Статті в журналах: "Tumor necrosis factor alpha (TNFalpha)"

1

Benbrahim-Tallaa, L., F. Boussouar, C. Rey, and M. Benahmed. "Tumor necrosis factor-alpha inhibits glutathione S-transferase-alpha expression in cultured porcine Sertoli cells." Journal of Endocrinology 175, no. 3 (December 1, 2002): 803–12. http://dx.doi.org/10.1677/joe.0.1750803.

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Glutathione S-transferases (GSTs) are a family of soluble enzymes of detoxification that use reduced glutathione in conjugation and reduction reactions. Toxic electrophiles are substrates for the GSTs. GSTalpha is expressed at high levels in different tIssues such as the testis. Among the different GSTs present in the testis, GSTalpha is specifically expressed in Leydig and Sertoli cells known to be under the control of hormonal and local regulatory factors. The present study investigated the regulatory action of tumor necrosis factor-alpha (TNFalpha) on basal and hormone (FSH and testosterone)-stimulated GSTalpha expression in cultured Sertoli cells. Treatment with TNFalpha (0-20 ng/ml, 48 h) induced a decrease in basal GSTalpha mRNA levels in a dose-dependent manner (fivefold decrease; P<0.001). The maximal and half maximal effects were observed at 20 ng/ml and 7 ng/ml respectively. The inhibitory effect of TNFalpha was also time-dependent with a maximal inhibitory effect (threefold decrease; P<0.001) observed at 48 h. The inhibitory effect of the cytokine was also observed on basal GSTalpha protein (28 kDa) levels. TNFalpha also inhibited the hormone-stimulated GSTalpha expression in Sertoli cells. The treatment of cultured Sertoli cells with both FSH and TNFalpha (100 ng/ml and 10 ng/ml respectively, 48 h) resulted in a complete suppression of the stimulatory action of FSH on GSTalpha mRNA levels. Similarly, in Sertoli cells treated with testosterone or its non-aromatizable metabolite dihydrotestosterone (100 ng/ml, 24 h), TNFalpha reduced the hormone-stimulated GSTalpha mRNA and protein levels. TNFalpha inhibited basal GSTalpha expression without affecting mRNA stability. Indeed, the decay curves (mRNA half-life time=18 h) for the GSTalpha basal mRNA levels in Sertoli cells was similar in the absence or presence of TNFalpha (10 ng/ml, 48 h). Testosterone increased GSTalpha mRNA without affecting the enzyme mRNA stability. TNFalpha antagonized the androgen-stimulated GSTalpha mRNA levels without affecting the enzyme mRNA stability, suggesting that the interaction between the androgen and the cytokine is mostly exerted at a transcriptional level. FSH increased GSTalpha mRNA levels through an increase in mRNA stability (increased mRNA half-life times to 119 h). TNFalpha antagonized the stimulatory effect of FSH on GSTalpha mRNA levels by antagonizing the stabilizing effect exerted by the hormone on GSTalpha mRNA. Together, these results suggest that the increase in the cytokine levels within the testis would alter the detoxification processes against genotoxic products during spermatogenesis.

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2

Warne, JP. "Tumour necrosis factor alpha: a key regulator of adipose tissue mass." Journal of Endocrinology 177, no. 3 (June 1, 2003): 351–55. http://dx.doi.org/10.1677/joe.0.1770351.

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In addition to its established role in the immune system, tumour necrosis factor alpha (TNFalpha) exerts complex regulatory actions on adipose tissue. TNFalpha is produced in and secreted by the adipocyte and thus is in a position to exert a paracrine and/or autocrine role within adipose tissue. TNFalpha affects many aspects of adipocyte function, from adipocyte development to lipid metabolism. Bringing together all of these diverse actions, TNFalpha appears to play a general role in reducing adipose tissue mass. Dysregulation of TNFalpha production and/or action could be one facet in the development of cachexia and obesity, as well as associated metabolic disorders such as insulin resistance.

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3

Brotas, Arles Martins, José Marcos Tellas Cunha, Eduardo Henrique Jorge Lago, Cristiane Chaves Nascentes Machado, and Sueli Coelho da Silva Carneiro. "Tumor necrosis factor-alpha and the cytokine network in psoriasis." Anais Brasileiros de Dermatologia 87, no. 5 (October 2012): 673–83. http://dx.doi.org/10.1590/s0365-05962012000500001.

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New molecular methods of research have greatly expanded the knowledge about the role of cytokines in several diseases, including psoriasis. The work orchestrated by these peptides is essential for the communication between resident inflammatory cells (keratinocytes and endothelial cells) and infiltrating cells (neutrophils, lymphocytes, Langerhans cells). This is a complex network due to redundancy, synergism and, sometimes, the antagonism of cytokines, which prevents full understanding of the pathogenesis of the disease. Currently, it seems premature to try to establish a main actor, but TNFalpha participates in all stages of psoriatic plaque development, as we shall see.

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Schmitz, H., M. Fromm, C. J. Bentzel, P. Scholz, K. Detjen, J. Mankertz, H. Bode, H. J. Epple, E. O. Riecken, and J. D. Schulzke. "Tumor necrosis factor-alpha (TNFalpha) regulates the epithelial barrier in the human intestinal cell line HT-29/B6." Journal of Cell Science 112, no. 1 (January 1, 1999): 137–46. http://dx.doi.org/10.1242/jcs.112.1.137.

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Cytokines are supposed to be mediators in diarrhoeal diseases. The aim of this study is to characterize the effect of tumor necrosis factor-alpha (TNFalpha) on epithelial barrier function in the colonic epithelial cell line HT-29/B6. Active ion transport and barrier function were measured as short-circuit current and transepithelial electrical resistance (Rt), respectively. In parallel, freeze-fracture electron microscopy (EM) of tight junctions (TJ) and immunofluorescence microscopy of the zonula occludens protein-1 (ZO-1) were performed. Serosal addition of TNF(alpha) (100 ng/ml) decreased Rt by 81%. This effect was dose-dependent and could be mimicked by antibodies against the p55 form of the TNF receptor. Cytotoxic effects were excluded by a negative lactate dehydrogenase (LDH) assay. Immunofluorescence localization with anti-ZO-1 antibodies revealed no evidence for disruption of the monolayer after TNFalpha treatment. In freeze-fracture EM, TJ complexity was decreased by TNFalpha, as indicated by a decrease in the number of strands from 4.7 to 3.4. The tyrosine kinase blocker genistein and the protein kinase A inhibitor H-8 reduced the effect of TNFalpha. A combination of TNFalpha with interferon-gamma acted synergistically on the epithelial barrier. In conclusion, TNFalpha impairs epithelial barrier function by altering structure and function of the tight junction, which could be of pathogenic relevance in intestinal inflammation.

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5

Nestor, Avgoustidis, Sipsas Nikolaos, Evangelou Konstantinos, and Pikazis Dimitrios. "Tuberculous bursitis of the wrist after anti-TNFalpha treatment: a case report." Open Medicine 5, no. 1 (February 1, 2010): 62–64. http://dx.doi.org/10.2478/s11536-009-0078-6.

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AbstractIn this report, we describe a case of tuberculous bursitis-osteomyelitis of the wrist, in an elderly patient with rheumatoid arthritis and anti-TNFalpha (anti-Tumor Necrosis Factor alpha) treatment.

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6

Gillio Tos, A., A. Cignetti, G. Rovera, and R. Foa. "Retroviral vector-mediated transfer of the tumor necrosis factor alpha gene into human cancer cells restores an apoptotic cell death program and induces a bystander-killing effect." Blood 87, no. 6 (March 15, 1996): 2486–95. http://dx.doi.org/10.1182/blood.v87.6.2486.bloodjournal8762486.

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Tumor necrosis factor alpha (TNFalpha) may induce tumor cell death by apoptosis, the physiologic program of cell death usually lost during neoplastic progression. However, many tumor cells are resistant to its effect unless high doses are administered. By retroviral vector- mediated gene transfer, we have transduced the TNFalpha gene into the DNA of human tumor cells to investigate whether the indefinite neoplastic cell proliferation could be blocked and the lost physiologic program of cell death restored. Evidence is provided that high-TNFalpha- producing clones generated from a human lymphoma T-cell line (ST4) can undergo apoptosis following transduction of the TNFalpha gene. Internucleosomal DNA cleavage was documented by May-Grunwald-Giemsa and by propidium iodide staining, as well as by gel electrophoresis. The induced apoptotic phenomenon is TNFalpha-mediated, since it can be reverted following incubation with anti-TNFalpha monoclonal antibodies (MoAbs), and it occurs with cytokine levels released in the supernatant by the engineered cells much lower(>100 times) than those required to promote the same effect on parental ST4 cells following administration of exogenous recombinant TNFalpha. The process is associated with a downregulation of the apoptosis-preventing gene, bcl-2, while the expression of bax and p53, genes usually involved in promoting apoptosis, persists. Mixed-culture experiments performed coincubating TNFalpha-transduced and untransduced ST4 cells allowed documentation of a bystander-killing effect on the parental cells. This phenomenon still occurred at transduced to parental cell ratios as low as 1:20 and was blocked in the presence of an anti-TNFalpha MoAb. These findings indicated that TNFalpha may play a regulatory role in the proliferation of human tumor cells, and suggest potential new antitumor therapeutic strategies based on the direct delivery of the TNFalpha gene into cancer cells.

