Готові списки джерел за темами / TNF INDUCED

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Добірка наукової літератури з теми "TNF INDUCED"

Автор: Grafiati
Опубліковано: 11 вересня 2023

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Статті в журналах з теми "TNF INDUCED"

1

Benveniste, E. N., J. Kwon, W. J. Chung, J. Sampson, K. Pandya, and L. P. Tang. "Differential modulation of astrocyte cytokine gene expression by TGF-beta." Journal of Immunology 153, no. 11 (December 1, 1994): 5210–21. http://dx.doi.org/10.4049/jimmunol.153.11.5210.

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Abstract In this study, we demonstrate that TGF-beta inhibits TNF-alpha expression, and induces/enhances IL-6 expression by primary rat astrocytes. Treatment of astrocytes with TGF-beta alone had no effect on TNF-alpha mRNA or protein expression; however, TGF-beta suppressed induction of TNF-alpha expression by three different stimuli (IFN-gamma/LPS, IFN-gamma/IL-1 beta, TNF-alpha) at both the protein and mRNA level. The extent of TGF-beta-mediated inhibition was greatest when astrocytes were pretreated with TGF-beta for 6 to 24 h, then exposed to the inducing stimuli. Inhibition of TNF-alpha mRNA steady-state levels by TGF-beta was a result of inhibition of TNF-alpha gene transcription, rather than degradation of the TNF-alpha message. In contrast, TGF-beta alone induced expression of IL-6 by astrocytes and synergized with two other cytokines, IL-1 beta and TNF-alpha, for enhanced IL-6 expression. TGF-beta-induced/enhanced IL-6 expression was mediated by transcriptional activation of the IL-6 gene. These results indicate that TGF-beta is an important regulator of cytokine production by astrocytes under inflammatory conditions in the brain.
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2

Kamijo, R., K. Takeda, M. Nagumo, and K. Konno. "Effects of combinations of transforming growth factor-beta 1 and tumor necrosis factor on induction of differentiation of human myelogenous leukemic cell lines." Journal of Immunology 144, no. 4 (February 15, 1990): 1311–16. http://dx.doi.org/10.4049/jimmunol.144.4.1311.

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Abstract Effects of transforming growth factor-beta 1 (TGF-beta 1), either alone or in combination with TNF, on the induction of differentiation of human myelogenous leukemic cell lines were examined. TGF-beta 1 alone induced differentiation of a human monocytic leukemia U-937 line into the cells with macrophage characteristics. When combined with TNF, TGF-beta 1 synergistically or additively induced differentiation associated properties. A human myeloblastic leukemia cell line, ML-1, differently responded to TGF-beta 1 in induction of differentiation. FcR activity and phagocytic activity induced by TNF were suppressed by TGF-beta 1. However, nitroblue tetrazolium reducing activity was synergistically induced by combinations of TGF-beta 1 and TNF. Scatchard analysis of TNF receptors indicated that the number of binding sites and dissociation constant of TNF for its receptors on U-937 or ML-1 cells were not changed by treatment with TGF-beta 1. Although IFN-gamma, IL-6, granulocyte CSF, and granulocyte-macrophage CSF-induced nitroblue tetrazolium reducing activity of U-937 cells, only IFN-gamma, and TNF induced it synergistically in combination with TGF-beta 1. Synergism between TGF-beta 1 and TNF was also observed in inhibition of growth of U-937 and ML-1 cells. Although TGF-beta 1 induction of differentiation of other monocytoid leukemic THP-1 cells was similar to that of U-937 cells, TGF-beta 1 only slightly induced differentiation of promyelocytic leukemic HL-60 cells, either alone or in combination with TNF. Our observations indicate that TGF-beta 1 strongly modulates differentiation and proliferation of human myelogenous leukemia cells, macrophage precursors.
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3

De Benedetti, F., LA Falk, LR Ellingsworth, FW Ruscetti, and CR Faltynek. "Synergy between transforming growth factor-beta and tumor necrosis factor-alpha in the induction of monocytic differentiation of human leukemic cell lines." Blood 75, no. 3 (February 1, 1990): 626–32. http://dx.doi.org/10.1182/blood.v75.3.626.626.

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Abstract We examined the effect of transforming growth factor-beta (TGF-beta) alone and in combinations with other factors on the growth and differentiation of the human promyelocytic cell line HL60 and the human monoblastic cell line U937. Treatment with TGF-beta alone did not significantly affect growth or differentiation of HL60 cells, while it significantly inhibited proliferation and induced monocytic differentiation of a small percentage of U937 cells. Combinations of TGF-beta and tumor necrosis factor-alpha (TNF-alpha) acted in synergy to inhibit cell proliferation and to induce monocytic differentiation of both HL60 and U937 cells. In contrast, no synergy was observed when HL60 cells were treated with TGF-beta in various combinations with interferon-alpha (IFN-alpha), interferon-gamma (IFN-gamma), and retinoic acid. Examination of TNF-alpha receptor expression on HL60 and U937 cells showed that these cell lines expressed comparable levels of high-affinity TNF-alpha binding sites. Treatment of HL60 and U937 cells with TGF-beta did not induce significant changes in TNF-alpha receptor expression in either cell line. In contrast, HL60 cells expressed much lower levels of TGF-beta receptors than did U937 cells. Treatment of both HL60 and U937 cells with TNF-alpha induced a dose-dependent increase in expression of TGF-beta receptors, suggesting that the synergy between TNF-alpha and TGF-beta may result, at least in part, from upregulation of TGF-beta receptor expression by TNF-alpha.
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4

De Benedetti, F., LA Falk, LR Ellingsworth, FW Ruscetti, and CR Faltynek. "Synergy between transforming growth factor-beta and tumor necrosis factor-alpha in the induction of monocytic differentiation of human leukemic cell lines." Blood 75, no. 3 (February 1, 1990): 626–32. http://dx.doi.org/10.1182/blood.v75.3.626.bloodjournal753626.

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Анотація:
We examined the effect of transforming growth factor-beta (TGF-beta) alone and in combinations with other factors on the growth and differentiation of the human promyelocytic cell line HL60 and the human monoblastic cell line U937. Treatment with TGF-beta alone did not significantly affect growth or differentiation of HL60 cells, while it significantly inhibited proliferation and induced monocytic differentiation of a small percentage of U937 cells. Combinations of TGF-beta and tumor necrosis factor-alpha (TNF-alpha) acted in synergy to inhibit cell proliferation and to induce monocytic differentiation of both HL60 and U937 cells. In contrast, no synergy was observed when HL60 cells were treated with TGF-beta in various combinations with interferon-alpha (IFN-alpha), interferon-gamma (IFN-gamma), and retinoic acid. Examination of TNF-alpha receptor expression on HL60 and U937 cells showed that these cell lines expressed comparable levels of high-affinity TNF-alpha binding sites. Treatment of HL60 and U937 cells with TGF-beta did not induce significant changes in TNF-alpha receptor expression in either cell line. In contrast, HL60 cells expressed much lower levels of TGF-beta receptors than did U937 cells. Treatment of both HL60 and U937 cells with TNF-alpha induced a dose-dependent increase in expression of TGF-beta receptors, suggesting that the synergy between TNF-alpha and TGF-beta may result, at least in part, from upregulation of TGF-beta receptor expression by TNF-alpha.
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5

HEGEWISCH, S. "TNF-induced cardiomyopathy." Lancet 335, no. 8684 (February 1990): 294–95. http://dx.doi.org/10.1016/0140-6736(90)90115-l.

