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1
Kang, J. H., and M. S. Lee. "In vitro inhibition ofHelicobacter pyloribyEnterococcus faeciumGM-1." Canadian Journal of Microbiology 51, no. 8 (August 1, 2005): 629–36. http://dx.doi.org/10.1139/w05-044.
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A strain of Enterococcus faecium that exhibits antibacterial activity against Helicobacter pylori was isolated from the feces of newborn babies. This strain was selected for its ability to inhibit the growth of H. pylori and to withstand harsh environmental conditions, such as acidic pH and high bile concentration. Biochemical tests and 16S rRNA sequencing specific for Enterococcus faecium GM-1 were used to identify the isolated bacterial strain. In vitro studies were used to investigate the inhibitory effects of E. faecium GM-1 on H. pylori. These results showed that the culture supernatant of E. faecium GM-1 significantly decreased the viability and urease activity of H. pylori. This inhibitory activity remained after adjustment of pH of culture supernatant to neutral. However, treatment with proteolytic enzymes reduced the anti-H. pylori activity of GM-1. Therefore, some substance(s) of E. faecium GM-1 other than pH and lactic acid might be associated with this inhibitory activity. Analysis by electron microscopy also demonstrated that the addition of GM-1 destroyed the cell structure of H. pylori. Additional studies suggested that the binding of H. pylori to human colonial cells decreased in the presence of GM-1.Key words: Enterococcus faecium, Helicobacter pylori, inhibition, human fecal strain, proteinaceous substance(s).
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Jeong, Su Jin, Kyoung Hwa Lee, Jie-Hyun Kim, Soon Young Park, and Young Goo Song. "Efficacy and Gut Dysbiosis of Gentamicin-Intercalated Smectite as a New Therapeutic Agent against Helicobacter pylori in a Mouse Model." Antibiotics 9, no. 8 (August 10, 2020): 502. http://dx.doi.org/10.3390/antibiotics9080502.
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Helicobacter pylori eradication rate with conventional standard therapy is decreasing owing to antibiotic resistance, necessitating novel antibacterial strategies against H. pylori. We evaluated the efficacy of a gentamicin-intercalated smectite hybrid (S-GM)-based treatment and analyzed fecal microbiome composition in H. pylori-infected mice. To evaluate anti-H. pylori efficacy, mice were divided into eight groups, and H. pylori eradication was assessed by a Campylobacter-like organism (CLO) test and PCR assay of H. pylori in gastric mucosa. One week after H. pylori eradication, pro-inflammatory cytokine levels and atrophic changes in gastric mucosa were examined. Stool specimens were collected and analyzed for microbiome changes. The S-GM-based triple regimen decreased bacterial burden in vivo, compared with that in untreated mice or mice treated with other regimens. The therapeutic reactions in the CLO test from gastric mucosa were both 90% in the standard triple therapy and S-GM therapy group, respectively. Those of H. pylori PCR in mouse gastric mucosa were significantly lower in standard triple therapy and S-GM therapy groups than in the non-treatment group. Toxicity test results showed that S-GM therapy reduced IL-8 level and atrophic changes in gastric mucosa. Stool microbiome analysis revealed that compared with mice treated with the standard triple therapy, mice treated with the S-GM therapy showed microbiome diversity and abundant microorganisms at the phylum level. Our results suggested that S-GM is a promising and effective therapeutic agent against H. pylori infection.
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Fan, K., Q. Ruan, L. Sensenbrenner, and B. D. Chen. "Up-regulation of granulocyte-macrophage colony-stimulating factor (GM-CSF) receptors in murine peritoneal exudate macrophages by both GM-CSF and IL-3." Journal of Immunology 149, no. 1 (July 1, 1992): 96–102. http://dx.doi.org/10.4049/jimmunol.149.1.96.
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Abstract Murine peritoneal exudate macrophages (PEM) display multiple CSF receptors. In this study, the expression of granulocyte-macrophage (GM)-CSF receptors in PEM was studied. PEM displayed over 5000 single type, high affinity GM-CSF receptors/cell with a Kd = 38 to 42 pM and an apparent molecular mass of 86,000 Da. Treatment of PEM with low, but not high, concentrations of recombinant murine (rMu) GM-CSF continuously for 24 h resulted in a marked up-regulation of GM-CSF receptors in PEM. A similar up-regulation of GM-CSF receptors also was detected in PEM cultures treated with rMuIL-3 (1-100 ng/ml) for 24 h or longer, regardless the doses of rMuIL-3 added in this case. Scatchard analysis of equilibrium binding showed that the enhanced binding activities in both cases were due to an increase in total number of GM-CSF receptors rather than changes in receptor affinity. Contrariwise, treatment with recombinant human macrophage-CSF (greater than 100-1000 ng/ml) partially inhibited the expression of GM-CSF receptors in PEM. Removal of rMuGM-CSF from culture medium 24 h after treatment led to a further up-regulation of GM-CSF receptors over a 4 to 24-h period, depending on the doses of initial treatment. On the other hand, removal of rMuIL-3 from culture medium after prolonged treatment did not result in further increase in GM-CSF receptors. The protein synthesis inhibitor cycloheximide abrogated GM-CSF receptor up-regulation induced by both rMuIL-3 and rMuGM-CSF, whereas actinomycin D inhibited only the second (8-24 h) phase of GM-CSF receptor up-regulation induced by exposure to high concentrations rMuGM-CSF (10 ng/ml). These findings suggest that rMuGM-CSF and rMuIL-3 up-regulate GM-CSF receptors in PEM in part through similar or identical metabolic pathways and provide further evidence of a close linkage between IL-3 and GM-CSF receptors.
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Ali, Arif, Haroon Khan, Danial Kahrizi, Samreen Pervez, Ghallab Alotaibi, and Luca Rastrelli. "Nephroprotective effects of Helianthus annuus seeds extract in gentamicin induced nephrotoxic male mice." Cellular and Molecular Biology 68, no. 1 (May 22, 2022): 1–7. http://dx.doi.org/10.14715/cmb/2022.68.1.1.
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Acute kidney injury (AKI) causes a decrease in renal function which leads to failure in balancing electrolyte, fluid and acid-base homoeostasis. AKI is a damaging and life-threatening disorder, but it can be managed if identified earlier. This study aimed to investigate the possible nephroprotective effect of Helianthus annuus seeds extract against gentamicin (GM) induced nephrotoxicity in male mice. The control group (0.5 ml normal saline i.p.,), Gentamycin (GM) group (GM 100 mg/kg i.p), silymarin + GM group (silymarin 50 mg/kg and GM 100 mg/kg i.p.,), H. annuus extract (HAE) and GM, group (HAE 250 mg/kg and GM 100 mg/kg i.p), HAE2 + GM group (HAE2; 500 mg/kg and GM 100 mg/kg i.p) and H. annuus oil (HAO) + GM (HAO 2.5 ml/kg and GM 100 mg/kg i.p). Serum creatinine, urea and blood urea nitrogen (BUN) were significantly (P< 0.001) elevated in the GM group compared to the control group. The elevated level of serum creatinine, urea and BUN were decreased significantly (P<0.001) in groups treated with HAE and HAO extracts compared to the GM group. The kidney histopathological study from the GM group showed tubular necrosis, vacuolation and fibrosis. However, the animal that received HAE and HAO showed no tubular necrosis and vacuolation. Only mild inflammation was observed compared to the GM group. In conclusion, the extract caused marked radical scavenger and protected the kidney from oxidative damage of GM. H. annuus seeds contain strong antioxidant compounds, including flavonoids, phenolic acids, tocopherols and minerals, which could be responsible for the current show.
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Campbell, Ian K., Melissa J. Rich, Robert J. Bischof, Ashley R. Dunn, Dianne Grail, and John A. Hamilton. "Protection from Collagen-Induced Arthritis in Granulocyte-Macrophage Colony-Stimulating Factor-Deficient Mice." Journal of Immunology 161, no. 7 (October 1, 1998): 3639–44. http://dx.doi.org/10.4049/jimmunol.161.7.3639.
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Abstract The involvement of granulocyte-macrophage CSF (GM-CSF) in collagen-induced arthritis (CIA) was examined using GM-CSF-deficient mice. Although CIA is generally considered to be restricted to mice of the H-2q or H-2r haplotypes, we examined the role of GM-CSF in the CIA model using GM-CSF-deficient (−/−) and wild-type (+/+) mice on a C57BL/6 (H-2b) background. Mice were immunized by intradermal injection at the base of the tail with chick type II collagen followed by a repeat injection 21 days later. We found, based on both clinical and histologic assessments, that wild-type mice on this background developed severe CIA, while the GM-CSF-deficient mice had virtually no disease. Mice that were heterozygous for the GM-CSF gene (+/−) collectively displayed an intermediate response between those of the GM-CSF+/+ and GM-CSF−/− groups, suggesting a gene dosage effect. GM-CSF+/+ and GM-CSF+/− mice exhibited CIA responses ranging from mild (single digits) to severe swelling of all four paws, while in the few GM-CSF−/− mice that developed CIA the disease was confined to single digits. Despite the putative role of GM-CSF in dendritic cell development, GM-CSF-deficient mice exhibited both humoral and cellular (delayed-type hypersensitivity) responses to type II collagen; however, the cellular response was significantly reduced in the GM-CSF-deficient mice compared with the wild-type controls. These findings suggest that GM-CSF is required for CIA development in mice and support the idea that GM-CSF is a key cytokine in inflammatory joint disease.
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Reshetnyak, Tatiana M., Irina A. Doroshkevich, Natalia V. Seredavkina, Evgeny L. Nasonov, Igor V. Maev, and Vasiliy I. Reshetnyak. "The Contribution of Drugs and Helicobacter pylori to Gastric Mucosa Changes in Patients with Systemic Lupus Erythematosus and Antiphospholipid Syndrome." International Journal of Rheumatology 2019 (May 5, 2019): 1–18. http://dx.doi.org/10.1155/2019/9698086.
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Background. The nature and rate of gastric mucosal (GM) damage in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) remain to be among the unsolved problems. Objective. To define the role of H. pylori and drugs in the development of GM damages in SLE and APS. Methods. A study was conducted on 85 patients with SLE and APS. All the patients underwent esophagogastroduodenoscopy with targeted biopsy of the mucosa of the gastric body and antrum. The presence of H. pylori in the gastric biopsy specimens was determined using polymerase chain reaction. Results. Endoscopic examination revealed that the patients with SLE and APS on admission had the following GM changes: antral gastritis (82.4%), erosions (24.7%), hemorrhages (8.2%), and pangastritis (8.2%). SLE and APS patients showed no direct correlation between the found GM damages and the presence of H. pylori. The use of glucocorticoid, low-dose acetylsalicylic acid, nonsteroidal anti-inflammatory drug, and anticoagulant in SLE and APS patients is accompanied by GM damage. Conclusion. There was no evidence of the role of H. pylori in GM damage in the SLE and APS patients. More frequent detection of H. pylori was observed in anticoagulants or low-dose acetylsalicylic acid users than in glucocorticoids and nonsteroidal anti-inflammatory drugs ones.
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Bhamre, P. R., and A. E. Desai. "Impact of heavy metal compounds on oxygen consumption of freshwater mussel Lamellidens consobrinus (Lea)." South Asian Journal of Experimental Biology 2, no. 1 (March 19, 2012): 01–04. http://dx.doi.org/10.38150/sajeb.2(1).p01-04.
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The purpose of this study was to assess the toxic effects of heavy metal compounds like Cadmium chloride (CdCl2) and Zinc sulphate (ZnSo4) on respiratory metabolism of the freshwater mussel Lamellidens consobrinus.The effect was observed for 24, 48, 72 and 96 h exposure. On exposure of mussels to toxic concentrations the respiratory metabolic rate was found profoundly decreased after two hours of intoxication in Cadmium chloride (0.0863 ± 0.0032 mg/gm/l/h) and Zinc sulphate (0.1517 ± .0018 mg/gm/l/h). The oxygen consumption was continuously decreased up to 96 h in CdCl2 (0.0303 ± 0.0019 mg/gm/l/h) and ZnSo4 (0.0746. ± 0.0019 mg/gm/l/h).The decrease in metabolic rate was more prominent in cadmium chloride than zinc sulphate. This impact may be due to inhibition of enzymatic pathways and osmoregulatory response which depends on the time of exposure to heavy metal compounds used for experimental work.