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7

Caux, C., B. Vanbervliet, C. Massacrier, I. Durand, and J. Banchereau. "Interleukin-3 cooperates with tumor necrosis factor alpha for the development of human dendritic/Langerhans cells from cord blood CD34+ hematopoietic progenitor cells." Blood 87, no. 6 (March 15, 1996): 2376–85. http://dx.doi.org/10.1182/blood.v87.6.2376.bloodjournal8762376.

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We have previously shown that tumor necrosis factor (TNF)alpha strongly potentiates the granulocyte-macrophage colony-stimulating factor (GM- CSF)/interleukin (IL)-3-dependent proliferation of CD34+ hematopoietic progenitor cells (HPC) through the recruitment of early progenitors with high proliferative potential. Furthermore, the combination of GM- CSF and TNFalpha allows the generation of large numbers of dendritic/Langerhans cells (D-Lc). Herein, we analyzed whether IL-3, when combined to TNFalpha would, as does GM-CSF, allow the generation of CD1a+ D-Lc. Accordingly, cultures of cord blood CD34+ HPC with IL-3 + TNFalpha yielded 20% to 60% CD14+ cells and 11% to 17% CD1a+ cells, while IL-3 alone did not generate significant numbers of CD1a+ cells. Although the percentage of CD1a+ cells detected in IL3 + TNFalpha was lower than that observed in GM-CSF + TNFalpha (42% to 78%), the strong growth induced by IL-3 + TNFalpha generated as many CD1a+ cells as did GM-CSF + TNFalpha. The CD14+ and CD1a+ cells generated with IL-3 + TNFalpha are similar to CD14+ and CD1a+ cells generated in GM-CSF alone and GM-CSF + TNFalpha, respectively. CD1a+ cells differed from CD14+ cells by (1) dendritic morphology, (2) higher expression of CD1a, CD1c, CD4, CD40, adhesion molecules (CD11c, CD54, CD58), major histocompatibility complex (MHC) class II molecules and CD28 ligands (CD80 and CD86), (3) lack of Fc receptor FcgammaRI (CD64) and complement receptor CR1 (CD35) expression, and (4) stronger induction of allogeneic T-cell proliferation. Thus, in combination with TNFalpha, IL-3 is as potent as GM-CSF for the generation of CD1a+ D-Lc from cord blood CD34+ HPC. The dendritic cell inducing ability of IL-3 may explain why mice with inactivated GM-CSF gene display dendritic cells.

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8

Jia, L., SM Kelsey, MF Grahn, XR Jiang, and AC Newland. "Increased activity and sensitivity of mitochondrial respiratory enzymes to tumor necrosis factor alpha-mediated inhibition is associated with increased cytotoxicity in drug-resistant leukemic cell lines." Blood 87, no. 6 (March 15, 1996): 2401–10. http://dx.doi.org/10.1182/blood.v87.6.2401.bloodjournal8762401.

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The drug-resistant leukemic cell lines, CEM/VLB100 and K/DAU600, are more sensitive to tumor necrosis factor alpha (TNFalpha)-mediated cytotoxicity compared with their parental cell lines, CCRF-CEM and K562 cl.6. Drug-resistant leukemic cell lines have more active mitochondrial function, which is associated with a greater susceptibility to TNFalpha- induced respiratory inhibition. TNFalpha blocked electron transfer at three sites, NADH dehydrogenase (complex I), succinate dehydrogenase (complex II), and cytochrome c oxidase (complex IV). Respiratory rate and electron transport chain enzyme activities were significantly inhibited in the drug-resistant, TNF-sensitive cell lines. Respiratory inhibition preceded cell death by at least 5 to 8 hours. The respiratory failure was not compensated for by appropriate up- regulation of the glycolytic pathway. Increasing mitochondrial respiratory rate and enzyme activities by long-term culture with 2 mmol/L adenosine 5′-diphosphate (ADP) and Pi sensitized both drug- sensitive and drug-resistant cells to TNFalpha-induced cytolysis. Intramitochondrial free radicals generated by paraquat only had a limited and delayed effect on respiratory inhibition and cytolysis in comparison with the effect of TNFalpha. We conclude that TNFalpha- induced cytotoxicity in leukemic cells is, at least in part, mediated by inhibition of mitochondrial respiration. Free radical generation by TNFalpha may not directly lead to the observed inhibition of the mitochondrial electron transport and other mechanisms must be involved.

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9

Fasshauer, M., J. Klein, S. Krahlisch, U. Lossner, M. Klier, M. Bluher, and R. Paschke. "GH is a positive regulator of tumor necrosis factor alpha-induced adipose related protein in 3T3-L1 adipocytes." Journal of Endocrinology 178, no. 3 (September 1, 2003): 523–31. http://dx.doi.org/10.1677/joe.0.1780523.

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Tumor necrosis factor (TNF) alpha-induced adipose-related protein (TIARP) has recently been cloned as a TNFalpha-stimulated protein expressed in adipocytes. Its expression is differentiation-dependent and potentially involved in mediating TNFalpha-induced insulin resistance. To further characterize regulation of TIARP gene expression, 3T3-L1 adipocytes were treated with key hormones modulating insulin sensitivity and influencing adipocyte metabolism, and TIARP gene expression was determined by quantitative real-time RT-PCR. Interestingly, TIARP mRNA expression was stimulated almost 9-fold after 500 ng/ml GH were added for 16 h whereas addition of 10 microM isoproterenol, 100 nM insulin and 100 nM dexamethasone for 16 h significantly decreased TIARP gene expression to between 35 and 50% of control levels. In contrast, angiotensin 2 (10 microM) and triiodothyronine (1 microM) did not have any effect. The stimulatory effect of GH was time- and dose-dependent with stimulation occurring as early as 1 h after effector addition and at concentrations as low as 5 ng/ml GH. Moreover, pharmacological inhibition of Janus kinase 2 and p42/44 mitogen-activated protein kinase reversed the stimulatory effect of GH, suggesting that both signaling molecules are involved in activation of TIARP gene expression by GH. Furthermore, an increase of TIARP mRNA could be completely reversed to control levels by withdrawal of GH for 24 h. Taken together, these results show that TIARP is not only responsive to TNFalpha but also to important other hormones influencing glucose homeostasis and adipocyte metabolism. Thus, this factor may play an integrative role in the pathogenesis of insulin resistance and its link to obesity.

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10

Lambert, GL, S. Barker, DM Lees, and R. Corder. "Endothelin-2 synthesis is stimulated by the type-1 tumour necrosis factor receptor and cAMP: comparison with endothelin-converting enzyme-1 expression." Journal of Molecular Endocrinology 24, no. 2 (April 1, 2000): 273–83. http://dx.doi.org/10.1677/jme.0.0240273.

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ABSTRACT The synthesis of the vasoconstrictor peptide endothelin-2 (ET-2) is dependent on hydrolysis of the biologically inactive intermediate big ET-2 by an endothelin-converting enzyme (ECE). Here, mechanisms inducing ET-2 synthesis have been investigated using the human renal adenocarcinoma cell line (ACHN). Synthesis of ET-2 by ACHN cells was inhibited by phosphoramidon (IC(50( congruent with11 microM). To determine whether ET-2 synthesis occurs in parallel with the metallopeptidase ECE-1, a putative processing peptidase for big ET-2, changes in the levels of their mRNAs were compared by semi-quantitative RT-PCR under conditions causing the upregulation of ET-2 synthesis. Tumour necrosis factor-alpha (TNFalpha), forskolin and a cell-permeable cAMP analogue (dibutyryl cAMP) caused concentration-dependent increases in ET-2 synthesis. Combination of forskolin or dibutyryl cAMP with TNFalpha produced a significantly greater increase in ET-2 production than these agents alone, indicating that adenylate cyclase and TNFalpha induce ET-2 synthesis by separate signalling pathways. Studies using receptor selective TNFalpha mutants, (125(I-TNFalpha binding and TNF receptor mRNA showed that type-1 TNF receptors mediate the ET-2 response to TNFalpha. PreproET-2 mRNA levels were increased by TNFalpha at 1 h and 2 h, but returned to control levels at 4 h. Treatment with forskolin significantly increased preproET-2 mRNA levels after 1 h and 4 h. ACHN cells expressed ECE-1b and ECE-1c, but not the ECE-1a isoform of this peptidase. RT-PCR for the combined isoforms ECE-1b/c/d showed TNFalpha to increase mRNA levels at 2 h and 4 h. Forskolin had no effect on ECE-1b/c/d mRNA levels. Thus, expression of ET-2 and ECE-1b/c/d mRNAs in ACHN cells do not display the co-ordinated regulation observed with typical peptide prohormone processing enzymes and their substrates.