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6

Los, Marek, Malgorzata Mozoluk, Davide Ferrari, Anna Stepczynska, Christopher Stroh, Andrea Renz, Zdenko Herceg, Zhao-Qi Wang, and Klaus Schulze-Osthoff. "Activation and Caspase-mediated Inhibition of PARP: A Molecular Switch between Fibroblast Necrosis and Apoptosis in Death Receptor Signaling." Molecular Biology of the Cell 13, no. 3 (March 2002): 978–88. http://dx.doi.org/10.1091/mbc.01-05-0272.

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Death ligands not only induce apoptosis but can also trigger necrosis with distinct biochemical and morphological features. We recently showed that in L929 cells CD95 ligation induces apoptosis, whereas TNF elicits necrosis. Treatment with anti-CD95 resulted in typical apoptosis characterized by caspase activation and DNA fragmentation. These events were barely induced by TNF, although TNF triggered cell death to a similar extent as CD95. Surprisingly, whereas the caspase inhibitor zVAD prevented CD95-mediated apoptosis, it potentiated TNF-induced necrosis. Cotreatment with TNF and zVAD was characterized by ATP depletion and accelerated necrosis. To investigate the mechanisms underlying TNF-induced cell death and its potentiation by zVAD, we examined the role of poly(ADP-ribose)polymerase-1 (PARP-1). TNF but not CD95 mediated PARP activation, whereas a PARP inhibitor suppressed TNF-induced necrosis and the sensitizing effect of zVAD. In addition, fibroblasts expressing a noncleavable PARP-1 mutant were more sensitive to TNF than wild-type cells. Our results indicate that TNF induces PARP activation leading to ATP depletion and subsequent necrosis. In contrast, in CD95-mediated apoptosis caspases cause PARP-1 cleavage and thereby maintain ATP levels. Because ATP is required for apoptosis, we suggest that PARP-1 cleavage functions as a molecular switch between apoptotic and necrotic modes of death receptor-induced cell death.
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7

Méndez-Samperio, Patricia, Marisol Hernandez-Garay та Angela Nuñez Vazquez. "Inhibition of Mycobacterium bovisBCG-Induced Tumor Necrosis Factor Alpha Secretion in Human Cells by Transforming Growth Factor β". Clinical Diagnostic Laboratory Immunology 5, № 4 (1 липня 1998): 588–91. http://dx.doi.org/10.1128/cdli.5.4.588-591.1998.

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ABSTRACT The effect of exogenous transforming growth factor β (TGF-β) onMycobacterium bovis BCG-induced tumor necrosis factor alpha (TNF-α) production by human mononuclear cells was studied. It was found that TNF-α production by human cells stimulated with BCG was significantly inhibited by TGF-β. The specificity of the observed inhibition was demonstrated, since the addition of an anti-TGF-β neutralizing monoclonal antibody completely reversed the inhibitory effect. Furthermore, the suppressive effect of TGF-β on TNF-α secretion in this system was not due to a direct cytotoxic effect, since cell viability was comparable in the presence or absence of TGF-β. Interestingly, our results demonstrated comparative suppressive effects of TGF-β and interleukin-10 on BCG-induced TNF-α secretion. Together, the data demonstrate, for the first time, that TGF-β inhibits BCG-induced TNF-α secretion by human cells.
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8

Panek, R. B., and E. N. Benveniste. "Class II MHC gene expression in microglia. Regulation by the cytokines IFN-gamma, TNF-alpha, and TGF-beta." Journal of Immunology 154, no. 6 (March 15, 1995): 2846–54. http://dx.doi.org/10.4049/jimmunol.154.6.2846.

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Abstract The molecular mechanism(s) by which three cytokines (IFN-gamma, TNF-alpha, TGF-beta) affect class II MHC gene expression in primary rat microglia was examined. IFN-gamma is a potent inducer of the class II gene, and this induction is unaffected by treatment with either TNF-alpha or TGF-beta. Transient transfection of primary rat microglia with an HLA-DRA promoter linked to the chloramphenicol acetyltransferase reporter gene (DRA-CAT) demonstrated that IFN-gamma acts at the transcriptional level to induce class II MHC gene expression, and that TNF-alpha and TGF-beta have no influence on IFN-gamma-induced promoter activity. Experiments using a series of DRA substitution mutants that individually affect the W, X1, X2, or Y elements, as well as a double mutation in both X1 and X2, indicate that all four of these elements are required for responsiveness of the DRA promoter to IFN-gamma. The effect of IFN-gamma and TNF-alpha on DNA binding proteins by microglia was examined. A constitutive complex with specificity for the X2 box was detected in extracts from unstimulated microglia. IFN-gamma treatment changed this complex to migrate with slower mobility, and TNF-alpha had no effect on either the constitutive or IFN-gamma-induced complexes. These studies provide information on the molecular regulation of the class II MHC gene in microglia, a cell type critically involved in immune regulation within the central nervous system.
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9

Kochumon, Shihab, Amnah Al-Sayyar, Texy Jacob, Amal Hasan, Fahd Al-Mulla, Sardar Sindhu та Rasheed Ahmad. "TNF-α Increases IP-10 Expression in MCF-7 Breast Cancer Cells via Activation of the JNK/c-Jun Pathways". Biomolecules 11, № 9 (13 вересня 2021): 1355. http://dx.doi.org/10.3390/biom11091355.

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IP-10 (also called CXCL10) plays a significant role in leukocyte homing to inflamed tissues, and increased IP-10 levels are associated with the pathologies of various inflammatory disorders, including type 2 diabetes, atherosclerosis, and cancer. TNF-α is a potent activator of immune cells and induces inflammatory cytokine expression in these cells. However, it is unclear whether TNF-α is able to induce IP-10 expression in MCF-7 breast cancer cells. We therefore determined IP-10 expression in TNF-α-treated MCF-7 cells and investigated the mechanism involved. Our data show that TNF-α induced/upregulated the IP-10 expression at both mRNA and protein levels in MCF-7 cells. Inhibition of JNK (SP600125) significantly suppressed the TNF-α-induced IP-10 in MCF-7 cells, while the inhibition of p38 MAPK (SB203580), MEK1/2 (U0126), and ERK1/2 (PD98059) had no significant effect. Furthermore, TNF-α-induced IP-10 expression was abolished in MCF-7 cells deficient in JNK. Similar results were obtained using MCF-7 cells deficient in c-Jun. Moreover, the JNK kinase inhibitor markedly reduced the TNF-α-induced JNK and c-Jun phosphorylation. The kinase activity of JNK induced by TNF-α stimulation of MCF-7 cells was significantly inhibited by SP600125. Altogether, our novel findings provide the evidence that TNF-α induces IP-10 expression in MCF-7 breast cancer cells via activation of the JNK/c-Jun signaling pathway.
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10

Kim, Han Geun, Joo Yun Kim, Min Geun Gim, Jung Min Lee та Dae Kyun Chung. "Mechanical stress induces tumor necrosis factor-α production through Ca2+ release-dependent TLR2 signaling". American Journal of Physiology-Cell Physiology 295, № 2 (серпень 2008): C432—C439. http://dx.doi.org/10.1152/ajpcell.00085.2008.