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Negrette-Guzmán, Mario, Wylly Ramsés García-Niño, Edilia Tapia, Cecilia Zazueta, Sara Huerta-Yepez, Juan Carlos León-Contreras, Rogelio Hernández-Pando, Omar Emiliano Aparicio-Trejo, Magdalena Madero, and José Pedraza-Chaverri. "Curcumin Attenuates Gentamicin-Induced Kidney Mitochondrial Alterations: Possible Role of a Mitochondrial Biogenesis Mechanism." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–16. http://dx.doi.org/10.1155/2015/917435.
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It has been shown that curcumin (CUR), a polyphenol derived fromCurcuma longa, exerts a protective effect against gentamicin- (GM-) induced nephrotoxicity in rats, associated with a preservation of the antioxidant status. Although mitochondrial dysfunction is a hallmark in the GM-induced renal injury, the role of CUR in mitochondrial protection has not been studied. In this work, LLC-PK1 cells were preincubated 24 h with CUR and then coincubated 48 h with CUR and 8 mM GM. Treatment with CUR attenuated GM-induced drop in cell viability and led to an increase in nuclear factor (erythroid-2)-related factor 2 (Nrf2) nuclear accumulation and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) cell expression attenuating GM-induced losses in these proteins.In vivo, Wistar rats were injected subcutaneously with GM (75 mg/Kg/12 h) during 7 days to develop kidney mitochondrial alterations. CUR (400 mg/Kg/day) was administered orally 5 days before and during the GM exposure. The GM-induced mitochondrial alterations in ultrastructure and bioenergetics as well as decrease in activities of respiratory complexes I and IV and induction of calcium-dependent permeability transition were mostly attenuated by CUR. Protection of CUR against GM-induced nephrotoxicity could be in part mediated by maintenance of mitochondrial functions and biogenesis with some participation of the nuclear factor Nrf2.
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Newton, Robert, Elizabeth M. King, Wei Gong, Christopher F. Rider, Karl J. Staples, Neil S. Holden, and Martin W. Bergmann. "Glucocorticoids inhibit IL-1β-induced GM-CSF expression at multiple levels: roles for the ERK pathway and repression by MKP-1." Biochemical Journal 427, no. 1 (March 15, 2010): 113–24. http://dx.doi.org/10.1042/bj20091038.
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In the present study, IL (interleukin)-1β increased GM-CSF (granulocyte/macrophage colony-stimulating factor) expression from pulmonary A549 cells and primary HBE (human bronchial epithelial) cells. These responses were repressed by the glucocorticoid dexamethasone, allowing the use of A549 cells as a relevant model. IL-1β induced GM-CSF release into the culture medium by 6 h and in cell lysates (cytosolic) at 2 h. These effects were profoundly inhibited by dexamethasone, yet IL-1β-induced GM-CSF mRNA and unspliced nRNA (nuclear RNA; a surrogate of transcription rate) were modestly inhibited by dexamethasone at times up to 2 h. Although this indicates an effect on protein synthesis, actinomycin D chase experiments also indicated post-transcriptional repression by dexamethasone. Dexamethasone-dependent mRNA repression increased with time and was prevented by translational blockade. In addition, dexamethasone and the dissociated steroid RU24858 repressed GM-CSF release in an actinomycin D-sensitive manner, thereby implicating glucocorticoid-induced gene expression. At 2 h, IL-1β-induced expression of GM-CSF protein, but not mRNA, was sensitive to the MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase] inhibitors PD098059 and U0126. Although this indicates a role for the MEK/ERK pathway in GM-CSF translation, PD098059 subsequently destabilized GM-CSF mRNA. Dexamethasone and RU24858 both reduced IL-1β-induced ERK phosphorylation and increased MKP-1 (MAPK phosphatase-1) expression. Inhibition of ERK phosphorylation was reproduced by MKP-1 overexpression and prevented by MKP-1-targeting siRNA (small interfering RNA). Since MKP-1 prevented GM-CSF expression by transcriptional, post-transcriptional and translational processes, we propose that glucocorticoids induce MKP-1 expression to reduce both MEK/ERK activation and GM-CSF protein synthesis. Thus de novo gene expression, particularly of MKP-1, is involved in the repressive effects of glucocorticoids.
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Waksman, Y., D. W. Golde, N. Savion, and I. Fabian. "Granulocyte-macrophage colony-stimulating factor enhances cationic antimicrobial protein synthesis by human neutrophils." Journal of Immunology 144, no. 9 (May 1, 1990): 3437–43. http://dx.doi.org/10.4049/jimmunol.144.9.3437.
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Abstract We analyzed the effect of recombinant human granulocyte macrophage CSF (GM-CSF) on protein synthesis in peripheral blood polymorphonuclear leukocytes. GM-CSF enhanced PMN 35S-methionine incorporation 1.5-fold over a 2-h incubation period. The effect of GM-CSF on the synthesis of specific proteins was investigated by separating the radiolabeled proteins on SDS-PAGE followed by autoradiography. Stimulation of protein synthesis by GM-CSF was rapid (2 h), dose dependent, and affected at least 10 separate polypeptides. Using ion exchange chromatography some of the GM-CSF-enhanced proteins were identified to have a cationic nature, including the 37- and the 57-kDA proteins whose synthesis was increased by GM-CSF 2.4-fold and 1.6-fold, respectively. The cationic protein fractions from GM-CSF-primed and control cells were eluted from an ion exchange column and tested for their antimicrobial activity. An overall twofold increase in the amount of cationic proteins was recovered from GM-CSF-treated cells as compared to control cells, and these proteins showed a proportional enhanced killing of S. typhimurium. These results suggest that enhanced cationic protein synthesis is an important mechanism whereby GM-CSF can increase neutrophil microbicidal activity via nonoxidative pathways.
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Rudolph, Jens, Christian Seyboldt, Harald Granzow, and Nikolaus Osterrieder. "The Gene 10 (UL49.5) Product of Equine Herpesvirus 1 Is Necessary and Sufficient for Functional Processing of Glycoprotein M." Journal of Virology 76, no. 6 (March 15, 2002): 2952–63. http://dx.doi.org/10.1128/jvi.76.6.2952-2963.2002.
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ABSTRACT The functional cooperation of equine herpesvirus 1 (EHV-1) glycoprotein M (gM) and the gene 10 (UL49.5) product was analyzed. Transient-transfection experiments using gM and UL49.5 expression plasmids as well as RK13 cell lines constitutively expressing UL49.5 (RK49.5) or gM (RKgM) demonstrated that the endo-β-N-acetylglucosaminidase H (endo H)-resistant mature form of gM was detectable only after coexpression of the two proteins. Deletion of the EHV-1 UL49.5-homologous gene 10 in strain KyA resulted in a small-plaque phenotype and up to 190-fold-reduced virus titers. The growth defects of the mutant KyAΔ49.5 virus, which were very similar to those of a gM-negative KyA virus, could be completely compensated for by growth of the mutant virus on RK49.5 cells or by repairing the deletion of gene 10 in the revertant virus KyAΔ49.5R. Analysis of cells infected with the UL49.5-negative EHV-1 demonstrated that gM was not transported to the trans-Golgi network in the absence of the UL49.5 product. In contrast, gM was efficiently transported and processed to the endo H-resistant mature form in KyAΔ49.5-infected RK49.5 cells. Furthermore, radioimmunoprecipitation experiments demonstrated that gM maturation was observed only if a 10,000-M r protein was coprecipitated with gM in KyA- or KyAΔ49.5R-infected cells or virions. This protein was absent in cells infected with KyΔ49.5 or KyAΔgM, suggesting that it was the EHV-1 UL49.5 product. Taken together, our results demonstrate that the expression of the EHV-1 UL49.5 product is necessary and sufficient for gM processing and that it is required for efficient virus replication.
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Lemaire, I., H. Yang, V. Lafont, J. Dornand, T. Commes, and M. F. Cantin. "Differential effects of macrophage- and granulocyte-macrophage colony-stimulating factors on cytokine gene expression during rat alveolar macrophage differentiation into multinucleated giant cells (MGC): role for IL-6 in type 2 MGC formation." Journal of Immunology 157, no. 11 (December 1, 1996): 5118–25. http://dx.doi.org/10.4049/jimmunol.157.11.5118.
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Abstract Macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage (GM)-CSF stimulate the differentiation of rat alveolar macrophages (AM) into multinucleated giant cells (MGC) with distinct phenotypes (type 1 and type 2 MGC). In the present study, we analyzed the profile of cytokine gene expression induced respectively, by M-CSF and GM-CSF during rat AM differentiation using reverse transcription-PCR. Enhanced mRNA expression for IL-1alpha, TNF-alpha, and TGF-beta1 was observed 3 h after treatment with M-CSF (50 U/ml) or GM-CSF (50 U/ml). In contrast, IL-6 mRNA expression was increased by GM-CSF but not M-CSF. Kinetic analysis indicated that GM-CSF stimulated IL-6 expression early (1.5 h), with maximal effect observed at 24 h and up to 5 days thereafter. Increased mRNA levels for IL-6 were associated with higher IL-6 activity in the culture media of differentiating AM. IL-6 activity was stimulated 3 h after treatment with GM-CSF and increased with time (up to 5 days). Interestingly, addition of exogenous IL-6 (20-100 ng/ml) alone or in combination with GM-CSF to AM cultures increased slightly and selectively the formation of MGC with type 2 phenotype. Conversely, neutralization of endogenous IL-6 during AM differentiation into MGC inhibited significantly (up to 50%) the formation of type 2 MGC. These results suggest a role for IL-6 in the formation of type 2 MGC and provide some insights into the mechanisms of MGC formation and the processes that regulate it positively.
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Agostini, C., L. Trentin, R. Zambello, P. Bulian, C. Caenazzo, A. Cipriani, P. Cadrobbi, S. Garbisa, and G. Semenzato. "Release of granulocyte-macrophage colony-stimulating factor by alveolar macrophages in the lung of HIV-1-infected patients. A mechanism accounting for macrophage and neutrophil accumulation." Journal of Immunology 149, no. 10 (November 15, 1992): 3379–85. http://dx.doi.org/10.4049/jimmunol.149.10.3379.
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Abstract In this paper, the release of granulocyte-macrophage colony-stimulating factor (GM-CSF) in the lung of patients with HIV-1 infection was evaluated. This cytokine has well recognized effects on granulocyte and macrophage growth and differentiation and plays some role in the mechanisms leading to the accumulation of alveolar macrophages (AM) in patients with interstitial lung disease. Detectable levels of GM-CSF (up to 10 pg/ml) were demonstrated in unconcentrated bronchoalveolar lavage fluid retrieved from HIV-1-seropositive patients, thus suggesting that the GM-CSF is released in vivo in the lung during HIV-1 infection. A statistically significant correlation was demonstrated between the bronchoalveolar lavage concentrations of GM-CSF and the absolute numbers of AM and lung neutrophils. Cell-free supernatants obtained from unstimulated 24-h cultured AM isolated from HIV-1-infected patients contained discrete amounts of GM-CSF, as demonstrated by an immunoenzymatic assay. AM lost the capability of releasing GM-CSF after 72 h of culture, thus suggesting that the production of GM-CSF is not constitutive in AM. After exposition of AM with LPS, the release of GM-CSF and the expression of its mRNA significantly increased with respect to the baseline values; interestingly, the amount of GM-CSF released by LPS-stimulated AM was more than 10-fold higher in HIV-1-infected patients than in healthy subjects. As demonstrated by flow cytometry analysis, more than 70% of freshly isolated AM efficiently bound phycoerythrin-GM-CSF, thus indicating that they express the receptor for GM-CSF. Determination of AM in G1, S, and G2+M by flow cytometry showed that, after 48 h of culture with GM-CSF, 5.5 to 7% of AM entered the proliferative phase of the cell cycle. Taken together, these findings suggest that AM might represent an important source of GM-CSF production in HIV-1 infection. In particular, the hypothesis is formulated that pulmonary opportunists might trigger AM to synthesize GM-CSF in situ. The local overproduction of this cytokine is likely to play a role in the pathogenic events leading to the local proliferation of AM and recruitment of neutrophils in AIDS-associated interstitial lung disease.
