Transbronchial human interleukin-10 gene transfer reduces acute inflammation associated with allograft rejection and intragraft interleukin-2 and tumor necrosis factor-α gene expression in a rat model of lung transplantation

2010 ◽  
Vol 29 (3) ◽  
pp. 360-367 ◽  
Author(s):  
Hisashi Oishi ◽  
Yoshinori Okada ◽  
Toshiaki Kikuchi ◽  
Yasushi Hoshikawa ◽  
Tetsu Sado ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis Factor ◽  
Allograft Rejection ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Acute Inflammation ◽  
Interleukin 2 ◽  
Interleukin 10 ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Association of expression of inflammatory response genes and DNA repair genes in colorectal carcinoma

Tumor Biology ◽  
2019 ◽  
Vol 41 (4) ◽  
pp. 101042831984304 ◽  
Author(s):  
Demétrius Eduardo Germini ◽  
Maria Isete Fares Franco ◽  
Fernando Luiz Affonso Fonseca ◽  
Flávia de Sousa Gehrke ◽  
Beatriz da Costa Aguiar Alves Reis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Repair ◽  
Tumor Necrosis Factor ◽  
Colorectal Carcinoma ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 2 ◽  
Repair System ◽  
Factor Α ◽  
Necrosis Factor

Inflammation is an important etiological factor of colorectal carcinoma and may be related to colorectal carcinoma growth and proliferation. This study aimed to verify whether the presence of chronic inflammation represented by tumor necrosis factor-α, interleukin-2, interleukin-6, and interleukin-10 gene expression is related to hMLH1, hMSH2, hMSH6, and PMS2 gene expression and the corresponding protein levels of these genes from the DNA repair system. A total of 83 patients were operated on for curative or palliative colorectal carcinoma. Expression of the inflammatory response genes tumor necrosis factor-α, interleukin-2, interleukin-6, and interleukin-10 as well as expression of the hMLH1, hMSH2, hMSH6, and PMS2 genes of the DNA repair system (mismatch repair) and the expression levels of the corresponding mismatch repair proteins were measured in neoplastic tissue by reverse transcription polymerase chain reaction and immunohistochemistry, respectively. Associations were observed between hMSH6 mRNA expression and interleukin-2 mRNA expression (p = 0.026) as well as between hMLH1 and hMSH2 gene expression and tumor necrosis factor-α gene expression (p = 0.042). Higher tissue levels of interleukin-2 and tumor necrosis factor-α gene expression were associated with lower hMSH6, hMLH1, and hMSH2 gene expression.

scholarly journals Targeted Deletion of Class A Macrophage Scavenger Receptor Increases the Risk of Cardiac Rupture After Experimental Myocardial Infarction

Circulation ◽  
2007 ◽  
Vol 115 (14) ◽  
pp. 1904-1911 ◽  
Author(s):  
Kenichi Tsujita ◽  
Koichi Kaikita ◽  
Takanori Hayasaki ◽  
Tsuyoshi Honda ◽  
Hironori Kobayashi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 10 ◽  
Experimental Myocardial Infarction ◽  
Cardiac Rupture ◽  
Infarcted Myocardium ◽  
Factor Α ◽  
Necrosis Factor

Background— Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A–deficient (SR-A −/− ) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction. Methods and Results— Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A −/− and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in SR-A −/− mice than in WT mice ( P =0.03). Importantly, death caused by cardiac rupture within 1 week after MI was 31% (17 of 54 mice) in SR-A −/− mice and 12% (6 of 51 mice) in WT mice ( P =0.01). In situ zymography demonstrated augmented gelatinolytic activity in the infarcted myocardium in SR-A −/− mice compared with WT mice. Real-time reverse transcription–polymerase chain reaction at day 3 after MI showed that the expression of matrix metalloproteinase-9 mRNA increased significantly in the infarcted myocardium in SR-A −/− mice compared with WT mice. Furthermore, SR-A −/− mice showed augmented expression of tumor necrosis factor-α and reduction of interleukin-10 in the infarcted myocardium at day 3 after MI. In vitro experiments also demonstrated increased tumor necrosis factor-α and decreased interleukin-10 expression in activated SR-A −/− macrophages. Conclusions— The present findings suggest that SR-A deficiency might cause impairment of infarct remodeling that results in cardiac rupture via insufficient production of interleukin-10 and enhanced expression of tumor necrosis factor-α and of matrix metalloproteinase-9. SR-A might contribute to the prevention of cardiac rupture after MI.

Aspirin Inhibits Tumor Necrosis Factor-α Gene Expression in Murine Tissue Macrophages

1997 ◽  
Vol 52 (3) ◽  
pp. 421-429 ◽  
Author(s):  
Rodney E. Shackelford ◽  
Paul B. Alford ◽  
Yan Xue ◽  
Sheau-Fung Thai ◽  
Dolph O. Adams ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Murine Tissue ◽  
Factor Α ◽  
Necrosis Factor

Lipopolysaccharide-induced interleukin-10 in mice: role of endogenous tumor necrosis factor-α

1995 ◽  
Vol 25 (10) ◽  
pp. 2888-2893 ◽  
Author(s):  
Johannes Barsig ◽  
Sabine Küsters ◽  
Kathrin Vogt ◽  
Hans-Dieter Volk ◽  
Gisa Tiegs ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 10 ◽  
Factor Α ◽  
Necrosis Factor
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