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11

Fasshauer, M., S. Kralisch, M. Klier, U. Lossner, M. Bluher, J. Klein, and R. Paschke. "Insulin resistance-inducing cytokines differentially regulate SOCS mRNA expression via growth factor- and Jak/Stat-signaling pathways in 3T3-L1 adipocytes." Journal of Endocrinology 181, no. 1 (April 1, 2004): 129–38. http://dx.doi.org/10.1677/joe.0.1810129.

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Various cytokines, including tumor necrosis factor (TNF) alpha, growth hormone (GH) and interleukin (IL)-6, induce insulin resistance. Recently, it was demonstrated that induction of suppressor of cytokine signaling (SOCS)-3 by TNFalpha and GH is an important mechanism by which these cytokines impair insulin sensitivity. The current study investigated in 3T3-L1 adipocytes whether TNFalpha and GH also upregulate SOCS-1 and SOCS-6, which have both been shown to inhibit insulin signaling potently, and whether IL-6 might alter synthesis of SOCS-1, -3 and -6. Interestingly, 10 ng/ml TNFalpha, 500 ng/ml GH and 30 ng/ml IL-6 induced SOCS-1 mRNA time-dependently with maximal stimulation detectable after 8 h of TNFalpha and 1 h of GH and IL-6 addition respectively. Furthermore, TNFalpha and GH caused sustained upregulation of SOCS-1 for up to 24 h, whereas stimulation by IL-6 was only transient, with SOCS-1 mRNA returning to basal levels 2 h after effector addition. Induction of SOCS-1 was dose-dependent, and significant stimulation was detectable at concentrations as low as 3 ng/ml TNFalpha, 50 ng/ml GH and 10 ng/ml IL-6. Furthermore, stimulation experiments and studies using pharmacologic inhibitors suggested that the positive effect of TNFalpha, GH and IL-6 on SOCS-1 mRNA is, at least in part, mediated by Janus kinase (Jak) 2. Finally, SOCS-3 expression was dose- and time-dependently induced by IL-6, at least in part via Jak2, but none of the cytokines affected SOCS-6 expression. Taken together, our results show a differential regulation of SOCS mRNA by insulin resistance-inducing hormones, and suggest that SOCS-1, as well as SOCS-3, may be an important intracellular mediator of insulin resistance in fat cells and a potential pharmacologic target for the treatment of impaired insulin sensitivity.

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12

P.O., Manafa, Osmond E.O., Onyenekwe C.C., Okeke C.O., Chukwuma G.O., Ihim A.C., Ogenyi S.I., Chukwuanukwu R.C., Manafa C.C. та Nnadi E.C. "Assessment Of Tumour Necrosis Factor-Alpha (Tnf- Α) And Creatinine Levels In Echis Ocellatus Bite Victims In Jos Metropolis, Nigeria". European Scientific Journal, ESJ 12, № 21 (29 липня 2016): 70. http://dx.doi.org/10.19044/esj.2016.v12n21p70.

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This study was designed to assess tumour necrosis factor-alpha and creatinine levels in Echis ocellatus bite victims. A total of 50 subjects were recruited. Out of this number, 40 were victims of E. ocellatus bite and the remaining 10 were non-victims of snake bite who served as the control group. Blood samples were collected from the victims within 24 hours of the snake bite and EchiTAb-G antivenom administered within the same period. Another batch of blood sample was collected 48 hours post-administration of the anti-venom. Tumour necrosis factor-alpha (TNF-alpha) levels were estimated by the Enzyme Linked Immunosorbent Assay technique while creatinine levels were determined using kinetic-spectrophotometric procedure. The mean serum levels of tumour necrosis factor-alpha and creatinine were significantly increased in E. ocellatus bite victims compared with the control group (P<0.05). Furthermore, the mean serum level of TNFalpha was significantly lower in E. ocellatus bite victims, post-administration of anti-venom, compared with the pre-administration of anti-venom (P<0.05). In contrast, no significant difference was observed in the mean serum level of creatinine in E. ocellatus bite victims, post-administration of anti-venom, compared with the pre-administration of anti-venom (P>0.05). Moreover, the mean serum level of creatinine was found to be significantly increased in E. ocellatus bite victims, post-administration of anti-venom, compared with the control group (P<0.05), while no significant difference was observed in the mean serum level of tumour necrosis factor-alpha in E. ocellatus bite victims, post-administration of anti-venom, compared with the control group(P>0.05). A positive correlation existed between tumour necrosis factor-alpha and creatinine levels in E. ocellatus bite subjects (r= 0.782). Echis ocellatus bite is a risk factor for renal damage indicated by an elevated serum creatinine, thus health authorities should make EchiTAb-G anti-venom freely available in health facilities and administered as quickly as possible to reduce the risk of renal damage in Echis ocellatus bite-prone areas.

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13

Ortiz, A., C. Lorz, S. González-Cuadrado, R. Garcia del Moral, F. O'Valle, and J. Egido. "Cytokines and Fas regulate apoptosis in murine renal interstitial fibroblasts." Journal of the American Society of Nephrology 8, no. 12 (December 1997): 1845–54. http://dx.doi.org/10.1681/asn.v8121845.

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Renal fibrosis is characterized by an increased number of fibroblasts and excessive deposition of extracellular matrix. Apoptotic cell death is a physiological mechanism to limit cell numbers, and an insufficient rate of death may contribute to fibroblast accumulation. However, little is known about the regulation of renal fibroblast survival. The authors have studied the interaction of cytokines and the Fas receptor in the regulation of apoptosis of renal fibroblasts and have observed that murine renal fibroblasts express Fas and the Fas ligand. Tumor necrosis factor alpha (TNFalpha) and agonistic anti-Fas antibodies induce apoptosis of renal fibroblasts in a time- and dose-dependent manner. Serum contains survival factors for renal fibroblasts. Both serum deprivation and TNFalpha increase the sensitivity to Fas-induced death and the expression of fas mRNA and Fas receptor. By contrast, insulin-like growth factor-1 decreases apoptosis induced by both serum deprivation and Fas activation and partially prevents the increase in Fas receptor expression induced by serum deprivation. Murine renal fibroblasts express constitutively both fas ligand mRNA and cell-surface Fas ligand, but the authors could not demonstrate a role for Fas ligand in the autocrine regulation of fibroblast survival. These data suggest that Fas and other cytokines cooperate to regulate renal fibroblast apoptosis. Modulation of the Fas death-signaling pathway in renal fibroblasts could represent a new therapeutic target for renal fibrosis.

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14

PATINO-GARCIA, A. "Analysis of the human tumour necrosis factor-alpha (TNFalpha ) gene promoter polymorphisms in children with bone cancer." Journal of Medical Genetics 37, no. 10 (October 1, 2000): 789–92. http://dx.doi.org/10.1136/jmg.37.10.789.

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15

MacKenzie, R. K., C. J. Holmes, A. Moseley, J. P. Jenkins, J. D. Williams, G. A. Coles, D. Faict, and N. Topley. "Bicarbonate/lactate- and bicarbonate-buffered peritoneal dialysis fluids improve ex vivo peritoneal macrophage TNFalpha secretion." Journal of the American Society of Nephrology 9, no. 8 (August 1998): 1499–506. http://dx.doi.org/10.1681/asn.v981499.

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Peritoneal macrophage (PMO) function was examined ex vivo after their in vivo exposure to either acidic, lactate-buffered solutions (PD4; 40 mM lactate, pH 5.2), bicarbonate/lactate-buffered solution (TBL; 25 mM/15 mM bicarbonate/lactate, pH 7.3), or bicarbonate-buffered solution (TB; 38 mM bicarbonate, pH 7.3), containing either 1.36 or 3.86% glucose. Initial experiments demonstrated that tumor necrosis factor-alpha (TNFalpha) release (assessed by TNF-direct immunoassay [DIA]) from PMO isolated from the peritoneal cavities of patients exposed to conventional fluid (PD4 1.36% glucose) was lowest after 30 min of intraperitoneal dwell (3591+/-1200 versus 28,946+/-9359 for 240-min dwell [pg/ml], n=5, P < 0.05). Five patients were exposed on 3 successive days to PD4, TBL, and TB for 30-min acute dwells containing 1.36% glucose in the first week and 3.86% glucose during the second. PMO TNFalpha release was assessed after ex vitro exposure to lipopolysaccharide (LPS). Exposure of PMO to TBL or TB (1.36% glucose) resulted in a significant increase in the generation of TNFalpha (pg/2 X 10(6) PMO) compared with PD4. TBL: 68,659+/-35,633, TB: 53,682+/-26,536 versus PD4 17,107+/-8996 (LPS 1.0 ng/ml, n=5 patients, P=0.043 versus PD4 for both). PMO that were recovered from PD4 and TB dwells (3.86% glucose) showed no significant difference in TNFalpha secretion (21,661+/-6934 and 23,923+/-9147, respectively). In contrast, exposure to TBL resulted in a significant increase (41,846+/-11,471) compared with PD4 (LPS 1.0 ng/ml, n=5 patients, P=0.043). These data demonstrate enhanced PMO function after in vivo exposure to bicarbonate- and bicarbonate/lactate-buffered solutions. This response was sustained in TBL alone at the highest glucose concentrations. These results suggest that the newer solutions, and particularly bicarbonate/lactate, might improve host defense status in peritoneal dialysis patients.

