carbon monoxide inhibits tenascin-c mediated inflammation via il-10 expression in a septic mouse model

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ID: 143301
2015
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Abstract
Tenascin-C (TN-C), an extracellular matrix (ECM) glycoprotein, is specifically induced upon tissue injury and infection and during septic conditions. Carbon monoxide (CO) gas is known to exert various anti-inflammatory effects in various inflammatory diseases. However, the mechanisms underlying the effect of CO on TN-C-mediated inflammation are unknown. In the present study, we found that treatment with LPS significantly enhanced TN-C expression in macrophages. CO gas, or treatment with the CO-donor compound, CORM-2, dramatically reduced LPS-induced expression of TN-C and proinflammatory cytokines while significantly increased the expression of IL-10. Treatment with TN-C siRNA significantly suppressed the effects of LPS on proinflammatory cytokines production. TN-C siRNA did not affect the CORM-2-dependent increase of IL-10 expression. In cells transfected with IL-10 siRNA, CORM-2 had no effect on the LPS-induced expression of TN-C and its downstream cytokines. These data suggest that IL-10 mediates the inhibitory effect of CO on TN-C and the downstream production of proinflammatory cytokines. Additionally, administration of CORM-2 dramatically reduced LPS-induced TN-C and proinflammatory cytokines production while expression of IL-10 was significantly increased. In conclusion, CO regulated IL-10 expression and thus inhibited TN-C-mediated inflammation in vitro and in vivo.
Reference Key
uddin2015mediatorscarbon Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Md. Jamal Uddin;Chun-shi Li;Yeonsoo Joe;Yingqing Chen;Qinggao Zhang;Stefan W. Ryter;Hun Taeg Chung
Journal polyhedron
Year 2015
DOI
10.1155/2015/613249
URL
http://dx.doi.org/10.1155/2015/613249
Keywords
pathology

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