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Fujiwara, Kunio, Masashi Shin, Hayato Matsunaga, Tetsuya Saita, and Lars-Inge Larsson. "Light-Microscopic Immunocytochemistry for Gentamicin and Its Use for Studying Uptake of the Drug in Kidney." Antimicrobial Agents and Chemotherapy 53, no. 8 (May 18, 2009): 3302–7. http://dx.doi.org/10.1128/aac.01627-08.
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ABSTRACT Gentamicin (GM) is a widely used antibiotic but shows renal toxicity. We produced a serum against GM (anti-GM) conjugated to bovine serum albumin with N-(gamma-maleimidobutyryloxy)succinimide. The antiserum was monospecific for GM and did not cross-react with the analog streptomycin, tobramycin, kanamycin, or amikacin. The antiserum also detected glutaraldehyde-fixed GM, and this enabled us to develop an immunocytochemical method for detecting the uptake of GM in rat kidney. Twelve hours after a single intravenous administration of GM, immunocytochemistry revealed that GM accumulated in the S1, S2, and S3 segments of the proximal tubules, as well as in the distal tubules and collecting ducts. By 12 h after injection, the drug was detected in cytoplasmic granules of the proximal tubule cells. However, early (1 h) after injection, drug accumulation was detected in the microvilli of these cells. The distal tubules and collecting ducts contained scattered swollen cells, reminiscent of necrotic cells, in which both the nuclei and the cytoplasm reacted strongly with GM. No staining occurred in the kidneys of saline-injected control rats. These results agree with previous studies showing that GM is endocytosed in the proximal tubules and accumulates in lysosomes. Additionally, our results show that GM also accumulates in the distal tubules and collecting ducts. This was achieved by systematically varying the pretreatment conditions—an approach necessary for detecting GM in different subcellular compartments. This approach should be useful for accurately detecting the uptake and toxicity of the antibiotic in different tissues.
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Ebisawa, M., M. C. Liu, T. Yamada, M. Kato, L. M. Lichtenstein, B. S. Bochner, and R. P. Schleimer. "Eosinophil transendothelial migration induced by cytokines. II. Potentiation of eosinophil transendothelial migration by eosinophil-active cytokines." Journal of Immunology 152, no. 9 (May 1, 1994): 4590–96. http://dx.doi.org/10.4049/jimmunol.152.9.4590.
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Abstract Activation of HUVEC monolayers by IL-1 beta or TNF-alpha induces migration of eosinophils across the endothelial monolayer (i.e., transendothelial migration) in vitro. In the present study, we demonstrate that culture of freshly isolated eosinophils in the presence of IL-5 for 24 to 48 h before use in the assay dramatically potentiated CD18-dependent eosinophil transendothelial migration through unstimulated endothelial monolayers. Granulocyte macrophage (GM)-CSF induced eosinophil transendothelial migration but did not induce neutrophil transendothelial migration. When IL-1 beta-activated endothelial cells were used, GM-CSF, IL-3, or IL-5 caused only modest potentiation of eosinophil transendothelial migration. Since activated endothelial cells are known to produce GM-CSF, we hypothesized that endothelial-derived GM-CSF might play a role in the process of IL-1 beta-induced eosinophil transendothelial migration. IL-1 beta-activated endothelial monolayers grown on the permeable supports produced 0.3 +/- 0.1 ng/ml of GM-CSF during a 4-h incubation and neutralizing Ab against GM-CSF inhibited eosinophil transendothelial migration by 48%, suggesting that endothelial-derived GM-CSF may participate in the response. Eosinophils purified from bronchoalveolar lavage 18 to 20 h after experimental Ag challenge in the lungs of allergic volunteers showed enhanced transendothelial migration, indicating that the cells may have undergone cytokine activation in vivo. Eosinophil-active cytokines may contribute to the preferential accumulation of eosinophils in vivo in part via potentiation of eosinophil transendothelial migration.
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Sukhan, D., and S. Vernigorodskiy. "Prognostic aspects of immunohistochemical assessment of cellular renewal and transcription factor SOX2 with precancerous changes in the gastric mucosa depending on the genotype of Helicobacter pylori in patients with various types of chronic gastritis." Reports of Vinnytsia National Medical University 22, no. 4 (December 28, 2018): 674–81. http://dx.doi.org/10.31393/reports-vnmedical-2018-22(4)-18.
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The precancerous potential of chronic gastritis (CG) associated with H. pylori is discussed in numerous writings, and today, CG is central to precancerous conditions of the stomach. A convincing theoretical basis for such an assessment of chronic gastritis is its characteristic feature — an interruption of cell renewal with the proliferation phase predominating over the differentiation phase. However, the determination of the degree of proliferative activity and impaired differentiation of the epithelium of the gastric mucosa (GM) remains not fully understood. The goal of our study was the immunohistochemical evaluation of the expression of Ki-67, Cyclin D1, p53, CPP32, HER2 and the Sox2 transcription factor in GM epithelial cells in patients with H. pylori-associated chronic gastritis.. To accomplish this goal, histological, cytological, immunohistochemical, molecular genetic, morphometric and statistical research methods were used. We found that in chronic H. pylori-associated non-atrophic gastritis (CNG) compared with H. pylori (-), the GM epithelium renewal rate increased, characterized by a significant increase in the expression of caspase-3 and Ki-67 proliferation markers, cyclin D1 (p <0.001) with expansion of the proliferative compartment and apoptosis zones. Ki-67, Cyclin D1, and p53 expression in severe dysplasia (SD) of GM was significantly (p <0.05) higher than the mild in patients with chronic non-atrophic and atrophic H. pylori-associated gastritis, despite a decrease in the expression of the transcription factor Sox2 and caspase-3 in cases of SD. The most specific marker for determining SD in patients with H. pylori-associated chronic gastritis was marker p53 (sensitivity 98.73%; specificity 83.38%, confidence interval 95%, p <0.05). Considering the immunohistochemical markers of H. pylori, a screening system has been developed for the early diagnosis of precancerous changes in the GM that will help optimize the treatment tactics of patients with chronic gastritis and increase the efficiency of detecting dysplastic and atrophic changes in the GM at their early stages of development.
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Beissert, S., J. Hosoi, S. Grabbe, A. Asahina, and R. D. Granstein. "IL-10 inhibits tumor antigen presentation by epidermal antigen-presenting cells." Journal of Immunology 154, no. 3 (February 1, 1995): 1280–86. http://dx.doi.org/10.4049/jimmunol.154.3.1280.
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Abstract IL-10 inhibits Langerhans cell (LC) Ag presentation to Th1 clones. As LC are capable of presenting tumor-associated Ags (TAA) for primary and secondary tumor immune responses, we examined the effect of IL-10 on LC Ag presentation in a model of immunity to the S1509a spindle cell tumor (H-2a). Because induction of immunity to S1509a requires exposure of LC to granulocyte-macrophage (GM)-CSF, this system also allowed us to study the regulatory interactions of GM-CSF and IL-10 on LC. Naive CAF1 (H-2a/d) mice could be immunized against S1509a by injection with GM-CSF-exposed and TAA-pulsed epidermal cells (EC) as assessed by inhibition of the growth of inoculated tumor cells. Incubation of EC in IL-10 before GM-CSF exposure completely inhibited Ag presentation in this system. Significantly, neither co-incubation of EC in IL-10 and GM-CSF (without preincubation in IL-10) nor IL-10 treatment after GM-CSF incubation was able to exert a down-regulatory effect. The ability of IL-10 to modulate EC presentation of TAA for a secondary immune response was also examined. EC were pulsed with TAA in vitro and then injected into a hind footpad of tumor-immune mice with 24 h swelling assessed as a measure of delayed-type hypersensitivity. Preincubation in IL-10 before TAA exposure significantly inhibited elicitation of delayed-type hypersensitivity with or without subsequent exposure to GM-CSF. Co-incubation of EC in IL-10 and GM-CSF or exposure to IL-10 after GM-CSF led to a normal response. These data indicate that IL-10 may serve as an important regulator of LC Ag-presenting function for tumor immune responses. IL-10 appears to specifically prevent the GM-CSF-induced maturation of LC Ag-presenting function when treatment with IL-10 occurs before exposure to GM-CSF but does not reverse the established mature state.
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DiPersio, J. F., P. Billing, R. Williams, and J. C. Gasson. "Human granulocyte-macrophage colony-stimulating factor and other cytokines prime human neutrophils for enhanced arachidonic acid release and leukotriene B4 synthesis." Journal of Immunology 140, no. 12 (June 15, 1988): 4315–22. http://dx.doi.org/10.4049/jimmunol.140.12.4315.
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Abstract Human recombinant granulocyte-macrophage CSF (GM-CSF) "primes" neutrophils for enhanced biologic responses to a number of secondary stimuli. Here, we examined the properties of neutrophil priming by GM-CSF and other growth factors such as human rTNF and granulocyte CSF. Although GM-CSF has a negligible direct effect on [3H]arachidonic acid release, it enhances or "primes" neutrophils for three- to fivefold increased release of [3H]arachidonic acid, induced by 1.0 microM A23187 and the chemotactants FMLP, platelet-activating factor, and leukotriene B4 (LTB4) (all 0.1 microM). The priming effects of GM-CSF were concentration- and time-dependent (maximum 100 pM, 1 h at 23 degrees C), and consistent with the determined dissociation constant of the human GM-CSF receptor. Indomethacin (10(-8) M), cycloheximide (100 micrograms/ml), and pertussis toxin (200 ng/ml, 2 h at 37 degrees C) had no effect on GM-CSF-, A23187, or platelet-activating factor-induced [3H]arachidonic acid release. The lipoxygenase inhibitor, nordihydroguaiaretic acid, however, totally abolished A23187-induced [3H]arachidonic acid release from both diluent- and GM-CSF-treated neutrophils. Consistent with this observation, we found that GM-CSF-pretreated neutrophils synthesize increased levels of LTB4 after stimulation with A23187 and chemotactic factors. GM-CSF enhances neutrophil arachidonic acid release and LTB4 synthesis, and thereby may amplify the inflammatory response to chemotactic factors and other physiologically relevant stimuli.
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Ren, Yudan, Susanne Bell, Helen L. Zenner, S. Y. Kathy Lau, and Colin M. Crump. "Glycoprotein M is important for the efficient incorporation of glycoprotein H–L into herpes simplex virus type 1 particles." Journal of General Virology 93, no. 2 (February 1, 2012): 319–29. http://dx.doi.org/10.1099/vir.0.035444-0.
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Herpes simplex virus type 1 glycoprotein M (gM) is a type III membrane protein conserved throughout the family Herpesviridae. However, despite this conservation, gM is classed as a non-essential protein in most alphaherpesviruses. Previous data have suggested that gM is involved in secondary envelopment, although how gM functions in this process is unknown. Using transfection-based assays, we have previously shown that gM is able to mediate the internalization and subcellular targeting of other viral envelope proteins, suggesting a possible role for gM in localizing herpesvirus envelope proteins to sites of secondary envelopment. To investigate the role of gM in infected cells, we have now analysed viral envelope protein localization and virion incorporation in cells infected with a gM-deletion virus or its revertant. In the absence of gM expression, we observed a substantial inhibition of glycoprotein H–L (gH–L) internalization from the surface of infected cells. Although deletion of gM does not affect expression of gH and gL, virions assembled in the absence of gM demonstrated significantly reduced levels of gH–L, correlating with defects of the gM-negative virus in entry and cell-to-cell spread. These data suggest an important role of gM in mediating the specific internalization and efficient targeting of gH–L to sites of secondary envelopment in infected cells.