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16

Jones, KL, DM de Kretser, IJ Clarke, JP Scheerlinck, and DJ Phillips. "Characterisation of the rapid release of activin A following acute lipopolysaccharide challenge in the ewe." Journal of Endocrinology 182, no. 1 (July 1, 2004): 69–80. http://dx.doi.org/10.1677/joe.0.1820069.

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A series of experiments were conducted in adult ewes to delineate the release profile of activin A and its relationship to other cytokines following an i.v. injection of the bacterial cell wall component, lipopolysaccharide (LPS). Following this challenge, plasma activin A increased rapidly and appeared to be released in a biphasic manner, slightly preceding the release of tumour necrosis factor-alpha (TNFalpha) and before elevation of interleukin (IL)-6 and follistatin levels. The concentration of activin A was correlated with body temperature during the response to LPS. A second experiment compared cytokine concentrations in matched blood and cerebrospinal fluid (CSF) samples. This revealed that activin A was not released centrally in the CSF following a peripheral LPS injection, nor was TNFalpha or the activin binding protein, follistatin, but IL-6 showed a robust elevation. In a third experiment, the stimulus for activin A release was examined by blocking prostaglandin synthesis. Flurbiprofen, a prostaglandin synthesis inhibitor, effectively attenuated the fever response to LPS and partly inhibited cortisol release, but the cytokine profiles were unaffected. Finally, the bioactivity of TNFalpha and/or IL-1 was blocked using soluble receptor antagonists. These treatments did not affect the initial release of activin A, but blockade of TNFalpha depressed the second activin peak. These studies define more rigorously the release of activin A into the circulation following acute inflammatory challenge. The response is rapid and probably biphasic, independent of prostaglandin- mediated pathways and does not depend upon stimulation by TNFalpha or IL-1. The data suggest that activin A release is an early event in the inflammatory cascade following the interaction of LPS with its cellular receptor.

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17

Milner, C. R. "No association between the 308 polymorphism in the tumour necrosis factor alpha (TNFalpha) promoter region and polycystic ovaries." Molecular Human Reproduction 5, no. 1 (January 1, 1999): 5–9. http://dx.doi.org/10.1093/molehr/5.1.5.

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18

Byrd, T. F. "Tumor necrosis factor alpha (TNFalpha) promotes growth of virulent Mycobacterium tuberculosis in human monocytes iron-mediated growth suppression is correlated with decreased release of TNFalpha from iron-treated infected monocytes." Journal of Clinical Investigation 99, no. 10 (May 15, 1997): 2518–29. http://dx.doi.org/10.1172/jci119436.

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19

Tsulukiya, I. T., E. I. Alexeeva, and T. M. Dvoryakovskaya. "Discontinuation of TNF-alpha inhibitors following remission in juvenile idiopathic arthritis without systemic manifestations." Voprosy praktičeskoj pediatrii 17, no. 4 (2022): 48–58. http://dx.doi.org/10.20953/1817-7646-2022-4-48-58.

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Juvenile idiopathic arthritis (JIA) is one of the most common and disabling rheumatic diseases in children. Pharmaceutical therapy for JIA can prevent the progression of the disease, achieve long-term remission, and significantly improve the quality of life in most patients. In cases where the initial therapy for JIA is not effective enough, it is recommended to escalate it, and vice versa, when remission is achieved, the de-escalation of therapy may be discussed. The latter is necessary due to the high risk of developing infectious complications and certain oncological diseases against the background of continuous biological treatment of JIA, as well as the negative impact of regular injections and/or infusions of medications on the quality of life, the interruption of educational process, the psychological burden of “lifelong” treatment with medications, and the economic burden on families and healthcare system. Currently, optimal regimens for the discontinuation of biopharmaceuticals, including TNFalpha inhibitors, remain a matter of debate. In this regard, the search for potential predictors of JIA exacerbation after withdrawal of biopharmaceuticals is relevant. Key words: juvenile idiopathic arthritis, biologic-free remission of JIA, tumor necrosis factor, inhibitors, etanercept, adalimumab, withdrawal, exacerbation, predictors

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Lindberg, MK, M. Erlandsson, SL Alatalo, S. Windahl, G. Andersson, JM Halleen, H. Carlsten, JA Gustafsson, and C. Ohlsson. "Estrogen receptor alpha, but not estrogen receptor beta, is involved in the regulation of the OPG/RANKL (osteoprotegerin/receptor activator of NF-kappa B ligand) ratio and serum interleukin-6 in male mice." Journal of Endocrinology 171, no. 3 (December 1, 2001): 425–33. http://dx.doi.org/10.1677/joe.0.1710425.

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Estrogens are important for the male skeleton. Osteoprotegerin (OPG), receptor activator of NF-kappa B ligand (RANKL), interleukin-6 (IL-6), IL-1 and tumor necrosis factor alpha (TNFalpha) have been suggested to be involved in the skeletal effects of estrogen. We treated orchidectomized mice with estradiol for 2 weeks and observed a 143% increase in the trabecular bone mineral density of the distal metaphysis of femur that was associated with a decreased OPG/RANKL mRNA ratio in vertebral bone. A similar decreased OPG/RANKL ratio was also seen after estrogen treatment of ovariectomized female mice. The effect of estrogen receptor (ER) inactivation on the OPG/RANKL ratio was dissected by using intact male mice lacking ER alpha (ERKO), ER beta (BERKO) or both receptors (DERKO). The expression of OPG was increased in ERKO and DERKO but not in BERKO male mice, resulting in an increased OPG/RANKL ratio. Furthermore, serum levels of IL-6 and tartrate-resistant acid phosphatase 5b (TRAP 5b) were decreased in ERKO and DERKO, but not in BERKO male mice. These results demonstrate that ER alpha, but not ER beta, is involved in the regulation of the vertebral OPG/RANKL ratio, serum levels of IL-6 and TRAP 5b in male mice.

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Gormley, Sheena M. C., William T. McBride, Marilyn A. Armstrong, Ian S. Young, Elizabeth McClean, Simon W. MacGowan, Gianfranco Campalani, and Terence J. McMurray. "Plasma and Urinary Cytokine Homeostasis and Renal Dysfunction during Cardiac Surgery." Anesthesiology 93, no. 5 (November 1, 2000): 1210–16. http://dx.doi.org/10.1097/00000542-200011000-00013.

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Background Cardiac surgery induces changes in plasma cytokines. Proinflammatory cytokines have been associated with a number of renal diseases. The proinflammatory cytokines interleukin 8 (IL-8), tumor necrosis factor alpha (TNFalpha), and interleukin 1beta (IL-1beta) are smaller than the antiinflammatory cytokines interleukin 10 (IL-10), interleukin 1 receptor antagonist (IL-1ra), and TNF soluble receptor 2 (TNFsr2), and thus undergo glomerular filtration more readily. Accordingly, this study investigated the relation between plasma and urinary cytokines and proximal renal dysfunction during cardiac surgery. Methods Twenty patients undergoing coronary artery bypass grafting with cardiopulmonary bypass (CPB) were studied. Blood and urine samples were analyzed for proinflammatory and antiinflammatory cytokines. Proximal tubular dysfunction was measured using urinary N-acetyl-beta-d-glucosaminidase (NAG)/creatinine and alpha1-microglobulin/creatinine ratios. Results Plasma IL-8, IL-10, IL-1ra, and TNFsr2 values were significantly elevated compared with baseline. Urinary IL-1ra and TNFsr2 were significantly elevated. Urinary NAG/creatinine and alpha1-microglobulin/creatinine ratios were also elevated. Plasma TNFalpha at 2 h correlated with urinary NAG/creatinine ratio at 2 and 6 h (P < 0.05) and with urinary IL-1ra at 2 h (P < 0.05). Plasma IL-8 at 2 h correlated with NAG/creatinine at 6 h (P < 0.05). Urinary IL-1ra correlated with urinary NAG/creatinine ratio after cross-clamp release and 2 and 6 h after CPB (P < 0.05). Conclusions Cardiac surgery using CPB leads to changes in plasma and urinary cytokine homeostasis that correlate with renal proximal tubular dysfunction. This dysfunction may be related to the renal filtration of proinflammatory mediators. Renal autoprotective mechanisms may involve the intrarenal generation of antiinflammatory cytokines.

