Effects of tumor necrosis factor (TNF) gene polymorphisms on the association between smoking and lung function among workers in swine operations

2021 ◽  
pp. 1-17
Author(s):  
Zhiwei Gao ◽  
James A. Dosman ◽  
Donna C. Rennie ◽  
David A. Schwartz ◽  
Ivana V. Yang ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Lung Function ◽  
Gene Polymorphisms ◽  
Tumor Necrosis ◽  
Swine Operations ◽  
Tnf Gene ◽  
Necrosis Factor

Relevance of IL-1 and TNF gene polymorphisms on interleukin-1β and tumor necrosis factor-α gastric mucosal production

2009 ◽  
Vol 70 (11) ◽  
pp. 935-945 ◽  
Author(s):  
María A. García-González ◽  
María A. Pérez Aísa ◽  
Mark Strunk ◽  
Rafael Benito ◽  
Elena Piazuelo ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Gene Polymorphisms ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 1Β ◽  
Tnf Gene ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor gene polymorphisms are associated with silicosis: a systemic review and meta-analysis

2019 ◽  
Vol 39 (2) ◽  
Author(s):  
Min Zhang ◽  
Ling-Long Peng ◽  
Xue-Lei Ji ◽  
Hai-Bing Yang ◽  
Ri-Sheng Zha ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Gene Polymorphisms ◽  
Tumor Necrosis ◽  
Literature Search ◽  
Meta Analysis ◽  
Asian Population ◽  
Systemic Review ◽  
Tnf Gene ◽  
Strength Of Association ◽  
Necrosis Factor

Abstract Studies investigating association between tumor necrosis factor (TNF) gene polymorphisms and silicosis susceptibility report conflicting results. The aim of this meta-analysis was to assess association between TNF gene polymorphisms and silicosis susceptibility. A systematic literature search was conducted to find relevant studies. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to estimate the strength of association. Finally, a total of 12 articles, involving 1990 silicosis patients and 1898 healthy controls were included in the meta-analysis. Overall, meta-analysis revealed a significant association between the TNF −308A allele and silicosis (OR = 1.348, 95%CI = 1.156–1.570, P<0.001). A significant association of AA+AG genotype of the TNF −308 A/G polymorphism with susceptibility to silicosis was also found (OR = 1.466, 95%CI = 1.226–1.753, P<0.001). After stratification by ethnicity, significant associations were detected under the genetic models (A allele and AA+AG genotype) for TNF −308A/G polymorphisms in the Asian population (P<0.05). Similarly, meta-analysis of the TNF −238A/G polymorphism revealed the same pattern as that shown by meta-analysis of TNF −308A/G. The meta-analysis suggests that the TNF −308A/G and −238A/G polymorphisms are associated with susceptibility to silicosis, especially in Asians.

scholarly journals Role of arachidonic acid metabolism in transcriptional induction of tumor necrosis factor gene expression by phorbol ester.

1989 ◽  
Vol 9 (1) ◽  
pp. 252-258 ◽  
Author(s):  
J Horiguchi ◽  
D Spriggs ◽  
K Imamura ◽  
R Stone ◽  
R Luebbers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Arachidonic Acid ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Leukotriene B4 ◽  
Mrna Levels ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
Tnf Gene ◽  
Necrosis Factor

The treatment of human HL-60 promyelocytic leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with induction of tumor necrosis factor (TNF) transcript. The study reported here has examined TPA-induced signaling mechanisms responsible for the regulation of TNF gene expression in these cells. Run-on assays demonstrated that TPA increases TNF mRNA levels by transcriptional activation of this gene. The induction of TNF transcripts by TPA was inhibited by the isoquinolinesulfonamide derivative H7 but not by HA1004, suggesting that this effect of TPA is mediated by activation of protein kinase C. TPA treatment also resulted in increased arachidonic acid release. Moreover, inhibitors of phospholipase A2 blocked both the increase in arachidonic acid release and the induction of TNF transcripts. These findings suggest that TPA induces TNF gene expression through the formation of arachidonic acid metabolites. Although indomethacin had no detectable effect on this induction of TNF transcripts, ketoconazole, an inhibitor of 5-lipoxygenase, blocked TPA-induced increases in TNF mRNA levels. Moreover, TNF mRNA levels were increased by the 5-lipoxygenase metabolite leukotriene B4. In contrast, the cyclooxygenase metabolite prostaglandin E2 inhibited the induction of TNF transcripts by TPA. Taken together, these results suggest that TPA induces TNF gene expression through the arachidonic acid cascade and that the level of TNF transcripts is regulated by metabolites of the pathway, leukotriene B4 and prostaglandin E2.

Tumor necrosis factor-α and interleukin-1β gene polymorphisms and risk of brain abscess in North Indian population

Cytokine ◽  
2015 ◽  
Vol 75 (1) ◽  
pp. 159-164 ◽  
Author(s):  
Priyanka Mishra ◽  
Kashi Nath Prasad ◽  
Kamini Singh ◽  
Anamika Bajpai ◽  
Rabi Narayan Sahu ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Brain Abscess ◽  
Gene Polymorphisms ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Indian Population ◽  
Interleukin 1Β ◽  
North Indian Population ◽  
Factor Α ◽  
Necrosis Factor

Role of arachidonic acid metabolism in transcriptional induction of tumor necrosis factor gene expression by phorbol ester

1989 ◽  
Vol 9 (1) ◽  
pp. 252-258
Author(s):  
J Horiguchi ◽  
D Spriggs ◽  
K Imamura ◽  
R Stone ◽  
R Luebbers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Arachidonic Acid ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Leukotriene B4 ◽  
Mrna Levels ◽  
Arachidonic Acid Release ◽  
Acid Release ◽  
Tnf Gene ◽  
Necrosis Factor

The treatment of human HL-60 promyelocytic leukemia cells with 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with induction of tumor necrosis factor (TNF) transcript. The study reported here has examined TPA-induced signaling mechanisms responsible for the regulation of TNF gene expression in these cells. Run-on assays demonstrated that TPA increases TNF mRNA levels by transcriptional activation of this gene. The induction of TNF transcripts by TPA was inhibited by the isoquinolinesulfonamide derivative H7 but not by HA1004, suggesting that this effect of TPA is mediated by activation of protein kinase C. TPA treatment also resulted in increased arachidonic acid release. Moreover, inhibitors of phospholipase A2 blocked both the increase in arachidonic acid release and the induction of TNF transcripts. These findings suggest that TPA induces TNF gene expression through the formation of arachidonic acid metabolites. Although indomethacin had no detectable effect on this induction of TNF transcripts, ketoconazole, an inhibitor of 5-lipoxygenase, blocked TPA-induced increases in TNF mRNA levels. Moreover, TNF mRNA levels were increased by the 5-lipoxygenase metabolite leukotriene B4. In contrast, the cyclooxygenase metabolite prostaglandin E2 inhibited the induction of TNF transcripts by TPA. Taken together, these results suggest that TPA induces TNF gene expression through the arachidonic acid cascade and that the level of TNF transcripts is regulated by metabolites of the pathway, leukotriene B4 and prostaglandin E2.

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