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Brock, T. G., R. W. McNish, M. J. Coffey, T. C. Ojo, S. M. Phare, and M. Peters-Golden. "Effects of granulocyte-macrophage colony-stimulating factor on eicosanoid production by mononuclear phagocytes." Journal of Immunology 156, no. 7 (April 1, 1996): 2522–27. http://dx.doi.org/10.4049/jimmunol.156.7.2522.
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Abstract Granulocyte-macrophage CSF (GM-CSF) primes granulocytes for leukotriene (LT) synthesis. Here, we examined the effects of GM-CSF on arachidonic acid (AA) metabolism in rat alveolar macrophages (AM), peritoneal macrophages, and human peripheral blood monocytes. Pretreatment of AMs with GM-CSF for 24 h significantly increased the synthesis of immunoreactive LTB4 upon subsequent stimulation with calcium ionophore. Enhanced LT synthesis required a minimum of 6 h of GM-CSF pretreatment, suggesting that protein synthesis was required for enhanced LT production; indeed, cycloheximide completely abolished the GM-CSF effect on LT synthesis. HPLC analysis confirmed that GM-CSF primed AMs for enhanced generation of LTB4, as well as the 5-lipoxygenase products LTC, and 5-HETE. Moreover, parallel increases in other AA metabolites and free AA were observed following GM-CSF pretreatment. The enhanced production of all AA metabolites indicated that GM-CSF up-regulated AA release. Consistent with this, whole cell lysates from GM-CSF-treated AMs demonstrated increased phospholipase A2 (PLA2) activity. The increased activity was resistant to DTT, indicating the involvement of a PLA2 other than the 14-kDa PLA2s. By immunoblot analysis, GM-CSF treatment caused an increase in the 85-kDa PLA2 protein comparable to the observed increase in PLA2 activity. Unlike AMs, neither peritoneal macrophages nor peripheral blood monocytes showed increased eicosanoid generation or increased expression of the 85-kDa PLA2 protein following GM-CSF pretreatment. These results indicate that GM-CSF increases the capacity of AMs, but not peritoneal macrophages or peripheral blood monocytes, to generate eicosanoids. This effect results from increased PLA2 activity, due at least in part to increased levels of the 85-kDa PLA2 protein.
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Vallance, S. J., C. P. Downes, E. J. Cragoe, and A. D. Whetton. "Granulocyte-macrophage colony-stimulating factor can stimulate macrophage proliferation via persistent activation of Na+/H+ antiport. Evidence for two distinct roles for Na+/H+ antiport activation." Biochemical Journal 265, no. 2 (January 15, 1990): 359–64. http://dx.doi.org/10.1042/bj2650359.
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Macrophages respond to a variety of extracellular stimuli which can modulate the proliferation, development, activation and functional activity of these cells. The effects of two such agents, granulocytemacrophage colony-stimulating factor (GM-CSF, which stimulates proliferation) and platelet-activating factor (PAF, which stimulates chemotaxis and bactericidal activity), on cellular signal transduction mechanisms were compared. PAF can stimulate inositol lipid hydrolysis leading to Ca2+ mobilization. GM-CSF on the other hand has no effect on these events. Both agonists do, however, share an ability to activate an amiloride-sensitive Na+/H+ antiport and, furthermore, amiloride analogues are shown to inhibit the proliferative effects of GM-CSF on these cells. Long-term incubations with either PAF or GM-CSF demonstrate that it is only those cells pretreated with the latter which show a persistent activation of the antiport together with a sustained increase in intracellular pH. PAF-treated cells exhibit only a transitory increase in antiport activity, their intracellular pH levels returning to resting levels in spite of the continuous presence of the agonist in the medium. These effects of GM-CSF and PAF on Na+/H+ exchange are observed in both bicarbonate-free and bicarbonate-containing medium. These results lead us to suggest that the Na+/H+ antiport has a role in macrophage proliferation and in the regulation of intracellular pH during the oxidative burst stimulated by PAF and other agonists, and that differential mechanisms whereby this antiport is regulated exist in macrophages.
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Alderson, M. R., T. W. Tough, S. F. Ziegler, and R. J. Armitage. "Regulation of human monocyte cell-surface and soluble CD23 (Fc epsilon RII) by granulocyte-macrophage colony-stimulating factor and IL-3." Journal of Immunology 149, no. 4 (August 15, 1992): 1252–57. http://dx.doi.org/10.4049/jimmunol.149.4.1252.
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Abstract We have investigated the regulation of expression of cell-surface and soluble CD23 (sCD23) by purified human peripheral blood monocytes and in cultures of human whole blood. IL-3, IL-4, and GM-CSF were found to markedly enhance the expression of CD23 on the surface of elutriated monocytes and to increase levels of sCD23 in monocyte-culture supernatants. The induction of CD23 expression by monocytes was confirmed at the mRNA level by Northern blot analysis. The ability of GM-CSF, IL-3, or IL-4 to induce cell-surface CD23 on monocytes was inhibited by specific neutralizing antibodies to the corresponding cytokine. IL-3 and GM-CSF induced maximal surface CD23 expression on monocytes by 24 to 48 h, followed by a slight decline at 72 and 96 h. In contrast, IL-4 induced a progressive increase in monocyte CD23 expression that reached a maximum at approximately 72 h. IL-4, GM-CSF, and IFN-gamma increased both surface and soluble CD23 expression by the monocytic cell line U937, whereas IL-3 had no effect. The plasma from fresh human whole blood or nonstimulated whole blood cultured for 24 to 48 h contained detectable sCD23, and addition of IL-3, IL-4, or GM-CSF to these cultures resulted in increased levels of this molecule. Two-color flow cytometry revealed that IL-3, but not GM-CSF, also enhanced CD23 expression by B cells enriched from PBMC, although the effect of IL-3 was weak in comparison with that of IL-4. These findings may have important implications for the in vivo therapeutic use of these cytokines.
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Mussi, Fernanda Carneiro, Andreia Santos Mendes, Tassia Lacerda de Queiroz, Ana Lúcia Siqueira Costa, Álvaro Pereira, and Bruno Caramelli. "Pre-hospital delay in acute myocardial infarction: judgement of symptoms and resistance to pain." Revista da Associação Médica Brasileira 60, no. 1 (February 2014): 63–69. http://dx.doi.org/10.1590/1806-9282.60.01.014.
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Objective To estimate the time of decision (TD) to look for medical care and the time of arrival (TA) at the health service for men (M) and women (W) suffering from acute myocardial infarction and to analyze the influence of the interpretation of pain and pain resistance behaviors during these times. Methods This is an exploratory research, performed at the university hospital in Salvador/Bahia. 43 W and 54 M were interviewed. To study the dependence among sociodemographic and gender variables, the Fisher Exact Test was used. To analyze times, a geometric mean (GM) was used. In order to verify the association between the GM of TD and TA and the judgment of pain, and between the GM of TD and TA and the behavior of resistance to pain, as well as to test the time of interaction between the gender variable and other variables of interest, the robust regression model was used. The statistical significance adopted was 5%. Results The GM of the TD for M was 1.13 h; for W, 0.74 h. The GM of the TA was 1.74 h for M and 1.47 h for W. Those who did not recognize the symptoms of AMI and presented behavior of resistance to pain had higher TD and TA, being the associations significant. Gender did not change the associations of interest. Conclusion The findings demonstrate the importance of health education aiming at the benefits of early treatment.
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Shieh, J. H., R. H. Peterson, and M. A. Moore. "Cytokines and dexamethasone modulation of IL-1 receptors on human neutrophils in vitro." Journal of Immunology 150, no. 8 (April 15, 1993): 3515–24. http://dx.doi.org/10.4049/jimmunol.150.8.3515.
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Abstract Modulation of IL-1R on human neutrophils was investigated after in vitro treatment of cells with human recombinant (hr) granulocyte (G)-CSF, hrgranulocyte-macrophage (GM)-CSF, hrCSF-1, hrIL-1 alpha, hrIL-2, hrIL-3, hrIL-4, hrIL-5, hrIL-6, hrIL-7, transforming growth factor-beta 1, or hrTNF-alpha. At 4 degrees C, 125I-IL-1 binding was competed by IL-1 but not by other cytokines tested. At 37 degrees C, GM-CSF, TNF-alpha, and IL-1 decreased 125I-IL-1 binding in a dose-dependent manner. Kinetic studies showed that GM-CSF reduced > 45% IL-1 binding within 15 min but later (8 h) produced a > 2-fold increase. In contrast, TNF decreased > 85% IL-1 binding within 15 min with a recovery of > 80% relative to that of control after 24 h. Scatchard analysis revealed that TNF or GM-CSF down-modulation of IL-1 binding was due to a decrease of IL-1R number. Further studies showed that dexamethasone and GM-CSF (or G-CSF) synergistically increased IL-1 binding after 8 h. This synergistic modulation was a cytokine dose- and time-dependent process, and was due to an increase in IL-1R numbers rather than a change in binding affinity. In addition, human bone marrow neutrophils, cord blood neutrophils, and several human hematopoietic cell lines (HL-60, U-937, and AML-193) responded to dexamethasone and GM-CSF (or G-CSF) with a superadditive increase in IL-1 binding. Because mammalian systems respond to bacterial endotoxins with secretion of TNF, IL-1, glucocorticoids, G-CSF and GM-CSF, our results shed additional light on this highly regulated cytokine network and revealed a novel role for GM-CSF.
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Heidenreich, S., J. H. Gong, A. Schmidt, M. Nain, and D. Gemsa. "Macrophage activation by granulocyte/macrophage colony-stimulating factor. Priming for enhanced release of tumor necrosis factor-alpha and prostaglandin E2." Journal of Immunology 143, no. 4 (August 15, 1989): 1198–205. http://dx.doi.org/10.4049/jimmunol.143.4.1198.
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Abstract The macrophage-activating properties of murine recombinant granulocyte-macrophage (GM)-CSF were studied in murine peritoneal macrophages with respect to metabolism, endocytosis, PGE2 and TNF-alpha release, and tumor cytotoxicity. GM-CSF was found to be a potent stimulus for RNA and protein synthesis, glucose consumption, pinocytosis, and FcR-independent phagocytosis. Macrophages were activated by GM-CSF to kill TNF-alpha-insensitive Eb lymphoma cells but failed to generate cytotoxicity against TNF-alpha-sensitive L929 cells. Although GM-CSF alone was incapable of stimulating TNF-alpha release, it primed macrophages for elevated TNF-alpha production in response to IFN-gamma plus LPS. The priming effect of GM-CSF disappeared upon longer incubation (greater than 12 h) and was followed by a strongly reduced responsiveness to stimuli that release TNF-alpha. Late-stage suppression could be reverted by treatment with the cyclooxygenase blocker indomethacin, and GM-CSF-induced priming for enhanced TNF-alpha release was entirely restored. The responsible arachidonic acid product mediating suppression was found to be PGE2, because 1) GM-CSF-primed macrophages released enhanced amounts of PGE2 and 2) indomethacin-restored macrophages were again suppressed when exogenous PGE2 was added back in amounts produced by GM-CSF-primed macrophages. Although GM-CSF potently induced TNF-alpha gene transcription by 20 h of treatment, PGE2 interfered with translation into the secreted TNF-alpha protein. These data show that GM-CSF is capable of priming for the enhanced release of two factors, initially for TNF-alpha and subsequently for PGE2. The temporally delayed generation of these two mediators suggests an autoregulatory circuit in which the later produced PGE2 limits GM-CSF-induced macrophage activation.