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Kawai, Y., Y. Matsumoto, K. Watanabe, H. Yamamoto, K. Satoh, M. Murata, M. Handa, and Y. Ikeda. "Hemodynamic forces modulate the effects of cytokines on fibrinolytic activity of endothelial cells." Blood 87, no. 6 (March 15, 1996): 2314–21. http://dx.doi.org/10.1182/blood.v87.6.2314.bloodjournal8762314.

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We investigated the effects of hemodynamic force on fibrinolytic activity of cultured human umbilical vein endothelial cells stimulated by cytokines, using a modified cone-plate viscometer in which well- controlled and -defined shear forces were generated. Treatment of the cells with interleukin (IL)-beta or tumor necrosis factor alpha (TNFalpha) under static conditions had no effect on tissue plasminogen activator (t-PA) secretion, while release of plasminogen activator inhibitor 1 (PAI-1) increased. When cells were exposed to increasing shear stress up to 24 dynes/cm2, levels of t-PA and t-PA/PAI-1 complex significantly increased relative to shear stress, while total PAI-1 and active PAI-1 secretion decreased gradually. In the presence of IL-1beta or TNFalpha, the increase in production of t-PA and the t-PA/PAI-1 complex was further augmented. Dot blot hybridization analysis of cultured cells in similar experimental conditions using t-PA and PAI-1 cDNA probes revealed no t-PA mRNA in 3 microg total RNA from static endothelial cells under resting or cytokine-stimulated conditions, but abundant t-PA mRNA was detected in cells subjected to a shear force of 18 dynes/cm2, and the increase was further augmented by addition of cytokines. In contrast, PAI-1 mRNA was detected in resting and cytokine- stimulated, nonsheared endothelial cells, but levels decreased after exposure to shear stress, even in the presence of cytokines. These results indicate a role for hemodynamic forces in regulating fibrinolytic activity with or without cytokine stimulation.

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Kroon, M. E., P. Koolwijk, B. van der Vecht, and V. W. van Hinsbergh. "Hypoxia in combination with FGF-2 induces tube formation by human microvascular endothelial cells in a fibrin matrix: involvement of at least two signal transduction pathways." Journal of Cell Science 114, no. 4 (February 15, 2001): 825–33. http://dx.doi.org/10.1242/jcs.114.4.825.

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Hypoxia in combination with a growth factor is a strong inducer of angiogenesis. Among several effects, hypoxia can activate endothelial cells directly, but the mechanism by which it acts is not fully elucidated. In vitro, human microvascular endothelial cells (hMVEC) form capillary-like tubules in fibrin solely after stimulation with a combination of fibroblast growth factor (FGF)-2 or vascular endothelial growth factor (VEGF) and the cytokine tumour necrosis factor (TNF)alpha. We show in this paper that in hypoxic conditions, FGF-2-stimulated hMVEC form tube-like structures in a fibrin matrix in the absence of TNFalpha. Hypoxia/FGF-2-stimulated cells express more urokinase-type plasminogen activator (u-PA) receptor than normoxia/FGF-2-stimulated cells and display a slightly higher turnover of u-PA. This small increase in u-PA activation probably cannot fully explain the hypoxia/FGF-2-induced tube formation. Hypoxia activated at least two signal pathways that may contribute to the enhanced angiogenic response. In hypoxia/FGF-2-stimulated hMVEC the transcription factor p65 was activated and translocated to the nucleus, whereas in normoxia/FGF-2-stimulated cells p65 remained inactive. Furthermore, in hypoxic conditions, the amounts of phosphorylated mitogen-activated protein kinases ERK1/2 were increased compared to normoxic conditions. We conclude that hypoxia is able to activate different signal pathways in FGF-2-stimulated human endothelial cells, which may be involved in hypoxia-induced angiogenesis.

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Lorenzin, M., A. Ortolan, G. Cozzi, A. Calligaro, M. Favaro, T. Del Ross, A. Doria та R. Ramonda. "AB0549 PREDICTIVE FACTORS FOR SWITCHING IN PATIENTS WITH PSORIATIC ARTHRITIS UNDERGOING ANTI-TNFα, ANTI-IL12/23 OR ANTI-IL17 DRUGS: A FIFTEEN-YEAR MONOCENTRIC REAL-LIFE STUDY". Annals of the Rheumatic Diseases 80, Suppl 1 (19 травня 2021): 1308.1–1308. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2019.

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Background:Biological Disease-Modifying Anti-Rheumatic Drugs (bDMARDs) targeting Tumor Necrosis Factor (TNF) alpha, Interleukin (IL) 12/23 and IL17, have been approved for Psoriatic Arthritis (PsA) treatment, in this chronological order.Objectives:The aims of our study were to evaluate 1) predictors of first bDMARD failure, including mechanism of action 2) factors associated to failure of multiple (>=2) therapies.Methods:Consecutive patients attending our Rheumatology Unit, classified as PsA according to CASPAR criteria and beginning treatment with bDMARDs in the period 2004-2020, were enrolled. Disease characteristics, previous/ongoing treatments, comorbidities and follow-up duration were recorded. Demographic, clinical and laboratory data, disease-activity and functional indexes [including Disease Activity in PSoriatic Arthritis (DAPSA), PASI (Psoriasis Area and Severity Index) and Health Assessment Questionnaire (HAQ)], were recorded at baseline and yearly and were compared between switchers (>=1 switch/swap) and non-switchers. Date and reason for switching were collected. Effectiveness was evaluated over-time with descriptive statistics. A multivariable Cox-Proportional-Hazard (PH) model was built to evaluate the influence of mechanism of action (anti-TNFalpha/anti-IL12/23/anti-IL17) and of negative prognostic factors for drug response on time to first bDMARD discontinuation. Furthermore, a multivariable logistic regression model was built to assess the association between negative prognostic factors for drug response (independent variables) and failure of>=2 bDMARDs (“multifailure”, outcome). Kaplan-Meier curves were used to assess differences in time-to-first bDMARD discontinuation according to the targeted cytokine. P values <=0.05 were considered significant. Infections and adverse events were recorded.Results:Our study included 264 patients, 117 (44.32%) females, mean age 56±12 years, mean PsA duration 15±3 years;117 (44.32%) switched bDMARDs at least once. Switchers were mostly females, with higher PASI and worse HAQ at baseline (Figure 1). Mean time-to-first bDMARD discontinuation was 72 months; 2-year and 5-year retention rate was 75% and 60%, respectively. Survival curves for anti-TNFalpha/anti-IL12/23/anti-IL17 were similar (log-rak test=0.83;p=0.66). Main reasons for switching were inefficacy (79) and adverse events (38). The Cox PH model showed that female sex was independently associated to a higher risk of first bDMARD discontinuation (HR=2.39; 95%CI:1.50-3.81), while initiating therapy before 2015 was protective (HR=0.40; 95%CI:0.22-0.73). Other independent variables, including mechanism of action (HR=0.76; 95%CI:0.30-1.74 for anti-IL17; HR=0.53; 95%CI 0.15-1.86 for anti-IL12/23; reference: anti-TNFalpha), age (HR=1.00; 95%CI:0.99-1.03), baseline DAPSA (HR=0.98; 95%CI:0.96-1.00), PASI (HR=0.95; 95%CI:0.86-1.04), HAQ (HR=1.29; 95%CI:0.91-1.83), Body Mass Index BMI (HR=1.02; 95%CI:0.98-1.07) and comorbidities (HR=1.10; 95%CI:0.92-1.31) were not associated to the outcome. In the logistic regression model, only female sex was significantly associated to failure of>=2 therapies (OR=1.99, 95%CI:1.07-3.69); bDMARD mechanism of action, age, and initiating therapy before 2015 were instead not independently associated.Conclusion:Survival rate was good for anti-TNFalpha and other bDMARDs. Female sex was a predictor of first bDMARD discontinuation, unlike mechanism of action, comorbidities and BMI.Figure 1.Disclosure of Interests:Mariagrazia Lorenzin: None declared., Augusta Ortolan: None declared., Giacomo Cozzi: None declared., Antonia Calligaro: None declared., Maria Favaro: None declared., Teresa Del Ross: None declared., Andrea Doria Grant/research support from: AD has received honoraria and speaker fees from Novartis, Abbvie, Pfizer, MSD, Janssen., Roberta Ramonda Grant/research support from: RR has received honoraria and speaker fees from Novartis, Abbvie, Pfizer, MSD, Janssen.

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Res, P., E. Martinez-Caceres, A. Cristina Jaleco, F. Staal, E. Noteboom, K. Weijer, and H. Spits. "CD34+CD38dim cells in the human thymus can differentiate into T, natural killer, and dendritic cells but are distinct from pluripotent stem cells." Blood 87, no. 12 (June 15, 1996): 5196–206. http://dx.doi.org/10.1182/blood.v87.12.5196.bloodjournal87125196.