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We studied centrifugation-mediated mechanical stress-induced tumor necrosis factor-α (TNF-α) production in the monocyte-like cell line THP-1. The induction of TNF-α by mechanical stress was dependent on the centrifugation speed and produced the highest level of TNF-α after 1 h of stimulation. TNF-α production returned to normal levels after 24 h of stimulation. Mechanical stress also induced Toll-like receptor-2 (TLR2) mRNA in proportion to the expression of TNF-α. The inhibition of TLR2 signaling by dominant negative myeloid differentiation factor 88 (MyD88) blocked TNF-α expression response to mechanical stress. After transient overexpression of TLR2 in HEK-293 cells, mechanical stress induced TNF-α mRNA production. Interestingly, mechanical stress activated the c-Src-dependent TLR2 phosphorylation, which is necessary to induce Ca2+ fluxes. When THP-1 cells were pretreated with BAPTA-AM, thapsigargin, and NiCl2·6H2O, followed by mechanical stimulation, both TLR2 and TNF-α production were inhibited, indicating that centrifugation-mediated mechanical stress induces both TLR2 and TNF-α production through Ca2+ releases from intracellular Ca2+ stores following TLR2 phosphorylation. In addition, TNF-α treatment in THP-1 cells induced TLR2 production in response to mechanical stress, whereas the preincubation of anti-TNF-α antibody scarcely induced the mechanical stress-mediated production of TLR2, indicating that TNF-α produced by mechanically stimulated THP-1 cells affected TLR2 production. We concluded that TNF-α production induced by centrifugation-mediated mechanical stress is dependent on MyD88-dependent TLR2 signaling that is associated with Ca2+ release and that TNF-α production induced by mechanical stress affects TLR2 production.
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Більше джерел

Дисертації з теми "TNF INDUCED"

1

Li, Rui Xin. "Scutellarin inhibits TNF-induced proliferative expansion of Tregs by blocking TNF-TNFR2 interactions." Thesis, University of Macau, 2018. http://umaclib3.umac.mo/record=b3952140.

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2

Bailey, Nicole. "TNF-dependent stress-induced plasticity in the hippocampus." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110419.

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Анотація:
Stress and stressful experiences are involved in the development and persistence of chronic physical and mental health disorders, and are an important concern for public health services. Previous studies have demonstrated acute stress can alter properties of neural circuits, specifically in the hippocampus. Tumour necrosis factor-alpha (TNF-alpha) is involved in AMPA-R trafficking, and evidence suggests it plays an important role in homeostatic, and possibly in Hebbian plasticity. Because TNF-alpha is regulated by stress, and is also important for plasticity; it is likely TNF-alpha is involved in stress-induced plasticity. Stress-induced changes in synaptic strength were recorded from 7 week old male wild-type, TNF-/- and DN-TNF (a dominant negative version of TNF) treated mice 24h after a 15 minute acute swim stress. DN-TNF, inhibits any soluble TNF-alpha while still permitting the action of membrane bound TNF-alpha. We recorded evoked excitatory postsynaptic currents from ventral hippocampal CA1 pyramidal cells in acute slices. We measured AMPA/NMDA ratios, as a measure of synaptic strength, along with rectification of the AMPA currents, to test for changes in AMPA receptor subunit composition. The present study demonstrates an increase in AMPA/NMDA ratio in stressed animals compared to unstressed controls, suggesting a stress-induced increase in synaptic strength in wild-type mice. Inhibition of TNF-alpha signalling prevents this stress-induced increase in synaptic strength, as DN-TNF treated mice had no change in AMPA/NMDA ratio following stress. Further, stress-induced synaptic changes were absent in TNF-/- mice. Stress does not affect the AMPA-R subunit composition at the 24h time point, as the rectification ratio was unaltered following stress. These results indicate stress induces an increase in synaptic strength within the CA1, in a manner dependent on TNF-alpha signalling.
Le stress et les expériences stressantes sont impliqués dans le développement et la persistance des troubles chroniques de santé physique et mentale, et elles représentent une préoccupation importante pour les services de santé publique. Des études antérieures ont démontré que le stress aigu peut modifier les propriétés des circuits neuronaux, en particulier dans l'hippocampe. Le facteur de nécrose tumorale-alpha (TNF-alpha) est impliqué dans le trafic des récepteurs AMPA (AMPA-R), et il semble qu'il joue un rôle important dans l'homéostasie, et peut-être dans la plasticité de Hebb. Puisque TNF-alpha est régulé par le stress et qu'il est également important pour la plasticité, il est probable que TNF-alpha soit impliqué dans la plasticité induite par le stress. Les changements de la force synaptique induits par le stress ont été enregistrées à partir de 7 semaines chez des souris (de type sauvage, TNF-alpha -/- et DN-TNF-alpha (une version dominante négative de TNF-alpha)) traitées 24h après 15 minutes de stress aigu dans l'eau. DN-TNF-alpha inhibe l'action de TNF-alpha soluble tout en permettant l'action de la membrane liée à TNF-alpha. Nous avons enregistré les courants postsynaptiques excitateurs évoqués à partir de cellules pyramidales dans des tranches aiguës de la région CA1 de l'hippocampe ventral. On a mesuré le ratio des récepteurs AMPA / NMDA pour quantifier la force synaptique en tenant compte de la correction des courants des récepteurs AMPA pour vérifier les changements dans la composition de leurs sous-unités. La présente étude démontre une augmentation du ratio des récepteurs AMPA / NMDA chez les animaux stressés par rapport aux animaux non stressés, ce qui suggère une augmentation de la force synaptique induite par le stress dans les souris de type sauvage. L'inhibition de la signalisation du TNF-alpha empêche cette augmentation de la force synaptique induite par le stress et les souris traitées avec DN-TNF-alpha n'ont pas modifié le rapport des récepteurs AMPA / NMDA en réponse au stress. En outre, les changements synaptiques induits par le stress étaient absents dans les souris TNF-alpha-/-. Le stress n'affecte ni la composition des sous-unités d'AMPA-R après 24h ni la correction des courants des récepteurs AMPA. Ces résultats indiquent que le stress induit une augmentation de la force synaptique dans la région CA1 via la signalisation de TNF-alpha.
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3

Williams, Richard Owen. "Strategies for immune intervention in murine collagen-induced arthritis." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309740.

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4

Ouellet, Sophie. "TNF-alpha production by alveolar macrophages in mineral-dust-induced fibrosis." Thesis, University of Ottawa (Canada), 1993. http://hdl.handle.net/10393/6641.