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Aust, G., A. Hofmann, S. Laue, S. Ode-Hakim, and W. A. Scherbaum. "Differential regulation of granulocyte-macrophage colony-stimulating factor mRNA and protein expression in human thyrocytes and thyroid-derived fibroblasts by interleukin-1α and tumour necrosis factor-α." Journal of Endocrinology 151, no. 2 (November 1996): 277–85. http://dx.doi.org/10.1677/joe.0.1510277.
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Abstract In this study, we provide the first report on the production of granulocyte-macrophage colony-stimulating factor (GM-CSF) by human thyroid epithelial cells. Primary cultures of highly purified thyrocytes and thyroid-derived fibroblasts (n=3) and three thyroid anaplastic and one largely papillary carcinoma cell lines were exposed to different potent GM-CSF stimulators, employing interleukin 1α (Il-1α) and tumour necrosis factor-α (TNF-α). Cytokine mRNA levels were monitored by semiquantitative reverse transcriptase-PCR including an internal heterologous competitor fragment after 3, 6 and 18 h of culture. Culture supernatants were assayed for GM-CSF using a highly sensitive ELISA (detection limit ≤ 0·5 pg/ml) after 24 h. Basal GM-CSF mRNA expression was higher in fibroblasts and SW 1736 cells compared with thyrocytes, C 634, 8505 C and HTh 74 cells. GM-CSF was spontaneously secreted by fibroblasts (means ± s.e.m.; 43 ± 15 pg/ml), SW 1736 (59 ± 4 pg/ml), HTh 74 (34 ± 4 pg/ml) and C 643 cells (12 ± 1 pg/ml) but not by thyrocytes and 8505 C cells. Treatment with Il-1α (10 U/ml) resulted in a marked increase of GM-CSF mRNA within 3 h and an increase or induction of protein expression in thyrocyte (2350 ± 214 pg/ml), fibroblast (5242 ± 1400 pg/ml), SW 1736 (20016 ± 280 pg/ml) and C 643 cultures (1285 ± 79 pg/ml). Stimulation with TNF-α (10 U/ml) yielded divergent results. No significant increase of GM-CSF mRNA or protein expression was found in thyrocytes although TNF-α receptor expression in these cells is well documented. Stimulation with TNF-α resulted in an increased GM-CSF production in fibroblasts (361 ± 14 pg/ml), HTh 74 (148 ± 51 pg/ml) and SW 1736 cultures (235 ± 43 pg/ml). TSH (10 mU/ml) did not stimulate GM-CSF secretion in thyrocytes and HTh 74 cells, both expressing the TSH receptor. Phorbol 12-myristate 13-acetate (10 ng/ml) enhanced GM-CSF mRNA and protein levels in all cell types investigated. Our data suggest that both thyrocytes and fibroblasts synthesize GM-CSF in response to Il-1α, but only fibroblasts respond to TNF-α with a significant increase in GM-CSF. Anaplastic thyroid carcinomas are potential GM-CSF producers. Journal of Endocrinology (1996) 151, 277–285
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Tan, Xiaorong, Jiangning Xu, Fangneng Li, Miao Wu, Ding Chen, and Yifeng Liang. "Improved GM (1,1) Model by Optimizing Initial Condition to Predict Satellite Clock Bias." Mathematical Problems in Engineering 2022 (June 16, 2022): 1–10. http://dx.doi.org/10.1155/2022/3895884.
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The variation law of satellite clock bias (SCB) can be regarded as a grey system because the spaceborne atomic clock is very sensitive and vulnerable to many factors. GM (1,1) model is the core and foundation of the grey system, which has been highly valued and successfully applied in SCB prediction since its production. However, there are still some problems to be further studied such as the lack of stability of its prediction effect in practical application. In view of this, an improved GM (1,1) model by optimizing the initial condition has been proposed in this paper so as to increase the prediction performance. The new initial condition is obtained by the weighted combination of the latest and oldest components of the original clock bias sequence. And the weight values of these two components are acquired from a method of minimizing the sum of squares of fitting errors. We adopt GPS rapid precision SCB data provided by the International GNSS Service (IGS) for 15 mins, 30 mins, 1 h, 3 h, 6 h, 12 h, and 24 h prediction experiments. The results show that the improved GM (1,1) model is effective and feasible, and its prediction accuracy and stability are significantly better than those of the traditional GM (1,1) model, ARIMA model, and QP model, even for the SCB signal with obvious fluctuation.
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Panchal, Rakeshkumar Ramanlal, and Piyushbhai Vishnubhai Desai. "Study of Gibberellic Acid Production by Solid State Fermentation Using Fusarium Moniliforme Sheldon." International Journal of Applied Sciences and Biotechnology 4, no. 3 (September 26, 2016): 402–7. http://dx.doi.org/10.3126/ijasbt.v4i3.15588.
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Gibberellic acid production using Fusarium moniliforme, isolated from wilted sugarcane plant has been investigated by solid state fermentation (SSF). The gibberellic acid production of 154mgm/gm was obtained on commercial wheat bran (CWB) mineral salt acid bed in 500 ml flasks after 168 h incubation. The gibberellic acid production rate was about 0.6 to 0.9 mgm/gm/hr during 96 to 168 h. Different carbon sources namely sucrose, lactose, maltose, soluble starch, glycerol, wheat flour and maize flour were tested as an additional substrate along with CWB at the concentration of 25% w/w or v/w base to observe its effects on gibberellic acid production. Soluble starch has been proved the best additional carbon source for gibberellic acid production, which yielded 1160mgm/gm of gibberellic acid after 168 h. Similarly, various nitrogen sources namely NH4Cl, NH4NO3, (NH4)2SO4, (NH4)MoO4 and urea were tested as an additional substrate at the concentration of 0.07% w/w of CWB. Urea was proved as the best nitrogen source which yielded 532 mgm/gm of gibberellic acid after 168 h incubation. We have observed about 7.5-fold and 3.5-fold increase in gibberellic acid production upon addition of soluble starch and urea respectively, in CWB using Fusarium moniliforme.Int J Appl Sci Biotechnol, Vol 4(3): 402-407
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Heufler, C., F. Koch, and G. Schuler. "Granulocyte/macrophage colony-stimulating factor and interleukin 1 mediate the maturation of murine epidermal Langerhans cells into potent immunostimulatory dendritic cells." Journal of Experimental Medicine 167, no. 2 (February 1, 1988): 700–705. http://dx.doi.org/10.1084/jem.167.2.700.
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Freshly isolated, murine epidermal Langerhans cells (LC) are weak accessory cells for primary T cell-dependent immune responses, but increase their stimulatory capacity at least 20-fold progressively over a 3-d culture with keratinocytes. We have studied the mediators of LC maturation. LC enriched from 12-h epidermal cultures by negative selection do not survive when cultured for 60 h in standard medium. LC survive and show increased stimulatory capacity for oxidative mitogenesis and the primary MLR when 30% keratinocyte-conditioned medium is included. Of the three cytokines that are known to be produced by keratinocytes, only granulocyte/macrophage CSF (GM-CSF) maintains viability and increases stimulatory capacity. IL-1 alone does not keep LC alive, but further enhances the stimulatory activity when combined with GM-CSF. IL-3 has no effect. The increase in LC stimulatory capacity is not due to increased Ia antigen expression, which does not change between 12 and 60 h. Function is not simply due to improved viability, as GM-CSF does not enhance the function of 12-h LC when added to the short-term oxidative mitogenesis assay. By generating LC with strong stimulating activity for resting T cells, GM-CSF and IL-1 may be critical in the sensitization phase of T cell-mediated immunity.
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Bickel, M., R. B. Cohen, and D. H. Pluznik. "Post-transcriptional regulation of granulocyte-macrophage colony-stimulating factor synthesis in murine T cells." Journal of Immunology 145, no. 3 (August 1, 1990): 840–45. http://dx.doi.org/10.4049/jimmunol.145.3.840.
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Abstract The granulocyte-macrophage CSF (GM-CSF) gene is known to be controlled at a variety of levels in different cell types. We showed previously that GM-CSF production by lectin or phorbol ester (12-O-tetradecanoyl-phorbol-13-acetate (TPA]-treated T cells was unaffected by cyclosporin A whereas IL-2 and IL-3 expression were. Cyclosporin A is thought to inhibit transcription that suggests that IL-2 and IL-3 are regulated primarily at the transcriptional level while GM-CSF is not. The lack of coordinate gene expression is of particular interest because all three mRNA share the presence of adenosine uridine-rich sequences in the 3' untranslated region and these sequences are believed to act by modulating mRNA stability. We measured the level of GM-CSF mRNA in untreated cells and found it to be extremely low. GM-CSF mRNA levels increased approximately 60-fold within 6 h of TPA-treatment. Nuclear run-on transcription analysis of the same cells showed readily detectable GM-CSF transcription in unstimulated cells that increased less than twofold after TPA treatment. However, IL-2 transcription was insignificant before TPA addition. Actinomycin D chase experiments showed that GM-CSF transcripts in untreated cells have a very short half-life (approximately 45 min) although transcripts in TPA-treated cells have a half-life exceeding 3 h. These findings indicate that GM-CSF production in EL-4 cells treated with TPA is regulated predominantly by modulation of cytoplasmic mRNA half-life.
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Xu, Xiaoxiang, Heyin Chen, Xia Wu, Sen Chen, Jing Qi, Zuhong He, Shengyu Zou, et al. "Hollow Mesoporous Silica@Zeolitic Imidazolate Framework Capsules and Their Applications for Gentamicin Delivery." Neural Plasticity 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/2160854.
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We have synthesized hollow mesoporous silica (HMS) at a zeolitic imidazolate framework (ZIF) capsule that can be used as a drug delivery system for gentamicin (GM). The GM is first loaded into HMS. Then, the outer surface of the GM/HMS is coated with uniformed ZIF nanoparticles (denoted as GM/HMS@ZIF). The GM/HMS@ZIF has been successfully prepared and acts as a capsule for GM. The GM/HMS@ZIF shows a good biocompatibility and a good cellular uptake in House Ear Institute-Organ of Corti 1 (HEI-OC1) cells. The GM is released slowly within 10 h under acidic conditions, which is used to simulate the pH of the endosome and lysosome compartments. The in vivo assay shows that the signal from fluorescein isothiocyanate (FITC) can be observed after 15 days, when the mice were injected with FITC/HMS@ZIF. This opens new opportunities to construct a delivery system for GM via one controlled low dose and sustained release for the therapy of Ménière’s disease.
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Greiber, Stefan, Barbara Müller, Petra Daemisch, and Hermann Pavenstädt. "Reactive Oxygen Species Alter Gene Expression in Podocytes: Induction of Granulocyte Macrophage-Colony-Stimulating Factor." Journal of the American Society of Nephrology 13, no. 1 (January 2002): 86–95. http://dx.doi.org/10.1681/asn.v13186.
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ABSTRACT. It has been suggested that reactive oxygen radicals (ROS) play a crucial role in the pathogenesis of proteinuria and podocyte injury. It was investigated whether changes in gene expression might account for ROS-induced podocyte dysfunction. Differentiated podocytes were incubated with control media or with exogenous ROS from the xanthine/xanthine-oxidase reaction for 4 h. A PCR-based suppressive subtractive hybridization assay was applied to isolate and clone mRNAs that were differentially expressed by exogenous ROS. One differentially expressed clone was identified as the proinflammatory cytokine granulocyte macrophage-colony-stimulating factor (GM-CSF). Regulation of GM-CSF in podocytes was further studied by Northern analysis and enzyme-linked immunosorbent assay. Exogenous ROS caused a concentration-dependent, >10-fold induction of GM-CSF mRNA after 4 h. A >50-fold increase in GM-CSF protein release in podocytes that had been stimulated with ROS could be detected. Induction of GM-CSF protein was inhibited by actinomycin D, which indicated that increased mRNA transcription was involved. The ROS scavengers dimethyl-thio-urea and pyrrolidone-dithio-carbamate strongly inhibited increased GM-CSF production induced by ROS. GM-CSF release was also induced when internal ROS production was triggered with NADH, whereas H2O2 had only a small effect. GM-CSF release by podocytes was also stimulated by lipopolysaccharide (LPS), interleukin-1 (IL-1), and phorbolester (PMA). Dimethyl-thio-urea significantly inhibited the LPS-, IL-1-, and PMA-induced GM-CSF production. Activation of the transcription factor nuclear factor-κB (NF-κB) but not activator protein-1 was involved in the upregulation of ROS-induced GM-CSF production. The data indicate that GM-CSF is differentially expressed by ROS in podocytes. ROS also partially mediate the effects of PMA and IL-1 on podocyte GM-CSF production. Because GM-CSF can enhance glomerular inflammation and induces mesangial proliferation, these data might provide further insight into the mechanisms of ROS-induced glomerular injury.