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Recently we reported that the human thymus contains a minute population of CD34+CD38dim cells that do not express the T-cell lineage markers CD2 and CD5. The phenotype of this population resembled that of CD34+CD38dim cells present in fetal liver, umbilical cord blood, and bone marrow known to be highly enriched for pluripotent hematopoietic stem cells. In this report we tested the hypothesis that the CD34+CD38dim thymocytes constitute the most primitive hematopoietic cells in the thymus using a combination of phenotypic and functional analyses. It was found that in contrast to CD34+CD38dim cells from fetal liver and bone marrow, CD34+CD38dim cells from the thymus express high levels of CD45RA and are negative for Thy-1. These data indicate that the CD34+CD38dim thymocytes are distinct from pluripotent stem cells. CD34+CD38dim thymocytes differentiate into T cells when cocultured with mouse fetal thymic organs. In addition, individual cells in this population can differentiate either to natural killer cells in the presence of stem cell factor (SCF), interleukin-7 (IL-7), and IL-2 or to dendritic cells in the presence of SCF, granulocyte- macrophage colony-stimulating factor, and tumor necrosis factor alpha(TNFalpha), indicating that CD34+CD38dim thymocytes contain multi- potential hematopoietic progenitors. To establish which CD34+ fetal liver subpopulation contains the cells that migrate to the thymus, we investigated the T-cell-developing potential of CD34+CD38dim and CD34+CD38+ fetal liver cells and found that the capacity of CD34+ fetal liver cells to differentiate into T cells is restricted to those cells that are CD38dim. Collectively, these findings indicate that cells from the CD34+CD38dim fetal liver cell population migrate to the thymus before upregulating CD38 and ommitting to the T-cell lineage.

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McMahon, CD, TH Elsasser, DR Gunter, LG Sanders, BP Steele, and JL Sartin. "Estradiol/progesterone implants increase food intake, reduce hyperglycemia and increase insulin resistance in endotoxic steers." Journal of Endocrinology 159, no. 3 (December 1, 1998): 469–78. http://dx.doi.org/10.1677/joe.0.1590469.

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High doses of lipopolysaccharide (LPS) induce transient hyperglycemia, then chronic hypoglycemia and increased insulin resistance. In addition, appetite is reduced, while body temperature and concentrations of cortisol and tumor necrosis factor alpha (TNFalpha) are elevated. Furthermore, concentrations of GH and IGF-I are reduced in cattle. The objectives of this study were to determine whether a gonadal steroid implant (20 mg estrogen and 200 mg progesterone) given to endotoxemic steers would: (1) reduce hyperglycemia, reduce hypoglycemia, reduce insulin resistance, (2) reduce changes in concentrations of GH and IGF-I, (3) reduce inappetence and reduce concentrations of blood urea nitrogen (BUN) and non-esterified fatty acids (NEFA), and (4) reduce fever and concentrations of TNFalpha and cortisol. Holstein steers were assigned within a 2x2 factorial arrangement of treatments as follows (n=5 per group): C/C, no steroid and vehicle; S/C, steroid and vehicle; C/E, no steroid and LPS (1 microg/kg body weight (BW), i.v.); S/E, steroid and endotoxin. Steroid implants were given at 20 weeks of age (day 0) and serial blood samples (15 min) were collected on day 14 for 8 h, with vehicle or LPS injected after 2 h. Intravenous glucose tolerance tests (100 mg/kg BW) were carried out at 6 h and 24 h. Hyperglycemia was 67% lower (P<0.05) in S/E- compared with C/E-treated steers between 30 and 150 min after i.v. injection of LPS. Hypoglycemia developed after 4 h and insulin resistance was greater in S/E- compared with C/E-treated steers (P<0. 05) at 6 and 24 h. Concentrations of IGF-I were restored earlier in steroid-treated steers than in controls. Concentrations of GH were not affected by steroids, but increased 1 h after injection of LPS, then were reduced for 2 h. Appetite was greater (P<0.05) in S/E- (2.1% BW) compared with C/E-treated steers (1.1% BW) (pooled s.e.m.=0.3). Concentrations of NEFA increased after injecting LPS, but concentrations were lower (P<0.05) in S/E- compared with C/E-treated steers. LPS did not affect concentrations of BUN, but concentrations were lower in steroid-treated steers. Steroids did not affect body temperature or concentrations of TNFalpha and cortisol. In summary, gonadal steroids reduce hyperglycemia, reduce inappetence and tissue wasting, but increase insulin resistance. Furthermore, concentrations of IGF-I are restored earlier in steroid-treated than in non-steroid-treated steers injected with LPS. It is concluded that gonadal steroids reduce severity of some endocrine and metabolic parameters associated with endotoxemia. However, it is unlikely that gonadal steroids acted via anti-inflammatory and immunosuppressive actions of glucocorticoids or through reducing concentrations of cytokines.

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Barrera, P. "Effects of treatment with a fully human anti-tumour necrosis factor alpha monoclonal antibody on the local and systemic homeostasis of interleukin 1 and TNFalpha in patients with rheumatoid arthritis." Annals of the Rheumatic Diseases 60, no. 7 (July 1, 2001): 660–69. http://dx.doi.org/10.1136/ard.60.7.660.

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Ognjanovic, S., S. Bao, SY Yamamoto, J. Garibay-Tupas, B. Samal, and GD Bryant-Greenwood. "Genomic organization of the gene coding for human pre-B-cell colony enhancing factor and expression in human fetal membranes." Journal of Molecular Endocrinology 26, no. 2 (April 1, 2001): 107–17. http://dx.doi.org/10.1677/jme.0.0260107.

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Pre-B-cell colony enhancing factor (PBEF) was first isolated from an activated peripheral blood lymphocyte cDNA library and was found to be involved in the maturation of B-cell precursors. It was subsequently identified as one of the genes upregulated by distending the human fetal membranes in vitro. Here we report on the genomic organization of this gene, which is composed of 11 exons and 10 introns, spanning 34.7 kb of genomic DNA. Neither the gene nor the protein has any homology with other cytokines in any currently available database. The use of two promoters (proximal and distal) may result in differential, tissue specific expression of the PBEF transcripts. The 5'-flanking region lacks the classical sequence motif that would place it with the hematopoietic cytokines; however, it has several putative regulatory elements, suggesting that this gene may be chemically and mechanically responsive to inducers of transcription. The three PBEF mRNA transcripts were observed in both normal and infected human fetal membranes but were significantly upregulated (P<0.05) in severe infection. The PBEF protein was immunolocalized, in both normal and infected tissues, to both the normal fetal cells of the amnion and chorion and the maternal decidua of the membranes, and to the invading neutrophils. These stained strongly and were likely to contribute to the increased expression in infection. The amniotic epithelial cell line (WISH cells) has been used as a model to study PBEF gene modulation. Lipopolysaccharide, interleukin (IL)-1beta, tumour necrosis factor (TNF)alpha and IL-6 all significantly increased the expression of PBEF in 4 h of treatment. The addition of dexamethasone to IL-1beta and TNFalpha significantly reduced the response of PBEF to these cytokines. IL-8 treatment failed to alter PBEF gene expression. Thus PBEF is a cytokine expressed in the normal fetal membranes and upregulated when they are infected. It is likely to have a central role in the mechanism of infection-induced preterm birth.

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Beksac, Meral, Merih Kizil, Ender A. Soydan, Esin Serbest, and Klara Dalva. "Interleukin-10(IL-10)1082-A and Tumor Necrosis Factor(TNF)-Alpha 238/308A Genotypes Are Associated with Earlier (Younger Than 55) Onset of Multiple Myeloma." Blood 104, no. 11 (November 16, 2004): 4869. http://dx.doi.org/10.1182/blood.v104.11.4869.4869.