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Macrophages are the predominant cell type in the chronic inflammatory reaction associated with the development of mineral-dust-induced fibrosis. Macrophages are potent producers of cytokines, which have recently emerged as potentially important mediators in regulating inflammatory states. I investigated cytokine production by alveolar macrophages (AM), with a special emphasis on tumor necrosis factor-$\alpha$, in experimental lung fibrosis induced by mineral dusts. Exposure to fibrigenic dusts had a bimodal effect on TNF-$\alpha$ production by AM. First, suppressed TNF-$\alpha$ production after 1 and 3 weeks of exposure. Second, after 6 weeks of exposure TNF-$\alpha$ production was high. By contrast, interleukin-1 (IL-1) and interleukin-6 (IL-6) production was increased in animals with inflammation with and without fibrosis. Potentiations in IL-1 and IL-6 production were associated with the early stage of the inflammatory reaction and were inversely correlated with TNF-$\alpha$ changes. Interestingly, alterations in TNF-$\alpha$ production were associated with definite shifts in the distribution size of AM suggesting that the overall production of TNF-$\alpha$ may be regulated by the specific class of AM present at sites of inflammation. To our knowledge, our study brings the first evidence for a negative modulation of TNF-$\alpha$ during inflammatory reactions leading to lung fibrosis. Furthermore, experiments with neutralizing antibody to TGF-$\beta$ suggest a role for TGF-$\beta$ in down-regulating TNF-$\alpha$ production in our system.
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5

Grabinger, Thomas [Verfasser]. "Mechanisms of TNF-induced apoptosis in intestinal epithelial cells / Thomas Grabinger." Konstanz : Bibliothek der Universität Konstanz, 2015. http://d-nb.info/1152947087/34.

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6

Reiss, Lucy Kathleen [Verfasser]. "A mouse intensive care unit to study TNF-induced sepsis and acid-induced lung injury / Lucy Kathleen Reiss." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2012. http://d-nb.info/1025698460/34.

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7

Garcia, Carbonell Ricard. "The role of RIPK1 in TNF-induced cell death in intestinal epithelial cells." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/462962.

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Inflammatory bowel diseases (IBD) are chronic inflammatory processes that affect the gastrointestinal tract. IBD is characterized by an intestinal inflammation and epithelial cell injury leading to a poor psychosocial wellbeing and increased the risk for cancer. IBD pathogenesis is multifactorial, involving genetic predisposition, epithelial barrier defects, dysregulated immune responses, and environmental factors. The current gold standard therapy is TNF blockade, a key proinflammatory cytokine. TNF activates the NF-κB pathway inducing an anti-apoptotic cell response and it plays an important role in the regulation of the intestinal homeostasis. However, in certain situations, TNF can also trigger cell death through different signaling cascades, a typical feature seen in IBD. This work shows how apoptotic IEC areas in IBD human samples co-localize with NF-κB activation and A20 upregulation. Furthermore, using animal models as well as in vitro studies, we show how NF-κB activation and A20 upregulation are required events to trigger TNF- dependent cell death in intestinal epithelial cells. We also show how other cytokines that are usually upregulated in IBD interact with TNF to induce cell death. Specifically, lymphotoxin β receptor activation synergizes with TNF to trigger apoptosis. We have proven that intestinal epithelial cells undergo apoptotsis downstream of TNFR in a RIPK1 dependent manner, and that kinase inhibition of RIPK1 prevents cell death. Chronic NF-κB induces apoptosis downstream of TNF in a ROS dependent manner and A20 requires its linear ubiquitin binding domain, zinc finger seven, to enhance the formation of complex IIb or ripoptosome after TNF stimulation. Overall these results help to further understand the pathogenesis of IBD and suggests RIPK1 as a possible target for new drugs to treat IB.
Les malalties inflamatòries intestinals (MII) són patologies caracteritzades per una inflamació crònica del tracte gastrointestinal que indueix dany a l’epiteli intestinal incrementant la morbiditat del pacient i el risc de desenvolupar càncer. La patogènesis de les MII és multifactorial, i inclou susceptibilitat genètica, defectes en la barrera epitelial, una resposta immunitària descontrolada i factors ambientals. El tractament estàndard per les MII és el bloqueig del TNF, una citocina pro- inflamatòria. El TNF activa la via de senyalització del NF-κB induint una resposta anti-apoptòtica, al mateix temps que té una funció important en la regulació de l’homeòstasi intestinal. No obstant, en certs casos, el TNF es capaç d’induir mort cel·lular, una característica típica de les MII, a través de diferents vies de senyalització. Aquesta tesis mostra com les àrees apoptòtiques en l’epiteli de les MII correlacionen amb una activació de la via del NF-κB i un increment de A20. Usant models animals i experiments in vitro, demostrem com l’activació de NF-κB així com l’augment de A20 en les cèl·lules del epiteli intestinal, són events necessaris per induir la mort cel·lular depenent de TNF. També demostrem com altres citocines, que generalment estan augmentades en les MII, afavoreixen l’apoptosis secundaria a TNF. Específicament, l’activació de receptor de la limfotoxina beta incrementa la capacitat del TNF per induir mort cel·lular. Ensenyem com aquesta mort és secundaria a l’activitat quinasa de RIPK1 i com inhibint-la es pot prevenir la mort cel·lular. També mostrem com l’activació crònica de NF-κB indueix apoptosis secundaria al TNF degut a un increment de ROS mentre que A20 requereix el seu domini d’unió a cadenes d’ubiquitines lineals per afavorir la formació del complexe IIb o ripoptosoma posterior a l’estimulació per TNF. Així doncs, aquest treball aprofundeix més en el coneixement de la patogènesis de les MII i suggereix la inactivació de l’activitat quinasa de RIPK1 com una possible diana terapèutica.
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8

Voigt, Susann [Verfasser]. "Induction, execution and clinical relevance of TNf- and TRAIL-induced necroptosis / Susann Voigt." Kiel : Universitätsbibliothek Kiel, 2017. http://d-nb.info/1137509740/34.

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9

Martín, Sara Rodríguez. "Investigation of MCMV-induced suppression of TNF production in vitro and in vivo." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4426.

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The murine cytomegalovirus (MCMV) immediate early 1 (IE1) protein has been described as a trans-activator of viral and host gene expression. However, the precise role that IE1 plays in the viral life cycle, and in particular its effect on the host immune response is not known. This thesis investigates the functional relationship of the IE1 protein and the immune response induced after infection. By using an ie1-deletion mutant MCMV (MCMVdie1) it was demonstrated that, early after infection, tumor necrosis factor (tnf ) gene activation and protein production was significantly induced in infected-primary macrophages (M ) to a much greater extent than its wild type counterpart. In addition, preliminary studies on the signalling pathways activated upon infection were carried out in order to gain information about the pathways that might be involved in MCMVinduced modulation of tnf activation. Initial observations on the MAPK family members Erk1/2, p38 and JNK did not revealed any differential activation in the absence of IE1. However, due to a number of limitations, it was not possible to draw any firm conclusions from this study. Investigation of the role of IE1 in the in vivo production of TNF were also performed in both susceptible (BALB/c) and resistant (C57Bl/6) mice. These experiments confirmed the attenuated phenotype of MCMVdie1 in vivo, whereby the mutant strain grew to much lower titers than wild type. When cytokine production was assessed in relation to PFU levels a significant production of TNF after infection is observed in different organs of both mice strains. This raises the question whether IE1 contributes to MCMV modulation of TNF production in the natural host. Although, because it is still unclear whether the phenotype of MCMVdie1 in vivo is due to a defect in the virus or the result of a immune response, it was not possible to conclude unequivocally that IE1 is responsible for dampening this cytokine response. This thesis also tested whether the attenuated replication of MCMVdie1 in vivo was due to the increased TNF production induced after infection. An initial investigation in tnf depleted mice revealed that the MCMVdie1 growth phenotype is not due to TNF response. Overall, this study has provided insight into a potential immune modulatory function by MCMV associated with IE1 protein and the regulation of TNF in vivo and in vitro.
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Mahony, Susan M. "Weight loss and metabolic alterations induced by recombinant tumour necrosis FACTOR-ALPHA (TNF)." Thesis, Aston University, 1989. http://publications.aston.ac.uk/12541/.