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Massey, W., B. Friedman, M. Kato, P. Cooper, A. Kagey-Sobotka, L. M. Lichtenstein, and R. P. Schleimer. "Appearance of granulocyte-macrophage colony-stimulating factor activity at allergen-challenged cutaneous late-phase reaction sites." Journal of Immunology 150, no. 3 (February 1, 1993): 1084–92. http://dx.doi.org/10.4049/jimmunol.150.3.1084.
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Abstract The cytokines IL-3 and granulocyte-macrophage CSF (GM-CSF) activate and/or prime monocytes, basophils, and eosinophils for a number of proinflammatory events in vitro. It was hypothesized that IL-3 and GM-CSF might also participate in the local inflammatory cascades that occur at cutaneous blister sites after Ag challenge in vivo. The M-07e megakaryocytic leukemia cell line, which proliferates in response to IL-3 or GM-CSF, was used to determine whether these cytokines were present in fluids derived after Ag challenge in the cutaneous blister chamber model. Fluids from blister chambers after either Ag (timothy grass, orchard grass, or ragweed) or vehicle control challenge were collected hourly for 12 h from nine patients with allergic rhinitis. Cytokine (IL-3/GM-CSF) activity was modestly elevated at 4 h after Ag challenge compared to control with the median of maximal proliferation 4% (range, 2 to 22%) vs 2% (range, 1 to 14%), respectively (Ag vs control, p < 0.03). Activity peaked at 7 h (Ag = 10%, range 1 to 12%, vs control = 1%, range 1 to 9%, p < 0.02) and then steadily declined. No increase in cytokine activity over control was seen in Ag-challenged nonatopics (n = 5, p = NS), indicating that release did not result from a nonspecific effect of the Ag solution. Neutralization of cytokine bioactivity in pooled late phase reaction (LPR) fluids from h 4 to 12 (n = 5) with anti-IL-3, anti-GM-CSF, or both antisera revealed that the majority of the activity was GM-CSF. To better quantify cytokine levels, pooled LPR fluids prepared from an additional 11 subjects were concentration-dialyzed (10x) and tested for cytokine activity. Pooled fluids from Ag-challenged sites contained a median of 625 pg/ml (range, 30 to 1250 pg/ml) GM-CSF equivalents, whereas those from the vehicle control-challenged sites contained a median 30 pg/ml (range, 30 to 300 pg/ml) GM-CSF equivalents (p < 0.004 Ag vs control groups, n = 11). Concentrated fluid from Ag- and control-challenged sites in two nonatopic subjects contained < 10 pg/ml cytokine activity. To evaluate the IL-3 and GM-CSF activity with a separate technique, ELISA were performed on separately pooled blister fluids from six atopic subjects. Although no IL-3 activity was detected after Ag challenge in these six subjects, all of them demonstrated levels of GM-CSF at Ag-challenged sites comparable to that found in the bioassay.(ABSTRACT TRUNCATED AT 400 WORDS)
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Das, Ashutosh, Mukta Das Gupta, Md Kabirul Islam Khan, Md Moksedul Momin, and Omar Faruk Miazi. "Genetic and phenotypic parameter estimates for body weight and egg production at sexual maturity in Hilly×Fayoumi crossbred chickens." Asian Journal of Medical and Biological Research 4, no. 2 (September 30, 2018): 186–92. http://dx.doi.org/10.3329/ajmbr.v4i2.38254.
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A crossbreeding experiment between Hilly, a locally adapted chicken type in Bangladesh and Fayoumi, an egg type light chicken breed was carried out to evaluate phenotypic performances and to estimate genetic parameters for body weight and egg production at sexual maturity. Results show the mean hatch weight of Hilly♂ × Fayoumi♀ (H♂×F♀) crosses was 35±0.1 gm. In this study, H♂×F♀ crossbred showed a heavier body weight (1551± 32.0 gm/bird) at 20 weeks in comparison with other indigenous chicken genotypes in Bangladesh. The highest body weight gain was found in 8-10 weeks of age. H♂×F♀ crossbred hens exhibited sexual maturity at an average age of 147.5±1.6 days with an average body weight of 1350± 16.8 gm/bird. The mean weight of eggs at sexual maturity was 33.7±0.5 gm/egg. The estimates of heritability for body weight were ranged from 0.15 to 0.26. We observed a positive genetic correlation between weight at sexual maturity (WSM) and egg weight at sexual maturity (EWSM), meaning that hens with high weight at sexual maturity would produce heavier eggs.Asian J. Med. Biol. Res. June 2018, 4(2): 186-192
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Blackwell, Brad G., James E. Leggett, Curtis A. Johnson, Stephen W. Zimmerman, and William A. Craig. "Ampicillin and Sulbactam Pharmacokinetics and Pharmacodynamics in Continuous Ambulatory Peritoneal Dialysis (CAPD)." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 10, no. 3 (July 1990): 221–26. http://dx.doi.org/10.1177/089686089001000307.
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The fixed combination antibiotic ampicillin/sulbactam may provide a new, safe, and effective method of treating dialysis-related bacterial peritonitis. The pharmacokinetics of this antibiotic combination were determined in patients receiving continuous ambulatory peritoneal dialysis (CAPD). The pharmacodynamic activity of this drug was also determined by use of mean bactericidal titers against selected bacterial strains. Six noninfected CAPD patients in a randomized twoway crossover study were given a fixed dose of ampicillin (2 gm) and sulbactam (1 gm) either intravenously or intra peritoneally. The mean peak ampicillin and sulbactam serum concentrations following intravenous dosing were 170.3 and 87.5 μg/mL, respectively. The mean peak serum concentrations of ampicillin and sulbactam following intraperitoneal dosing were 48.0 an d 27.8 μg/mL, respectively. Absolute bioavailabilities of the intraperitoneal ampicillin and sulbactam doses were 60% and 68%. Both drugs exhibited similar distribution and elimination characteristics. Renal failure markedly reduced drug elimination. Intraperitoneal administration of ampicillin/sulbactam provided satisfactory inhibitory and bactericidal antibiotic titers for most organisms in dialysate at 6 h but not 24 h. Ampicillin/sulbactam (2 gm/1 gm) should be administered every 12 h to patients with peritoneal dialysis-related peritonitis.
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Catalá, M. G., D. Izquierdo, R. Romaguera, M. Roura, and M. T. Paramio. "334 EFFECT OF A GROWTH MEDIUM DURING IVM ON EMBRYO DEVELOPMENT OF PREPUBERTAL EWE OOCYTES." Reproduction, Fertility and Development 22, no. 1 (2010): 323. http://dx.doi.org/10.1071/rdv22n1ab334.
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The aim of this study was to assess the effect of an in vitro growth medium (De Wu et al. 2006 Biol. Rep. 75, 547-554) in prepubertal ewe oocytes selected by the brilliant cresyl blue (BCB) test. Prepubertal ewe oocytes were recovered by slicing ovaries of slaughtered animals and immediately exposed during 1 h to 13 μM BCB and classified according to their cytoplasm coloration (Rodriguez-Gonzalez E et al. 2002 Theri- ogenology 57(5), 1397-1409): BCB+ (blue cytoplasm, hypothetically grown oocytes) and BCB- (uncolored cytoplasm, hypothetically growing oocytes). Uncolored oocytes (BCB-) were matured using three culture media: growth medium (GM: TCM-199, 0.04 μg mL-1 FSH, 0.04 μg mL-1 LH, 0.004 μg mL-1 estradiol, 100 μg mL-1 ascorbic acid, and 5 μL mL-1 ITS: insulin transferrin selenium), conventional maturation medium (CM: TCM-199, 10 μg mL-1 FSH, 10 μg mL-1 LH and 1 μg mL-1 estradiol) and modified maturation medium (MM: CM with the addition of 100 μg mL-1 ascorbic acid and 5 μL mL-1 ITS). Oocytes were matured in GM for 12 h and then separated into 2 groups, CM (GM+CM) and MM (GM+MM) for another 12 h of maturation. Two extra groups of BCB- oocytes were directly cultured for 24 h in CM or MM media (BCB-/CM and BCB-/MM). Colored oocytes (BCB+) and a control group (oocytes not exposed to BCB) were matured for 24 h in CM. All groups were cultured at 38.5°C and 5% CO2 in humidified atmosphere. Fertilization took place in SOF medium supplemented with 10% of estrous sheep serum during 20 h with a sperm concentration of 1 × 106 spermatozoa/mL. Presumptive zygotes were cultured for 8 days in SOF with 10% FCS at 38.5°C, 5% CO2 and 5% O2. Results are shown in Table 1. The percentage of morula plus blastocyst obtained from BCB - oocytes was significantly increased in oocytes exposed to growth medium (containing ITS, ascorbic acid and low hormone concentrations; groups GM+CM and GM+MM) for the first 12 h. An increasing tendency has also been observed in blastocyst yield in these two groups. Regarding maturation rate, no differences were found in all groups (data not shown). In conclusion, as De Wu et al. (2006) showed in prepubertal gilts, we also achieved some improvements in embryo development of growing oocytes when the first 12 h of maturation took place in a growth medium. However, embryo developmental potential of BCB- oocytes is still lower compared with that of BCB+ oocytes. Table 1.Effect of GM on embryo development of BCB- oocytes Grant sponsor Spanish Ministry of Science and Innovation.Code: AGL2007-60227-CO2-01
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Burg, Jürgen, Vera Krump-Konvalinkova, Fernando Bittinger, and Charles James Kirkpatrick. "GM-CSF expression by human lung microvascular endothelial cells: in vitro and in vivo findings." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 2 (August 1, 2002): L460—L467. http://dx.doi.org/10.1152/ajplung.00249.2001.
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Recently, many findings indicate that granulocyte-macrophage colony-stimulating factor (GM-CSF) plays an important role in the pathogenesis of acute and chronic lung diseases. In the present paper, the production of this cytokine in human pulmonary microvascular endothelial cells (HPMEC) is investigated. In an in vitro study, quiescent HPMEC did not express GM-CSF, either at the transcriptional or at the protein level. After activation for 4 h with tumor necrosis factor (TNF)-α (30/300 U/ml), lipopolysaccharide (LPS; 0.1/1 μg/ml), or interleukin (IL)-1β (100 U/ml), a significant release of GM-CSF was measured by enzyme-linked immunosorbent assay, with a time-dependent increase over 72 h. IL-8 (4, 16, or 64 ng/ml) or IL-1β at a concentration of 10 U/ml did not induce the release of GM-CSF. Human umbilical vein endothelial cells (HUVEC) and the angiosarcoma cell line HAEND served as reference cell lines. GM-CSF release in HPMEC was significantly ( P < 0.025–0.05) less inducible by IL-1β than in HUVEC. A constitutive expression of GM-CSF by HAEND was observed. Additionally, GM-CSF expression in vivo by the lung microvasculature was confirmed by immunohistochemistry in lung tissue. To our knowledge, this is the first report of the ability of human pulmonary endothelial cells to synthesize and release GM-CSF. These results support the hypothesis that the lung microvasculature via the production of GM-CSF is a potential contributor to the cytokine network in lung diseases. This could be of particular importance in the pathogenesis of the acute respiratory distress syndrome in which endothelial dysfunction plays a central pathogenetic role.
