期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 484, 期 2, 页码 205-213出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2008.11.027
关键词
Transepithelial resistance; Inflammation; LPS; Oxidant; Wound repair; Occludin; Claudin
资金
- NIH [HL60812, HL068865, HL074295]
Acute airway inflammation is associated with enhanced production of nitric oxide (NO center dot) and altered airway epithelial barrier function, suggesting a role of NO center dot or its metabolites in epithelial permeability. While high concentrations of S-nitrisothiols disrupted transepithelial resistance (TER) and increased permeability in 16HBE14o- cells, no significant barrier disruption was observed by NONOates, in spite of altered distribution and expression of some TJ proteins. Barrier disruption of mouse tracheal epithelia[ (MTE) cell monolayers in response to inflammatory cytokines was independent of NOS2, based on similar effects in MTE cells from NOS2-/- mice and a lack of effect of the NOS2-inhibitor 1400W. Cell pre-incubation with LPS protected MTE cells from TER loss and increased permeability by H2O2, which was independent of NOS2. However, NOS2 Was found to contribute to epithelial wound repair and TER recovery after mechanical injury. Overall, our results demonstrate that epithelial NOS2 is not responsible for epithelial barrier dysfunction during inflammation, but may contribute to restoration of epithelial integrity. (C) 2008 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据