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Книги з теми "TNF INDUCED"

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Mahony, Susan Maria. Weight loss and metabolic alterations induced by recombinant tumour necrosis FACTOR-ALPHA (TNF). Birmingham: Aston University. Department of Pharmaceutical Sciences, 1989.

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2

Rogler, Gerhard. Gastrointestinal system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0021.

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Rheumatic diseases and diseases of the gastrointestinal (GI) tract are connected in two ways. The extraintestinal manifestations of inflammatory GI diseases such as inflammatory bowel disease affect joints in up to one-third of patients. On the other hand, several rheumatic diseases such as vasculitis or systemic lupus erythematosus (SLE) induce a wide spectrum of gastrointestinal manifestations. The GI tract constitutes a huge area in contact with the environment. It is exposed to billions of food antigens, commensal bacteria, and potential pathogens. Some of those antigens are thought to play a role in the pathogenesis of rheumatic diseases. The intestinal barrier function and the gut immune system are tightly regulated, as on one hand tolerance for food antigens and the resident commensal flora needs to be maintained, and on the other hand pathogens need to be rapidly and effectively eliminated. Non-infectious, chronic inflammatory diseases of the small and large intestine with rheumatic manifestations have been well known for decades. Among the susceptibility genes for Crohn's disease and ulcerative colitis are some that also cause susceptibility to rheumatoid arthritis or SLE, indicating a shared susceptibility and overlapping pathological mechanisms. Subsequently, similar therapeutic principles have successfully been applied in autoimmune GI and rheumatological diseases such as steroids, immunosuppressants, and anti-TNF (tumour necrosis factor) antibodies.
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Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
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4

(Contributor), WHO, ed. Non-Ionizing Radiation, Part 1: Static and Extremely Low-Frequency (ELF) Electric and Magnetic Fields (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans). World Health Organisation, 2002.

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Частини книг з теми "TNF INDUCED"

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Wolchok, Jedd, Adam Cohen, and David Schaer. "Glucocorticoid-Induced TNF Receptor (GITR)." In Cancer Therapeutic Targets, 243–50. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_6.

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Wolchok, Jedd, Adam Cohen, and David Schaer. "Glucocorticoid-Induced TNF Receptor (GITR)." In Cancer Therapeutic Targets, 1–8. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6613-0_6-2.

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Akassoglou, Katerina, George Kassiotis, George Kollias, Lesley Probert, Jan Bauer, and Hans Lassmann. "Transgenic Models of Tnf Induced Demyelination." In Advances in Experimental Medicine and Biology, 245–59. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4685-6_20.

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4

Haegeman, Guy, and Walter Fiers. "TNF-induced Mechanisms for IL6 Gene Induction." In Signalling Mechanisms — from Transcription Factors to Oxidative Stress, 375–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79675-3_26.

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Vini, Ravindran, Sreeja Sreekumar, Juberiya M. Azeez, and Sreeja Sreeharshan. "Pomegranate Extract Protects Endothelial Cells from TNF-α Associated Damage." In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 276–89. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_27.

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AbstractPomegranates are known for being rich in polyphenols and are considered to have immense therapeutic potential. The present study investigates the hypothesis that the Methanolic Extract of Pomegranate (PME), a rich source of antioxidants, may reverse the adverse effects of TNF-α in endothelial cells. This was done by pre-treating the endothelial cells EA.hy926 with PME (80 µg/ml) before subjecting them to apoptotic stimuli, which was TNF-α in combination with cyclohexamide. PME was found to rescue a population of cells from apoptosis induced by TNF-α modulating the levels of BCL2 and BAX involved in intrinsic apoptotic pathway. PME was found to increase the BCL-2/BAX ratio and reverse the elevated levels of effector caspase and thus assist cells to escape from apoptotic stimuli. Also, the extract was found to attenuate oxidative stress by reducing the levels of Reactive Oxygen Species (ROS). Supplementing its anti-atherosclerotic potential, PME pre-treatment diminished the elevated levels of adhesion molecules like VCAM upon TNF-α treatment. PME may therefore have therapeutic implications in protecting the endothelium from TNF-α triggered atherosclerosis.
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Choksi, Swati, Gourav Choudhary, and Zheng-Gang Liu. "Transition from TNF-Induced Inflammation to Death Signaling." In Methods in Molecular Biology, 73–80. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-1130-2_5.

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7

Gentle, Ian E., and John Silke. "New Perspectives in TNF-R1-Induced NF-κB Signaling." In Advances in Experimental Medicine and Biology, 79–88. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6612-4_8.

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8

Emmerich, Christoph H., Anna C. Schmukle, Tobias L. Haas, Björn Gerlach, Stefanie M. Cordier, Eva Rieser, and Henning Walczak. "The Linear Ubiquitin Chain Assembly Complex (LUBAC) Forms Part of the TNF-R1 Signalling Complex and Is Required for Effective TNF-Induced Gene Induction and Prevents TNF-Induced Apoptosis." In Advances in Experimental Medicine and Biology, 115–26. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6612-4_12.

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9

Cho, YoungSik, Sreerupa Challa, and Francis Ka-Ming Chan. "A RNA Interference Screen Identifies RIP3 as an Essential Inducer of TNF-Induced Programmed Necrosis." In Advances in Experimental Medicine and Biology, 589–93. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6612-4_62.

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Waldherr, Steffen, Jan Hasenauer, Malgorzata Doszczak, Peter Scheurich, and Frank Allgöwer. "Global Uncertainty Analysis for a Model of TNF-Induced NF-κB Signalling." In Advances in the Theory of Control, Signals and Systems with Physical Modeling, 365–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-16135-3_29.

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Тези доповідей конференцій з теми "TNF INDUCED"

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Wolfe, Valerie M., Seonghun Park, Marjana Tomic, Peter A. Torzilli, and C. T. Christopher Chen. "Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176541.

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Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α. TNF-α is known to bind its receptor (TNFR1) to cause a cascade that ends with degradation of an inhibitor, IκBα, and release of the transcription factor NF-κB [3]. The actions of TNF-α are also known to be affected by at least three NF-κB independent pathways including the p38, ERK, and JNK pathways [4]. The objective of this study was to determine whether cyclic compression could affect TNF-α induced cartilage degradation and to determine the roles of p38, ERK, and JNK pathways in TNF-induced cartilage degradation. We hypothesized that cyclic loading would inhibit the degradative effects caused by TNF-α.
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Liu, J. "SMOR1, a Novel TNFa-SpecificModulatorOrRegulator, Specifically Regulates TNF-a Induced JNK Activation in Inflammation." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5467.

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3

Pryhuber, GS, та HL Huyck. "TNF Receptor Associated Factor 1 (TRAF1) Enhances Silica Induced Macrophage Retension Potentiating TNF-α Dependent Fibrosis." У American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1320.

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Fikry, A., and P. Faridin. "363 Anti – tnf alfa induced lupus : a case report." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.363.

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Leaver, Susannah K., Gregory Quinlan, Timothy W. Evans, and Anne Burke-Gaffney. "TNF ± MODIFIES THIOREDOXIN-INDUCED CYTOKINE RELEASE FROM HUMAN MONOCYTES." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6150.