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Shieh, J. H., R. H. Peterson, and M. A. Moore. "Bacterial endotoxin regulation of cytokine receptors on murine bone marrow cells: in vivo and in vitro study." Journal of Immunology 152, no. 2 (January 15, 1994): 859–66. http://dx.doi.org/10.4049/jimmunol.152.2.859.
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Abstract Bacterial endotoxin (LPS) modulation of CSF-1, granulocyte-macrophage (GM)-CSF, G-CSF, IL-1, TNF, and Kit Ligand receptors on murine bone marrow cells (BMC) in vivo and in vitro was investigated. In vivo LPS reduced the binding of hrIL-1 (> 90%), mrTNF (> 62%), mrGM-CSF (> 42%) and hrG-CSF (> 91%) to BMC within 2 h, but elevated IL-1 binding (> 8.4-fold) between 8 to 48 h. In vitro, LPS decreased G-CSF and IL-1 binding after 8 h yet increased TNF binding in a dose-dependent manner, suggesting that in vivo, the LPS up-regulation of IL-1 binding to BMC was indirect. Because in vivo LPS elevated the levels of TNF, IL-6, GM-CSF, and glucocorticoids, we further examined GM-CSF and TNF modulation of cytokine receptors on BMC in vivo. In vivo, TNF decreased the binding of TNF (> 88%), G-CSF (> 89%), and IL-1 (> 73%) within 30 min, but increased IL-1 binding (> 4.8-fold) after 10 h. In contrast, in vitro TNF decreased IL-1 binding after 8 h, implying that in vivo TNF up-regulation of Il-1 binding to BMC was also due to an indirect mechanism. However, GM-CSF increased IL-1 binding to BMC both in vivo and in vitro after 8 h. Further studies showed that in vitro GM-CSF and dexamethasone synergistically increased IL-1 binding to BMC in a time- and dose-dependent manner. This synergistic modulation depended on synthesis of protein and mRNA, and was due to an increase in receptor number rather than an increase in receptor affinity. Because in vivo, LPS and LPS-induced cytokines (IL-1 and TNF) elicited the secretion of glucocorticoid and CSF activities, our results revealed a mechanism for LPS up-modulation of IL-1R on BMC in vivo.
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Lalor, D. J., B. Truong, S. Henness, A. E. Blake, Q. Ge, A. J. Ammit, C. L. Armour, and J. M. Hughes. "Mechanisms of serum potentiation of GM-CSF production by human airway smooth muscle cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 5 (November 2004): L1007—L1016. http://dx.doi.org/10.1152/ajplung.00126.2004.
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Inflammation and vascular leakage are prevalent in asthma. This study aimed to elucidate the mechanisms involved in serum potentiation of cytokine-induced granulocyte macrophage colony stimulating factor (GM-CSF) production by human airway smooth muscle cells and to identify possible factors responsible. Serum-deprived cells at low density were stimulated with TNF-α and IL-1β for 24 h. Human AB serum (10%), inhibitors of RNA and protein synthesis or specific signaling molecules, or known smooth muscle mitogens were then added for 24 h. Culture supernatants were analyzed for GM-CSF levels, and cells were harvested to assess viability, cell cycle progression, GM-CSF-specific mRNA content, and p38 phosphorylation. Serum potentiated GM-CSF release when added before, together with (maximal), or after the cytokines. The potentiation involved both new GM-CSF-specific mRNA production and protein synthesis. The mitogens IGF, PDGF, and thrombin all potentiated GM-CSF release, and neutralizing antibodies for EGF, IGF, and PDGF reduced the serum potentiation. Inhibitor studies ruled as unlikely the involvement of p70S6kinase and the MAPK p42/p44, two signaling pathways implicated in proliferation, and the involvement of the MAPK JNK, while establishing roles for p38 MAPK and NF-κB in the potentiation of GM-CSF release. Detection of significant p38 phosphorylation in response to serum stimulation, through Western blotting, further demonstrated the involvement of p38. These studies have provided evidence to support p38 being targeted to interrupt the cycle of inflammation, vascular leakage and cytokine production in asthma.
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Lardon, F., DR Van Bockstaele, HW Snoeck, and ME Peetermans. "Quantitative cell-cycle progression analysis of the first three successive cell cycles of granulocyte colony-stimulating factor and/or granulocyte-macrophage colony-stimulating factor-stimulated human CD34+ bone marrow cells in relation to their colony formation." Blood 81, no. 12 (June 15, 1993): 3211–16. http://dx.doi.org/10.1182/blood.v81.12.3211.3211.
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Abstract The bromodeoxyuridine (BrdU)-Hoechst flow cytometric technique was applied to study the immediate cell kinetic response of highly purified human (h) bone marrow progenitor cells (CD(34+)-sorted fraction) to h granulocyte colony-stimulating factor (G-CSF) and/or h granulocyte- macrophage colony-stimulating factor (GM-CSF). The technique permits us to differentiate cycling from noncycling cells and to make a quantitative assessment of cell cycles after stimulation. Semisolid agar and single-cell liquid cultures were also performed to compare these initial events to the effects observed after 14 days of culture. The combination of G-CSF plus GM-CSF, acting synergistically in day 14 cultures, was found to have a subadditive effect in the first cell cycles, thereby indicating partial overlap of the different target cells. However, this combination accelerated transit through the cell cycle, as could be seen from the higher number of cells in the third cell cycle after 72 hours of stimulation. We conclude that, apart from the unresponsive cells, the CD34+ compartment consists of cells responsive to both G-CSF and GM-CSF, and cells responsive to either one of the CSFs alone, and that the combination of the two CSFs speeds up the cell cycle traverse rate for a significant fraction of the target cells that are initially responsive for both G-CSF and GM-CSF. The latter supports the hypothesis of an overlapping signalling pathway of G-CSF and GM-CSF.
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Lardon, F., DR Van Bockstaele, HW Snoeck, and ME Peetermans. "Quantitative cell-cycle progression analysis of the first three successive cell cycles of granulocyte colony-stimulating factor and/or granulocyte-macrophage colony-stimulating factor-stimulated human CD34+ bone marrow cells in relation to their colony formation." Blood 81, no. 12 (June 15, 1993): 3211–16. http://dx.doi.org/10.1182/blood.v81.12.3211.bloodjournal81123211.
Full textAbstract:
The bromodeoxyuridine (BrdU)-Hoechst flow cytometric technique was applied to study the immediate cell kinetic response of highly purified human (h) bone marrow progenitor cells (CD(34+)-sorted fraction) to h granulocyte colony-stimulating factor (G-CSF) and/or h granulocyte- macrophage colony-stimulating factor (GM-CSF). The technique permits us to differentiate cycling from noncycling cells and to make a quantitative assessment of cell cycles after stimulation. Semisolid agar and single-cell liquid cultures were also performed to compare these initial events to the effects observed after 14 days of culture. The combination of G-CSF plus GM-CSF, acting synergistically in day 14 cultures, was found to have a subadditive effect in the first cell cycles, thereby indicating partial overlap of the different target cells. However, this combination accelerated transit through the cell cycle, as could be seen from the higher number of cells in the third cell cycle after 72 hours of stimulation. We conclude that, apart from the unresponsive cells, the CD34+ compartment consists of cells responsive to both G-CSF and GM-CSF, and cells responsive to either one of the CSFs alone, and that the combination of the two CSFs speeds up the cell cycle traverse rate for a significant fraction of the target cells that are initially responsive for both G-CSF and GM-CSF. The latter supports the hypothesis of an overlapping signalling pathway of G-CSF and GM-CSF.
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Koyama, Sekiya, Etsuro Sato, Tsuyoshi Masubuchi, Akemi Takamizawa, Hiroshi Nomura, Keishi Kubo, Sonoko Nagai, and Takateru Izumi. "Human lung fibroblasts release chemokinetic activity for monocytes constitutively." American Journal of Physiology-Lung Cellular and Molecular Physiology 275, no. 2 (August 1, 1998): L223—L230. http://dx.doi.org/10.1152/ajplung.1998.275.2.l223.
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We determined whether human lung fibroblasts (HLFs) might release mediators that are responsible for monocyte chemokinetic activity (MCA) constitutively. HLF supernatant fluids showed MCA in a time-dependent manner ( P < 0.001). Checkerboard analysis of 24- and 72-h supernatant fluids showed that the activity was chemokinetic. Partial characterization of 24- and 72-h supernatant fluids revealed that the mediators released after 24 h were predominantly composed of lipid-soluble activity, and MCA was blocked by lipoxygenase inhibitors. The mediators released after 72 h were predominantly trypsin sensitive and blocked by cycloheximide. Molecular-sieve column chromatography identified four peaks of MCA. A polyclonal antibody to monocyte chemoattractant protein-1 (MCP-1) inhibited MCA by 20% after 24 h and by 40% after 72 h. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and transforming growth factor-β (TGF-β) antibodies attenuated MCA released after 72 h by 30 and 10%, respectively. These antibodies inhibited corresponding molecular-weight peaks separated by molecular-sieve column. The concentrations of MCP-1, GM-CSF, and TGF-β were 4,698 ± 242, 26.8 ± 3.8, and 550 ± 15 pg/ml, respectively. A leukotriene B4(LTB4)-receptor antagonist attenuated the total MCA and the lowest molecular weight peak of MCA. The concentrations of LTB4were 153.4 ± 12.4 (24 h) and 212 ± 16.6 (72 h) pg/ml. These findings suggest that HLFs may modulate the recruitment of monocytes into the lung by releasing MCP-1, GM-CSF, TGF-β, and LTB4constitutively.
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Jiang, Yuhang, Yasir Arafat, Puleng Letuma, Liaqat Ali, Muhammad Tayyab, Muhammad Waqas, Yanchun Li, Weiwei Lin, Sheng Lin, and Wenxiong Lin. "Restoration of Long-Term Monoculture Degraded Tea Orchard by Green and Goat Manures Applications System." Sustainability 11, no. 4 (February 15, 2019): 1011. http://dx.doi.org/10.3390/su11041011.
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Tea is an economic shrubby plant in tropical and subtropical regions of the world. To obtain high yield in tea cultivation, chemical fertilizer application rates have generally been used. However, a large quantity of chemical fertilizer application in a long-term continuously ratooned and monoculture tea orchard can inevitably lead to soil acidification and a decline in fertility. Therefore, the restoration of soil fertility and the sustainable development of tea planting by organic ways are critical for the tea industry. In this study, field trials were conducted in the tea orchard that was continuously ratooned and mono-cultured for 20 years. Nitrogen fertilizer (NF), Laredo soybeans green manure (LF), and goat manure (GM) treatments were applied to restore optimum acidity, soil fertility, microbial activity, and the community structure of a long-term continuously monoculture tea orchard. This paper investigated that the pH value was increased from 4.23 to 4.32 in GM and LF, respectively. Similarly, the content of exchangeable acidity (EA) was decreased by 1.21 and 1.46 cmol·kg−1 in GM and LF, respectively. Available nutrient results indicated that the content of NH4+-N was increased by 3.96, 4.38, NO3−-N by 1.07, 2.16, AP by 3.46, 6.86, AK by 0.26, 0.3 mg kg−1 in GM and LF treatments, respectively. Enzyme analysis revealed that the activity of urease and sucrase was promoted by 7.98 mg·g−1·24 h−1 and 6.77 mg·g−1·24 h−1, respectively, in LF treatment. Likewise, the activity of acid phosphatase and polyphenol oxidase was sharply increased by 2.3 mg·g−1 h−1 and 63.07 mg·g−1 h−1 in LF treatments. Additionally, the activity of urease, sucrase, acidic phosphatase, polyphenol oxidase, and peroxidase were also significantly increased by applying GM treatments. Meanwhile, LF and GM treatments significantly improved soil microbial biomass as well as low weight organic acid content in degraded tea rhizosphere. Furthermore, high throughput sequence results illustrated that the relative abundance of Rhizobiaceae and Bradyrhizobiaceae families increased in LF and GM treatments, respectively, which are mostly a kind of nitrogen fixer and plant growth promoting bacteria. Taken together, the physiological traits of the new sprouts and the biochemical components of new tea leaves were also significantly improved by GM and LF treatments. From this study, it is concluded that LF and GM are good agriculture management practices, which promote plant growth, yield, and nutrient availability by maintaining and improving pH, enhancing available nutrients status, improving the secretion of low molecular weight organic acids, and balancing the microbial community structure in the long-term mono-cultured tea orchard.
