科研之友
微信
新浪微博
Facebook
分享链接
摘要
Li Y, Dinwiddie DL, Harrod KS, Jiang Y, Kim KC. Anti-inflammatory effect of MUC1 during respiratory syncytial virus infection of lung epithelial cells in vitro. Am J Physiol Lung Cell Mol Physiol 298: L558-L563, 2010. First published January 15, 2010; doi:10.1152/ajplung.00225.2009.-MUC1 is a transmembrane glycoprotein expressed on the apical surface of airway epithelial cells and plays an anti-inflammatory role during airway bacterial infection. In this study, we determined whether the anti-inflammatory effect of MUC1 is also operative during the respiratory syncytial virus (RSV) infection. The lung epithelial cell line A549 was treated with RSV, and the production of TNF alpha and the levels of MUC1 protein were monitored temporally during the course of infection by ELISA and Western blot analysis. Small inhibitory RNA ( siRNA) transfection was utilized to assess the role of MUC1 in regulating RSV-mediated inflammatory responses by lung epithelial cells. Our results revealed that: 1) following RSV infection, an increase in MUC1 level was preceded by an increase in TNF alpha production and completely inhibited by soluble TNF receptor ( TNFR); and 2) knockdown of MUC1 using MUC1 siRNA resulted in a greater increase in TNF alpha level following RSV infection compared with control siRNA treatment. We conclude that the RSV-induced increase in the TNF alpha levels upregulates MUC1 through its interaction with TNFR, which in turn suppresses further increase in TNF alpha by RSV, thus forming a negative feedback loop in the control of RSV-induced inflammation. This is the first demonstration showing that MUC1 can suppress the virus-induced inflammatory responses.
- 出版日期2010-4
- 单位南方医科大学