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Horan, Ian, Amy Langton, Stuart Farrow, Edwin R. Chilvers, and Helen Parfrey. "TRUSS Is A Regulator Of TNF± Induced IL-8." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6384.

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7

PONTES, JADY ELEN DE, MARILIA BARRETO GAMEIRO SILVA, BÁRBARA STADLER KAHLOW, DEBORAH CRISTYNE COLOMBO, and JULIANA DELFINO. "INTERSTITIAL GRANULOMATOUS DERMATITIS INDUCED BY ANTI-TNF: CASE REPORT." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-141.

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8

Kim, J., J. Sohn, Y. Shin, C. Hong та J. Park. "TNF-α Blockade Attenuates German Cockroach Extract-Induced Allergic Asthma." У American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4230.

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BETANCOURT, LORENA ELIZABETH, VALDIRENE SILVA SIQUEIRA, ERIVELTON AZEVEDO LOPES, GISSELA RIOS MACHADO, PABLO ARTURO OLIVO PALLO, GIOVANNY HOMERO JÁCOME, MARIELY FERNANDA SILVA HELBINGEN, FERNANDO HENRIQUE CARLOS SOUZA, and SAMUEL KATSUYUKI SHINJO. "ANTI-TNF-ALPHA INDUCED-SYSTEMIC AUTOIMMUNE MYOPATHIES: A CASE SERIES." In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-027.

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10

Kashyap, Meghana, Kristen T. Carter, Brent C. Sauer та Christopher T. Chen. "NF-κB Mediates Cartilage Degradation Induced by Trauma Injury and Interleukin-1". У ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14513.

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Chondrocyte death, induced by impact injury (necrosis) and/or apoptotic inducers such as cytokines, and high level of nitric oxide, is important for the development of post-traumatic arthritis (PTA) [1–3]. The upregulation of pro-inflammatory cytokines, such as interleukin −1 (IL-1) and Tumor necrosis factor (TNF) α, is known to mediate cartilage degradation in inflammatory diseases and after trauma injury [1,2, 6–9]. IL-1 induces the degradation of proteoglycan (PG) in cartilage through NF-κB and Mitogen-activated protein kinases (MAPK: p38, ERK and JNK) pathways [1,2,6]. IL-1 is highly upregulated in synovial joint after impact injury, but the role of IL-1 induced chondrocyte death and matrix/PG degradation in injured cartilage is not completely clear.
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Звіти організацій з теми "TNF INDUCED"

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Wang, Jun, Congcong Wang, Hongjuan Fu, Zezhong Liu, Yimin Zhang, and Tong Zhang. TNF alpha antagonists improve oxidative stress and atherosclerosis induced by rheumatoid arthritis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2023. http://dx.doi.org/10.37766/inplasy2023.1.0033.

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2

Schwartz, Bertha, Vaclav Vetvicka, Ofer Danai, and Yitzhak Hadar. Increasing the value of mushrooms as functional foods: induction of alpha and beta glucan content via novel cultivation methods. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600033.bard.

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During the granting period, we performed the following projects: Firstly, we differentially measured glucan content in several pleurotus mushroom strains. Mushroom polysaccharides are edible polymers that have numerous reported biological functions; the most common effects are attributed to β-glucans. In recent years, it became apparent that the less abundant α-glucans also possess potent effects in various health conditions. In our first study, we explored several Pleurotus species for their total, β and α-glucan content. Pleurotuseryngii was found to have the highest total glucan concentrations and the highest α-glucans proportion. We also found that the stalks (stipe) of the fruit body contained higher glucan content then the caps (pileus). Since mushrooms respond markedly to changes in environmental and growth conditions, we developed cultivation methods aiming to increase the levels of α and β-glucans. Using olive mill solid waste (OMSW) from three-phase olive mills in the cultivation substrate. We were able to enrich the levels mainly of α-glucans. Maximal total glucan concentrations were enhanced up to twice when the growth substrate contained 80% of OMSW compared to no OMSW. Taking together this study demonstrate that Pleurotuseryngii can serve as a potential rich source of glucans for nutritional and medicinal applications and that glucan content in mushroom fruiting bodies can be further enriched by applying OMSW into the cultivation substrate. We then compared the immune-modulating activity of glucans extracted from P. ostreatus and P. eryngii on phagocytosis of peripheral blood neutrophils, and superoxide release from HL-60 cells. The results suggest that the anti-inflammatory properties of these glucans are partially mediated through modulation of neutrophileffector functions (P. eryngiiwas more effective). Additionally, both glucans dose-dependently competed for the anti-Dectin-1 and anti-CR3 antibody binding. We then tested the putative anti-inflammatory effects of the extracted glucans in inflammatory bowel disease (IBD) using the dextran sulfate sodium (DSS)–induced model in mice. The clinical symptoms of IBD were efficiently relieved by the treatment with two different doses of the glucan from both fungi. Glucan fractions, from either P. ostreatus or P. eryngii, markedly prevented TNF-α mediated inflammation in the DSS–induced inflamed intestine. These results suggest that there are variations in glucan preparations from different fungi in their anti-inflammatory ability. In our next study, we tested the effect of glucans on lipopolysaccharide (LPS)-induced production of TNF-α. We demonstrated that glucan extracts are more effective than mill mushroom preparations. Additionally, the effectiveness of stalk-derived glucans were slightly more pronounced than of caps. Cap and stalk glucans from mill or isolated glucan competed dose-dependently with anti-Dectin-and anti-CR-3 antibodies, indicating that they contain β-glucans recognized by these receptors. Using the dextran sulfate sodium (DSS)-inflammatory bowel disease mice model, intestinal inflammatory response to the mill preparations was measured and compared to extracted glucan fractions from caps and stalks. We found that mill and glucan extracts were very effective in downregulatingIFN-γ and MIP-2 levels and that stalk-derived preparations were more effective than from caps. The tested glucans were equally effective in regulating the number of CD14/CD16 monocytes and upregulating the levels of fecal-released IgA to almost normal levels. In conclusion, the most effective glucans in ameliorating some IBD-inflammatory associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii. These spatial distinctions may be helpful in selecting more effective specific anti-inflammatory mushrooms-derived glucans. We additionally tested the effect of glucans on lipopolysaccharide-induced production of TNF-α, which demonstrated stalk-derived glucans were more effective than of caps-derived glucans. Isolated glucans competed with anti-Dectin-1 and anti-CR3 antibodies, indicating that they contain β-glucans recognized by these receptors. In conclusion, the most effective glucans in ameliorating IBD-associated symptoms induced by DSS treatment in mice were glucan extracts prepared from the stalk of P. eryngii grown at higher concentrations of OMSW. We conclude that these stress-induced growing conditions may be helpful in selecting more effective glucans derived from edible mushrooms. Based on the findings that we could enhance glucan content in Pleurotuseryngii following cultivation of the mushrooms on a substrate containing different concentrations of olive mill solid waste (OMSW) and that these changes are directly related to the content of OMSW in the growing substrate we tested the extracted glucans in several models. Using dextran sulfate sodium (DSS)–inflammatory bowel disease (IBD) mice model, we measured the colonic inflammatory response to the different glucan preparations. We found that the histology damaging score (HDS) resulting from DSS treatment reach a value of 11.8 ± 2.3 were efficiently downregulated by treatment with the fungal extracted glucans, glucans extracted from stalks cultivated at 20% OMSWdownregulated to a HDS value of 6.4 ± 0.5 and at 80% OMSW showed the strongest effects (5.5 ± 0.6). Similar downregulatory effects were obtained for expression of various intestinal cytokines. All tested glucans were equally effective in regulating the number of CD14/CD16 monocytes from 18.2 ± 2.7 % for DSS to 6.4 ± 2.0 for DSS +glucans extracted from stalks cultivated at 50% OMSW. We finally tested glucans extracted from Pleurotuseryngii grown on a substrate containing increasing concentrations of olive mill solid waste (OMSW) contain greater glucan concentrations as a function of OMSW content. Treatment of rat Intestinal epithelial cells (IEC-6) transiently transfected with Nf-κB fused to luciferase demonstrated that glucans extracted from P. eryngii stalks grown on 80% OMSWdownregulatedTNF-α activation. Glucans from mushrooms grown on 80% OMSW exerted the most significant reducing activity of nitric oxide production in lipopolysaccharide (LPS) treated J774A.1 murine macrophages. The isolated glucans were tested in vivo using the Dextran Sodium Sulfate (DSS) induced colitis in C57Bl/6 mice and found to reduce the histology damaging score resulting from DSS treatment. Expression of various intestinal cytokines were efficiently downregulated by treatment with the fungal extracted glucans. We conclude that the stress-induced growing conditions exerted by OMSW induces production of more effective anti-inflammatory glucans in P. eryngii stalks.
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3