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Alnaseri, Yahya A. A. M., and Sundus A. Alabdulla. "Study of growth and yield of maize (Zea mays L.) under levels of nitrogen and potassium fertilization." Muthanna Journal for Agricultural Sciences 8, no. 1 (December 23, 2020): 55–62. http://dx.doi.org/10.52113/mjas04/8.1/8.
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"A field experiment was conducted during the autumn season 2018 at Al- Zinawiya site 10 km south-east of center Al- Nasiriya Governorate, to determine the effect of four levels of Nitrogen fertilizer (0.120,180 and 240 kg N ha-1 ) and four levels of Potassium fertilizer (0,80,120 and 160 kg K ha-1 ) and The interaction between them, on growth and yield of corn (Zea mays L.) Fajer-1 variety. Factorial experiment according to Randomized complete block design (R.C.B.D) was used in this study with three replicates The results showed the level 240 kg N ha-1 achieved significant superiority in the Days to Tasselling, Days to silking, Plant height, Leaf area, number of grains per ear, weight 500 grain, grain yield, the concentration of nitrogen and potassium in leaves (54.09 Days, 57.58 Days, 166.17cm, 399.29cm2 , 404.83per ear-1 , 158.20gm, 6.702t h-1 , 1.46Mg gm-1 , 1.28Mg gm-1 respectively). The level of 160 kg K-1 was significant superior among other levels by giving the best results of studied characters, (Days to Tasselling, Days to silking, Plant height, Leaf area, number of grains per ear, grain yield and the concentration of nitrogen in the leaves.) (54.09 Days, 57.58days, 138.42cm, 338.05 cm2 , 338.58 per ear, 5.250 t h-1 , 1.44Mg gm-1 respectively). The interaction for the treatment (240 kg N h-1 + 160 kg K h-1 ) was superior grain number of per ear (430.00), weight 500 grain (160.40 gm), and grain yield (7.060 t h-1)"
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Wu, Shuling, Sven Enders, Thomas Burmeister, Daniel Nowak, Mark Reinwald, and Eckhard Thiel. "GM-CSF Stimulates IL-8 Expression in Human Bone Marrow Stromal Cells Via Activation of NADPH Oxidases." Blood 110, no. 11 (November 16, 2007): 4109. http://dx.doi.org/10.1182/blood.v110.11.4109.4109.
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Abstract The self-renewal, proliferation, and mobilization of hematopoietic progenitor cells (HPC) depend on complex interactions involving cytokines and bone marrow (BM) stromal microenvironment. Little is known about the effect of mobilizing agents such as granulocyte-macrophage colony-stimulating factor (GM-CSF) on BM stromal cells and their contribution to the mobilization of peripheral blood stem cells. In the present study we show that, 3 hours after addition, GM-CSF distinctly upregulated IL-8 mRNA expression and protein secretion in cultured human BM stromal cells. Furthermore, GM-CSF stimulated the generation of reactive oxygen species (ROS) in a dose- and time-dependent manner. Intracellular levels of ROS correlated with the extent of IL-8 production and IL-8 promotor activity as determined by luciferase reporter assay. Using western blot analysis, we showed that BM stromal cells expressed both phagocytic and non-phagocytic NAD(P)H oxidase components such as gp91phox, NOX1, p22phox, p47phox, p67phox, and NOXO1, suggesting that the upregulation of IL-8 expression induced by GM-CSF may be associated with the activation of stromal cell NADPH oxidase activity. GM-CSF directly stimulated the phosphorylation of p47phox, a key event in NAD(P)H oxidase activation. Inhibitors of the ERK1/2 and AKT pathways abrogated GM-CSF-induced phosphorylation of p47phox, indicating that GM-CSF-induced phosphorylation of p47phox is mediated by these pathways in BM stromal cells. Accordingly, the transactivation of IL-8 promotor activity induced by GM-CSF was suppressed by these inhibitors and the antioxidants diphenylene iodonium (DPI) and N-acetyl-l-cysteine (NAC). In conclusion, these findings show that GM-CSF elicits the activation of the redox-sensitive signaling via ROS, resulting in stromal cell function such as cytokine production and therefore possibly impacts on hematopoiesis.
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Cantón, Emilia, Javier Pemán, Amparo Valentín, Ana Espinel-Ingroff, and Miguel Gobernado. "In Vitro Activities of Echinocandins against Candida krusei Determined by Three Methods: MIC and Minimal Fungicidal Concentration Measurements and Time-Kill Studies." Antimicrobial Agents and Chemotherapy 53, no. 7 (April 20, 2009): 3108–11. http://dx.doi.org/10.1128/aac.00160-09.
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ABSTRACT We evaluated the in vitro activities of anidulafungin, micafungin, and caspofungin against Candida krusei by determining MIC and minimum fungicidal concentration (MFC) measurements and by the time-kill method. The geometric mean (GM)-MIC/GM-MFC values were 0.1/0.34, 0.25/0.44, and 1/2.29, respectively. The mean times to reach 99.9% growth reduction were 19.1 ± 18.2 h (mean ± standard deviation) for 2 mg/liter anidulafungin, 37.4 ± 8.8 h for 2 mg/liter caspofungin, and 30.7 ± 12.2 h for 1 mg/liter micafungin. Anidulafungin exhibited the highest time-kill rate, followed by micafungin. The three echinocandins showed fungicidal activity at concentrations reached in serum.
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Orbulov, Imre Norbert, and Kornél Májlinger. "Characterisation of Hybrid Metal Matrix Syntactic Foams." Materials Science Forum 812 (February 2015): 219–25. http://dx.doi.org/10.4028/www.scientific.net/msf.812.219.
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High quality aluminium matrix syntactic foams (AMSFs) were produced by pressure infiltration. This method can ensure the maximal volume fraction of the reinforcing hollow spheres and very low amount of unwanted or matrix porosities. By this method hybrid MMSFs with mixed metal and ceramic hollow spheres were also produced. The matrix material was AlSi12 alloy and two different types – produced by Hollomet GmbH in Germany – of hollow spheres were used: Globomet (GM) and Globocer (GC). The geometrical properties of the hollow spheres were similar (average outer diameter), but their base material was pure iron and Al2O3+SiO2 in the case of GM and GC hollow spheres respectively. The volume fraction of the reinforcing hollow spheres were maintained at ~65 vol%, but the ratio of them was altered in 20% steps (100% GM + 0% GC, 80% GM + 20% GC...). The results of the compression tests showed, that the compressive strength, yield strength, plateau strength, structural stiffness and the absorbed mechanical energy values increased with higher ceramic hollow sphere reinforcement ratio. The fracture strains of the investigated MMSFs decreased with the higher GC ratio. Generally the strength values also increased with higher diameter to height (H/D) ratio from H/D=1 to H/D=1.5 and 2.
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Hart, P. H., G. A. Whitty, D. S. Piccoli, and J. A. Hamilton. "Synergistic activation of human monocytes by granulocyte-macrophage colony-stimulating factor and IFN-gamma. Increased TNF-alpha but not IL-1 activity." Journal of Immunology 141, no. 5 (September 1, 1988): 1516–21. http://dx.doi.org/10.4049/jimmunol.141.5.1516.
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Abstract TNF-alpha and IL-1 activities and PGE2 levels were investigated in the supernatants of highly purified human monocytes cultured for 18 h with recombinant human granulocyte-macrophage CSF (GM-CSF). GM-CSF alone did not stimulate IL-1 or TNF-alpha activities or the production of PGE2. GM-CSF with IFN-gamma, but not with LPS, consistently activated the monocytes for TNF-alpha activity. In contrast, for increased IL-1 activity, GM-CSF synergized weakly and irregularly with LPS, but not at all with IFN-gamma. For the third monocyte product investigated, GM-CSF was a weak and inconsistent inducer of PGE2 and only in the co-presence of IFN-gamma. Thus, GM-CSF can elicit different responses in human monocytes depending both on the co-stimulus as well as the monocyte product being investigated.
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Wang, SY, YM Li, LY Chen, RC Wang, CK Lin, and CK Ho. "Detection of the target progenitor cells of granulomonopoietic enhancing activity." Blood 76, no. 3 (August 1, 1990): 495–500. http://dx.doi.org/10.1182/blood.v76.3.495.495.
Full textAbstract:
Abstract Macrophage-derived granulomonopoietic enhancing activity (GM-EA) is a novel mediator that amplifies colony formation of myeloid progenitor cells (CFU-GM) in conjunction with colony-stimulating factors (CSFs), and is distinct from other hematopoietic synergizing factors such as interleukin (IL)-1, IL-4, and IL-6. In the present study, we try to ascertain whether or not there is a GM-EA-specific responsive myeloid progenitor cell population. Human bone marrow cells deleted of adherent cells and T lymphocytes were separated by velocity sedimentation into three subpopulations with respective sedimentation rates (millimeters per hour) of 7.4 +/- 0.4, 6.0 +/- 0.6, and 4.7 +/- 0.3. These subpopulations corresponded to the day 7 CFU-GM, day 14 CFU-GM, and the earlier myeloid progenitor cells, pre-CFU-GM, respectively. Pre-CFU-GM failed to respond to the colony-inducing effect of GM-CSF but could be stimulated by GM-EA alone to generate small clusters (5 to 25 cells) in soft agar after 14 days of incubation. Correspondingly, suspension preculture of the fractionated bone marrow cells also showed that only the progenitor cells with low sedimentation rate (4.7 mm/h) could be activated by GM-EA to generate CFU-GM. Taken together, our results suggest that the specific target cell of GM-EA is the pre-CFU-GM, and that GM-EA acts on these cells as a growth/maturation factor, but on the day 7 and day 14 CFU-GM as a synergistic growth factor.
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Wang, SY, YM Li, LY Chen, RC Wang, CK Lin, and CK Ho. "Detection of the target progenitor cells of granulomonopoietic enhancing activity." Blood 76, no. 3 (August 1, 1990): 495–500. http://dx.doi.org/10.1182/blood.v76.3.495.bloodjournal763495.
Full textAbstract:
Macrophage-derived granulomonopoietic enhancing activity (GM-EA) is a novel mediator that amplifies colony formation of myeloid progenitor cells (CFU-GM) in conjunction with colony-stimulating factors (CSFs), and is distinct from other hematopoietic synergizing factors such as interleukin (IL)-1, IL-4, and IL-6. In the present study, we try to ascertain whether or not there is a GM-EA-specific responsive myeloid progenitor cell population. Human bone marrow cells deleted of adherent cells and T lymphocytes were separated by velocity sedimentation into three subpopulations with respective sedimentation rates (millimeters per hour) of 7.4 +/- 0.4, 6.0 +/- 0.6, and 4.7 +/- 0.3. These subpopulations corresponded to the day 7 CFU-GM, day 14 CFU-GM, and the earlier myeloid progenitor cells, pre-CFU-GM, respectively. Pre-CFU-GM failed to respond to the colony-inducing effect of GM-CSF but could be stimulated by GM-EA alone to generate small clusters (5 to 25 cells) in soft agar after 14 days of incubation. Correspondingly, suspension preculture of the fractionated bone marrow cells also showed that only the progenitor cells with low sedimentation rate (4.7 mm/h) could be activated by GM-EA to generate CFU-GM. Taken together, our results suggest that the specific target cell of GM-EA is the pre-CFU-GM, and that GM-EA acts on these cells as a growth/maturation factor, but on the day 7 and day 14 CFU-GM as a synergistic growth factor.