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Abstract The individual differences among the polymorphic regions of the cytokine genes involved in the pathogenesis of myeloma have been investigated by various groups: Neben et al have found the TNF238 A allel to be associated with a higher serum level of TNF-alpha and with better response to Thalidomide. The IL 10-1082 G promoter gene genotype have been found to be associated with high secretory pattern and in increased frequency among myeloma patients compared to normal controls by Zheng et al. Van Ness et al have reported the IL-10-G genotype to be associated with shorter survival compared to IL-10-A allele carriers None of these groups have analyzed the impact of these genotypes on age of onset. With an aim to analyze the association between the frequencies of the cytokines known to be important in the pathogenesis of Myeloma, TNF-alpha, IL-6, IL-10 and the age of diagnosis, we have isolated DNA from peripheral blood of 59 patients. Patients with a median age of 56(28–83)M/F:35/24 diagnosed and treated in our center between 2002–2004 were analyzed. To determine the TNF 238 and 308(G/A), IL-6 174(G/C), IL-10 1082(G/A),819(T/C) and 592(A/C) bp polymorphic allele frequencies Cytokine Genotyping Kit (Pel-Freeze) and/or Cytgen (OneLambda) Genotyping Trays have been used. Evaluation of results were done as described in the worksheets. Interpretation and definition of phenotypes(low and high secretory patterns) were based on the previously published reports. 30 patients(50,8%) were younger than 56 (median=the cutoff:56). TNF-A homozygous alelle couldnot be observed among all patients. The frequencies of all alleles were: TNF-alfa308A, TNF-alfa238A, IL-10 1082 G 20%, 20%, 12% respectively. IL-6 -GG/GC alleles which have been linked with high secretory pattern constituted the majority of the patients(58/59). When TNFalfa-A were detected based on the 238 bp reactivity the association of low phenotype with elder age was remarkable(p=0.019). This finding wasnot valid for the 308 bp location. IL-10 phenotypes were more complicated with an accumulation in the intermediate level of secretion. The impact of TNF was varified with the separate evaluation of this group, based on their TNF-238/308 genotype, p=0.031). Conclusion: There is a trend towards younger age of onset in Myeloma. Genetic factors for susceptibility have not been defined yet. The new tools for detection of single nucleotide polymorphisms have a promising role in this field. In our prospective study we have found a predominance of low IL-10 secretory A genotype and the high secretory TNF-A genotype among patients younger than 56. To our knowledge this is the first report on such an association. Investigation of other genes in linkeage with TNF on the neighboring MHC region may be necessary for understanding myeloma pathogenesis. Age TNF 238 H/L TNF 308 H/L TNF 238,308 H/L IL-10 H/I/L IL-10 I,TNF H(238 or 308)/ IL-10 I,TNF L(238 or308) L:Low, H: High,I:Intermediate secretory, TNF238A:H, TNF238G:L, TNF308A:H, TNF308G:L, IL-10G: H ≤55 5 / 7 6 / 24 7 / 5 1 /16 / 13 5 / 2 >55 1 / 16 6 / 23 4 / 13 6 /13 / 8 1 / 6 N=29, p=0.019 N=59, p=0.948 N=29, p=0.057 N=57, p=0.085 N=14, p=0.031

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Humby, Frances, Patrick Durez, Maya H. Buch, Myles J. Lewis, Michele Bombardieri, Christopher John, Hasan Rizvi, et al. "Rituximab versus tocilizumab and B-cell status in TNF-alpha inadequate-responder rheumatoid arthritis patients: the R4-RA RCT." Efficacy and Mechanism Evaluation 9, no. 7 (August 2022): 1–58. http://dx.doi.org/10.3310/gopl1729.

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Background Although biological therapies have transformed the outlook for those with rheumatoid arthritis, there is a lack of any meaningful response in approximately 40% of patients. The role of B cells in rheumatoid arthritis pathogenesis is well recognised and is supported by the clinical efficacy of the B-cell-depleting agent rituximab (MabThera, F. Hoffman La-Roche Ltd, Basel, Switzerland). Rituximab is licensed for use in rheumatoid arthritis following failure of conventional synthetic disease-modifying antirheumatic drugs and tumour necrosis factor inhibitor therapy. However, over 50% of patients show low/absent synovial B-cell infiltration, suggesting that, in these patients, inflammation is driven by alternative cell types. This prompted us to test the hypothesis that, in synovial biopsy B-cell-poor patients, tocilizumab (RoActemra, F. Hoffman La-Roche Ltd, Basel, Switzerland) (targeting interleukin 6) is superior to rituximab (targeting CD20+/B cells). Design The R4–RA (A Randomised, open-labelled study in anti-TNFalpha inadequate responders to investigate the mechanisms for Response, Resistance to Rituximab versus Tocilizumab in Rheumatoid Arthritis patients) trial is a 48-week Phase IV, open-label, randomised controlled trial conducted in 19 European centres that recruited patients failing on or intolerant to conventional synthetic disease-modifying antirheumatic drug therapy and at least one tumour necrosis factor inhibitor. Participants Synovial tissue was obtained at trial entry and classified histologically as B-cell rich or B-cell poor to inform balanced stratification. Patients were randomised on a 1 : 1 basis to receive standard therapy with rituximab or tocilizumab. B-cell-poor/-rich molecular classification was also carried out. The study was powered to test the superiority of tocilizumab over rituximab at 16 weeks in the B-cell-poor population. Main outcome measures The primary end point was defined as an improvement in the Clinical Disease Activity Index (CDAI) score of ≥ 50% from baseline. In addition, patients were considered to be non-responders if they did not reach an improvement in CDAI score of ≥ 50% and a CDAI score of < 10.1, defined for simplicity as CDAI major treatment response (CDAI-MTR). Secondary outcomes included the assessment of CDAI response in the B-cell-rich cohort, in which the non-inferiority of rituximab compared with tocilizumab was evaluated. Safety data up to week 48 are reported. Results In total, 164 patients were randomised: 83 patients received rituximab and 81 received tocilizumab. Eighty-one out of 83 rituximab patients and 73 out of 81 tocilizumab patients completed treatment up to week 16 (primary end point). Baseline characteristics were comparable between the treatment groups. In the histologically classified B-cell-poor population (n = 79), no significant difference was observed in the primary outcome, an improvement in CDAI score of ≥ 50% from baseline (risk ratio 1.25, 95% confidence interval 0.80 to 1.96). A supplementary analysis of the CDAI-MTR, however, did reach statistical significance (risk ratio 1.96, 95% confidence interval 1.01 to 3.78). In addition, when B-cell-poor classification was determined molecularly, both the primary end point and the CDAI-MTR were statistically significant (risk ratio 1.72, 95% confidence interval 1.02 to 2.91, and risk ratio 4.12, 95% confidence interval 1.55 to 11.01, respectively). Moreover, a larger number of secondary end points achieved significance when classified molecularly than when classified histologically. In the B-cell-rich population, there was no significant difference between treatments in the majority of both primary and secondary end points. There were more adverse events and serious adverse events, such as infections, in the tocilizumab group than in the rituximab group. Conclusion To our knowledge, this is the first biopsy-based, multicentre, randomised controlled trial of rheumatoid arthritis. We were unable to demonstrate that tocilizumab was more effective than rituximab in patients with a B-cell-poor pathotype in our primary analysis. However, superiority was shown in most of the supplementary and secondary analyses using a molecular classification. These analyses overcame possible unavoidable weaknesses in our original study plan, in which the histological method of determining B-cell status may have misclassified some participants and our chosen primary outcome was insufficiently sensitive. Given the significant results observed using the molecular classification, future research will focus on refining this stratification method and evaluating its clinical utility. Trial registration Current Controlled Trials ISRCTN97443826. Funding This project was funded by the Efficacy and Mechanism Evaluation (EME) programme, a Medical Research Council and National Institute for Health and Care Research (NIHR) partnership. This will be published in full in Efficacy and Mechanism Evaluation; Vol. 9, No. 7. See the NIHR Journals Library website for further project information.

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Myśliwska, J., E. Bryl, P. Trzonkowski, and A. Myśliwski. "Compensatory effect of TNFalpha on low natural killer activity in the elderly." Acta Biochimica Polonica 47, no. 2 (June 30, 2000): 301–11. http://dx.doi.org/10.18388/abp.2000_4010.

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Regulatory effect of CD25, an activation antigen the alpha subunit of interleukin 2 receptor (IL2R) on the activity of natural killer (NK) cells was studied in fifty elderly (57-70 years old) and fifty young people (19-35 years old). Cytotoxic NK activity was assessed by 51Cr release assay, the levels of interleukin 2 (IL2) and tumour necrosis factors alpha (TNFalpha) were measured using bioassays and expression of CD16 and CD25 proteins by flow cytometry. Low NK activity in the elderly was associated with decline of full health, lowered serum concentration of IL2 and increased production of TNFalpha during NK reaction. Inhibition of TNFalpha activity by anti-TNF monoclonal antibody suppressed exclusively NK activity of low NK responders. Moreover, stimulation in vitro of blood mononuclear cells, with TNFalpha induced in the elderly low NK responders a significantly higher increase of the CD25 expression on the surface of NK cells as compared with that in the elderly high responders. Since the CD25 molecule constitutes a subunit of the high affinity receptor, binding IL2 to immunocompetent cells, its increased expression on NK cells of low NK responders would enable them to bind even low amounts of the endogenous IL2 available in this group of the elderly. Thus, an overproduction of TNFalpha seems to be a mechanism compensating, in the non-fully healthy elderly, for the decreased IL2 production, promoting efficient cytotoxic reaction.

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Say, Rıdvan, Ebru Birlik Özkütük, Özlem Biçen Ünlüer, Deniz Uğurağ, and Arzu Ersöz. "Nano anti-tumor necrosis factor-alpha based potentiometric sensor for tumor necrosis factor-alpha detection." Sensors and Actuators B: Chemical 209 (March 2015): 864–69. http://dx.doi.org/10.1016/j.snb.2014.12.063.