Elmann, Anat, Orly Lazarov, Joel Kashman, and Rivka Ofir. therapeutic potential of a desert plant and its active compounds for Alzheimer's Disease. United States Department of Agriculture, March 2015. http://dx.doi.org/10.32747/2015.7597913.bard.

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We chose to focus our investigations on the effect of the active forms, TTF and AcA, rather than the whole (crude) extract. 1. To establish cultivation program designed to develop lead cultivar/s (which will be selected from the different Af accessions) with the highest yield of the active compounds TTF and/or achillolide A (AcA). These cultivar/s will be the source for the purification of large amounts of the active compounds when needed in the future for functional foods/drug development. This task was completed. 2. To determine the effect of the Af extract, TTF and AcA on neuronal vulnerability to oxidative stress in cultured neurons expressing FAD-linked mutants.Compounds were tested in N2a neuroblastoma cell line. In addition, we have tested the effects of TTF and AcA on signaling events promoted by H₂O₂ in astrocytes and by β-amyloid in neuronal N2a cells. 3. To determine the effect of the Af extract, TTF and AcA on neuropathology (amyloidosis and tau phosphorylation) in cultured neurons expressing FAD-linked mutants. 4. To determine the effect of A¦ extract, AcA and TTF on FAD-linked neuropathology (amyloidosis, tau phosphorylation and inflammation) in transgenic mice. 5. To examine whether A¦ extract, TTF and AcA can reverse behavioral deficits in APPswe/PS1DE9 mice, and affect learning and memory and cognitive performance in these FAD-linked transgenic mice. Background to the topic.Neuroinflammation, oxidative stress, glutamate toxicity and amyloid beta (Ab) toxicity are involved in the pathogenesis of Alzheimer's diseases. We have previously purified from Achilleafragrantissimatwo active compounds: a protective flavonoid named 3,5,4’-trihydroxy-6,7,3’-trimethoxyflavone (TTF, Fl-72/2) and an anti-inflammatory sesquiterpenelactone named achillolide A (AcA). Major conclusions, solutions, achievements. In this study we could show that TTF and AcA protected cultured astrocytes from H₂O₂ –induced cell death via interference with cell signaling events. TTF inhibited SAPK/JNK, ERK1/2, MEK1 and CREBphosphorylation, while AcA inhibited only ERK1/2 and MEK1 phosphorylation. In addition to its protective activities, TTF had also anti-inflammatory activities, and inhibited the LPS-elicited secretion of the proinflammatorycytokinesInterleukin 6 (IL-6) and IL-1b from cultured microglial cells. Moreover, TTF and AcA protected neuronal cells from glutamate and Abcytotoxicity by reducing the glutamate and amyloid beta induced levels of intracellular reactive oxygen species (ROS) and via interference with cell signaling events induced by Ab. These compounds also reduced amyloid precursor protein net processing in vitro and in vivo in a mouse model for Alzheimer’s disease and improvedperformance in the novel object recognition learning and memory task. Conclusion: TTF and AcA are potential candidates to be developed as drugs or food additives to prevent, postpone or ameliorate Alzheimer’s disease. Implications, both scientific and agricultural.The synthesis ofAcA and TTF is very complicated. Thus, the plant itself will be the source for the isolation of these compounds or their precursors for synthesis. Therefore, Achilleafragrantissima could be developed into a new crop with industrial potential for the Arava-Negev area in Israel, and will generate more working places in this region.
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Meidan, Rina, and Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
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5

Ngan, Elaine, and Betty Diamond. LPP is Required for TGF-Beta Induced Motility and Invasion of Neu/ErbB-2 Expressing Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada568114.

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6

Liao, Dezhong J. Mechanisms for c-myc Induced Mouse Mammary Gland Carcinogenesis and for the Synergistic Role of TGF(alpha) in the Process. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396362.

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7

Clausen, Jay, Richard Hark, Russ Harmon, John Plumer, Samuel Beal, and Meghan Bishop. A comparison of handheld field chemical sensors for soil characterization with a focus on LIBS. Engineer Research and Development Center (U.S.), February 2022. http://dx.doi.org/10.21079/11681/43282.

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Анотація:
Commercially available handheld chemical analyzers for forensic applications have been available for over a decade. Portable systems from multiple vendors can perform X-ray fluorescence (XRF) spectroscopy, Raman spectroscopy, Fourier transform infrared(FTIR) spectroscopy, and recently laser-induced breakdown spectroscopy (LIBS). Together, we have been exploring the development and potential applications of a multisensor system consisting of XRF, Raman, and LIBS for environmental characterization with a focus on soils from military ranges. Handheld sensors offer the potential to substantially increase sample throughput through the elimination of transport of samples back to the laboratory and labor-intensive sample preparation procedures. Further, these technologies have the capability for extremely rapid analysis, on the order of tens of seconds or less. We have compared and evaluated results from the analysis of several hundred soil samples using conventional laboratory bench top inductively coupled plasma atomic emission spectroscopy (ICP-AES) for metals evaluation and high-performance liquid chromatography (HPLC) and Raman spectroscopy for detection and characterization of energetic materials against handheld XRF, LIBS, and Raman analyzers. The soil samples contained antimony, copper, lead, tungsten, and zinc as well as energetic compounds such as 2,4,6-trinitrotoluene(TNT), hexahydro-1,3,5-triazine (RDX), nitroglycerine (NG), and dinitrotoluene isomers (DNT). Precision, accuracy, and sensitivity of the handheld field sensor technologies were compared against conventional laboratory instrumentation to determine their suitability for field characterization leading to decisional outcomes.
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8

Blumwald, Eduardo, and Avi Sadka. Citric acid metabolism and mobilization in citrus fruit. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7587732.bard.

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Accumulation of citric acid is a major determinant of maturity and fruit quality in citrus. Many citrus varieties accumulate citric acid in concentrations that exceed market desires, reducing grower income and consumer satisfaction. Citrate is accumulated in the vacuole of the juice sac cell, a process that requires both metabolic changes and transport across cellular membranes, in particular, the mitochondrial and the vacuolar (tonoplast) membranes. Although the accumulation of citrate in the vacuoles of juice cells has been clearly demonstrated, the mechanisms for vacuolar citrate homeostasis and the components controlling citrate metabolism and transport are still unknown. Previous results in the PIs’ laboratories have indicated that the expression of a large number of a large number of proteins is enhanced during fruit development, and that the regulation of sugar and acid content in fruits is correlated with the differential expression of a large number of proteins that could play significant roles in fruit acid accumulation and/or regulation of acid content. The objectives of this proposal are: i) the characterization of transporters that mediate the transport of citrate and determine their role in uptake/retrieval in juice sac cells; ii) the study of citric acid metabolism, in particular the effect of arsenical compounds affecting citric acid levels and mobilization; and iii) the development of a citrus fruit proteomics platform to identify and characterize key processes associated with fruit development in general and sugar and acid accumulation in particular. The understanding of the cellular processes that determine the citrate content in citrus fruits will contribute to the development of tools aimed at the enhancement of citrus fruit quality. Our efforts resulted in the identification, cloning and characterization of CsCit1 (Citrus sinensis citrate transporter 1) from Navel oranges (Citrus sinesins cv Washington). Higher levels of CsCit1 transcripts were detected at later stages of fruit development that coincided with the decrease in the juice cell citrate concentrations (Shimada et al., 2006). Our functional analysis revealed that CsCit1 mediates the vacuolar efflux of citrate and that the CsCit1 operates as an electroneutral 1CitrateH2-/2H+ symporter. Our results supported the notion that it is the low permeable citrateH2 - the anion that establishes the buffer capacity of the fruit and determines its overall acidity. On the other hand, it is the more permeable form, CitrateH2-, which is being exported into the cytosol during maturation and controls the citrate catabolism in the juice cells. Our Mass-Spectrometry-based proteomics efforts (using MALDI-TOF-TOF and LC2- MS-MS) identified a large number of fruit juice sac cell proteins and established comparisons of protein synthesis patterns during fruit development. So far, we have identified over 1,500 fruit specific proteins that play roles in sugar metabolism, citric acid cycle, signaling, transport, processing, etc., and organized these proteins into 84 known biosynthetic pathways (Katz et al. 2007). This data is now being integrated in a public database and will serve as a valuable tool for the scientific community in general and fruit scientists in particular. Using molecular, biochemical and physiological approaches we have identified factors affecting the activity of aconitase, which catalyze the first step of citrate catabolism (Shlizerman et al., 2007). Iron limitation specifically reduced the activity of the cytosolic, but not the mitochondrial, aconitase, increasing the acid level in the fruit. Citramalate (a natural compound in the juice) also inhibits the activity of aconitase, and it plays a major role in acid accumulation during the first half of fruit development. On the other hand, arsenite induced increased levels of aconitase, decreasing fruit acidity. We have initiated studies aimed at the identification of the citramalate biosynthetic pathway and the role(s) of isopropylmalate synthase in this pathway. These studies, especially those involved aconitase inhibition by citramalate, are aimed at the development of tools to control fruit acidity, particularly in those cases where acid level declines below the desired threshold. Our work has significant implications both scientifically and practically and is directly aimed at the improvement of fruit quality through the improvement of existing pre- and post-harvest fruit treatments.
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9

Meir, Shimon, Michael S. Reid, Cai-Zhong Jiang, Amnon Lers, and Sonia Philosoph-Hadas. Molecular Studies of Postharvest Leaf and Flower Senescence. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7592657.bard.

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Original objectives: To understand the regulation of abscission by exploring the nature of changes of auxin-related gene expression in tomato (Lycopersicon esculatumMill) abscission zones (AZs) following organ removal, and by analyzing the function of these genes. Our specific goals were: 1) To complete the microarray analyses in tomato flower and leaf AZs, for identifying genes whose expression changes early in response to auxin depletion; 2) To examine, using virus-induced gene silencing (VIGS), the effect of silencing target genes on ethylene sensitivity and abscission competence of the leaf and flower AZs; 3) To isolate and characterize promoters from AZ-specific genes to be used in functional analysis; 4) To generate stable transgenic tomato plants with selected genes silenced with RNAi, under the control of an AZ-specific promoter, for further characterization of their abscission phenotypes. Background: Abscission, the separation of organs from the parent plant, results in postharvest quality loss in many ornamentals and other fresh produce. The process is initiated by changes in the auxin gradient across the AZ, and is triggered by ethylene. Although changes in gene expression have been correlated with the ethylene-mediated execution of abscission, there is almost no information on the initiation of the abscission process, as the AZ becomes sensitized to ethylene. The present project was focused on elucidating these early molecular regulatory events, in order to gain a better control of the abscission process for agricultural manipulations. Major conclusions, solutions, achievements: Microarray analyses, using the Affymetrix Tomato GeneChip®, revealed changes in expression, occurring early in abscission, of many genes with possible regulatory functions. These included a range of auxin- and ethylene-related transcription factors (TFs), other TFs that are transiently induced just after flower removal, and a set of novel AZ-specific genes. We also identified four different defense-related genes, including: Cysteine-type endopeptidase, α- DOX1, WIN2, and SDF2, that are newly-associated with the late stage of the abscission process. This supports the activation of different defense responses and strategies at the late abscission stages, which may enable efficient protection of the exposed tissue toward different environmental stresses. To facilitate functional studies we implemented an efficient VIGS system in tomato, and isolated two abscission-specific promoters (pTAPG1 and pTAPG4) for gene silencing in stable transformation. Using the VIGS system we could demonstrate the importance of TAPGs in abscission of tomato leaf petioles, and evaluated the importance of more than 45 genes in abscission. Among them we identified few critical genes involved in leaf and flower abscission. These included: PTRP-F1, PRP, TKN4, KNOTTED-like homeobox TF, KD1, and KNOX-like homeodomain protein genes, the silencing of which caused a striking retardation of pedicel abscission, and ERF1, ERF4, Clavata-like3 protein, Sucrose transporter protein, and IAA10 genes, the silencing of which delayed petiole abscission. The importance of PRPand KD1 genes in abscission was confirmed also by antisense–silencing using pTAPG4. Experiments testing the effects of RNAi silencing of few other genes are still in progress, The analysis of the microarray results of flower and leaf AZs allowed us to establish a clear sequence of events occurring during acquisition of tissue sensitivity to ethylene, and to confirm our hypothesis that acquisition of ethylene sensitivity in the AZ is associated with altered expression of auxin-regulated genes in both AZs. Implication, both scientific and agricultural: Our studies had provided new insights into the regulation of the abscission process, and shaded light on the molecular mechanisms that drive the acquisition of abscission competence in the AZ. We pointed out some critical genes involved in regulation of abscission, and further expanded our knowledge of auxin-ethylene cross talk during the abscission process. This permits the development of novel techniques for manipulating abscission, and thereby improving the postharvest performance of ornamentals and other crops.
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