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Donnelly, Jennifer, Sharon Cooley, Joanna Balding, Ciaran Murphy, Tom Walsh, Owen Smith, Michael Geary, and Corrina M. C. Mahon. "Obesity, tumor necrosis factor-alpha and tumor necrosis factor-alpha −308 polymorphism in normal pregnancy." American Journal of Obstetrics and Gynecology 193, no. 6 (December 2005): S160. http://dx.doi.org/10.1016/j.ajog.2005.10.643.

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ÇAYAKAR, Ahmet. "What is Tumor Necrosis Factor Alpha ?" Turkiye Klinikleri Journal of Internal Medicine 3, no. 2 (2018): 67–76. http://dx.doi.org/10.5336/intermed.2018-61424.

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Nabe, T. "Tumor Necrosis Factor Alpha-Mediated Asthma." International Archives of Allergy and Immunology 160, no. 2 (2013): 111–13. http://dx.doi.org/10.1159/000342420.

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Satoh, Mamoru, Motoyuki Nakamura, Hidetoshi Satoh, Hidenori Saitoh, Ikuo Segawa, and Katsuhiko Hiramori. "Expression of tumor necrosis factor-alpha–converting enzyme and tumor necrosis factor-alpha in human myocarditis." Journal of the American College of Cardiology 36, no. 4 (October 2000): 1288–94. http://dx.doi.org/10.1016/s0735-1097(00)00827-5.

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37

Karim, Bahija, Roland Béliard, Jean-Jacques Huart, and Dominique Bourel. "Four epitopes on tumor necrosis factor-alpha defined by murine anti-tumor necrosis factor-alpha monoclonal antibodies." Immunology Letters 41, no. 2-3 (July 1994): 139–45. http://dx.doi.org/10.1016/0165-2478(94)90124-4.

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38

Galbraith, Gillian M. P., R. Britt Steed, John J. Sanders, and Janardan P. Pandey. "Tumor Necrosis Factor Alpha Production by Oral Leukocytes: Influence of Tumor Necrosis Factor Genotype." Journal of Periodontology 69, no. 4 (April 1998): 428–33. http://dx.doi.org/10.1902/jop.1998.69.4.428.

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39

Sullivan, K. E., A. B. M. Reddy, K. Dietzmann, A. R. Suriano, V. P. Kocieda, M. Stewart, and M. Bhatia. "Epigenetic Regulation of Tumor Necrosis Factor Alpha." Molecular and Cellular Biology 27, no. 14 (May 21, 2007): 5147–60. http://dx.doi.org/10.1128/mcb.02429-06.

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ABSTRACT Tumor necrosis factor alpha (TNF-α) is a potent cytokine which regulates inflammation via the induction of adhesion molecules and chemokine expression. Its expression is known to be regulated in a complex manner with transcription, message turnover, message splicing, translation, and protein cleavage from the cell surface all being independently regulated. This study examined both cell lines and primary cells to understand the developmental regulation of epigenetic changes at the TNF-α locus. We demonstrate that epigenetic modifications of the TNF-α locus occur both developmentally and in response to acute stimulation and, importantly, that they actively regulate expression. DNA demethylates early in development, beginning with the hematopoietic stem cell. The TNF-α locus migrates from heterochromatin to euchromatin in a progressive fashion, reaching euchromatin slightly later in differentiation. Finally, histone modifications characteristic of a transcriptionally competent gene occur with myeloid differentiation and progress with differentiation. Additional histone modifications characteristic of active gene expression are acquired with stimulation. In each case, manipulation of these epigenetic variables altered the ability of the cell to express TNF-α. These studies demonstrate the importance of epigenetic regulation in the control of TNF-α expression. These findings may have relevance for inflammatory disorders in which TNF-α is overproduced.

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Baud, Laurent, Bruno Fouqueray, Carole Philippe, and Abdelaziz Amrani. "Tumor necrosis factor alpha and mesangial cells." Kidney International 41, no. 3 (March 1992): 600–603. http://dx.doi.org/10.1038/ki.1992.90.

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Rockstrom, Matthew D., Liangyu Chen, Ping Taishi, Joseph T. Nguyen, Cody M. Gibbons, Sigrid C. Veasey, and James M. Krueger. "Tumor necrosis factor alpha in sleep regulation." Sleep Medicine Reviews 40 (August 2018): 69–78. http://dx.doi.org/10.1016/j.smrv.2017.10.005.

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42

Dorhoi, Anca, and Stefan H. E. Kaufmann. "Tumor necrosis factor alpha in mycobacterial infection." Seminars in Immunology 26, no. 3 (June 2014): 203–9. http://dx.doi.org/10.1016/j.smim.2014.04.003.

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McDonough, Paul G., Joseph A. Hill, and Deborah J. Anderson. "Tumor Necrosis Factor-Alpha and Sperm Function?" Fertility and Sterility 57, no. 3 (March 1992): 705–7. http://dx.doi.org/10.1016/s0015-0282(16)54930-9.

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44

Liu, Hongqun, and Sam S. Lee. "Tumor necrosis factor-alpha in cirrhotic cardiomyopathy." Journal of Hepatology 36 (April 2002): 11. http://dx.doi.org/10.1016/s0168-8278(02)80028-9.

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45

Robicheaux Clementine, Rochelle, Justin Lyman, Jerald Zakem, Jyothi Mallepalli, Stephen Lindsey, and Robert Quinet. "Tumor Necrosis Factor-Alpha Antagonist-Induced Sarcoidosis." JCR: Journal of Clinical Rheumatology 16, no. 6 (September 2010): 274–79. http://dx.doi.org/10.1097/rhu.0b013e3181efa190.

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46

Malangoni, Mark A. "Interferon Gamma and Tumor Necrosis Factor Alpha." Archives of Surgery 125, no. 4 (April 1, 1990): 444. http://dx.doi.org/10.1001/archsurg.1990.01410160030005.

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47

Lisby, S., and C. Hauser. "Transcriptional regulation of tumor necrosis factor-alpha in keratinocytes mediated by interleukin-1beta and tumor necrosis factor-alpha." Experimental Dermatology 11, no. 6 (December 2002): 592–98. http://dx.doi.org/10.1034/j.1600-0625.2002.110612.x.

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Blankenstein, T., Z. H. Qin, K. Uberla, W. Müller, H. Rosen, H. D. Volk, and T. Diamantstein. "Tumor suppression after tumor cell-targeted tumor necrosis factor alpha gene transfer." Journal of Experimental Medicine 173, no. 5 (May 1, 1991): 1047–52. http://dx.doi.org/10.1084/jem.173.5.1047.

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The tumor necrosis factor alpha (TNF-alpha) gene was introduced by retroviral gene transfer into the TNF-alpha-insensitive tumor cell line J558L. Production of 40 pg/ml TNF-alpha by clone J2T12 consistently did not change the growth rate in vitro, but drastically suppressed tumor growth when injected into syngeneic BALB/c mice. Within 2 wk, 90% of the mice inoculated with J558L cells developed a tumor, but none of the mice injected with J2T12 did so. Within the observation period (greater than 3 mo), 60% of the mice inoculated with J2T12 did not develop a tumor. In the other 40% of the mice, tumor manifestation was significantly delayed. Mice injected simultaneously with J2T12 cells and an anti-TNF-alpha monoclonal antibody developed tumors similar to parental J558L cells. Similarly, the tumor-suppressive effects of TNF-alpha were abolished, e.g., by injection of an anti-type 3 complement receptor (CR3) monoclonal antibody that is known to prevent migration of inflammatory cells. These results and the observation of tumor-infiltrating macrophages suggest that lack of tumorigenicity of J2T12 cells is due to the TNF-alpha secretion by the tumor cells and that TNF-alpha acts indirectly by a mechanism that involves chemotactic recruitment and activation of cells, predominantly of macrophages. In contrast, the tumor growth was not affected when, instead of TNF-alpha, interleukin 6 was expressed by J558L cells. Together, our results support the concept of tumor cell-targeted cytokine gene transfer as a tool for cancer treatment, and particularly demonstrate that extremely low doses of TNF-alpha produced by tumor cells are sufficient to inhibit tumor growth without detectable side effects.

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Leitman, D. C., R. C. Ribeiro, E. R. Mackow, J. D. Baxter, and B. L. West. "Identification of a tumor necrosis factor-responsive element in the tumor necrosis factor alpha gene." Journal of Biological Chemistry 266, no. 15 (May 1991): 9343–46. http://dx.doi.org/10.1016/s0021-9258(18)92822-x.

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Kristiansson, Marianne, Michael Soop, Agneta Shanwell, and Karl-Gosta Sundqvist. "Presence of Tumor Necrosis Factor alpha and Tumor Necrosis Factor Soluble Receptors in Erythrocyte Concentrates." Anesthesiology 84, no. 1 (January 1, 1996): 243–44. http://dx.doi.org/10.1097/00000542-199601000-00042.

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