Neutrophils and inflammatory resolution in the mucosa

被引:41
作者
Colgan, Sean P. [1 ]
机构
[1] Univ Colorado, Sch Med, Dept Med, Mucosal Inflammat Program, Aurora, CO 80045 USA
基金
美国国家卫生研究院;
关键词
Metabolism; Hypoxia-inducible factor; Inflammation; Nucleoside; Nucleotidase; Mucosa; Colitis; Epithelium; Endothelium; Murine model; INDUCIBLE FACTOR-I; KAPPA-B-ALPHA; BARRIER FUNCTION; EXPERIMENTAL COLITIS; ADENOSINE RECEPTORS; ATP RELEASE; CYCLIC-AMP; HYPOXIA; INHIBITION; TIGHT;
D O I
10.1016/j.smim.2015.03.007
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Inflammatory diseases in mucosal organs as diverse as the lung, liver and intestine inevitably require the intimate interactions between neutrophils and epithelia. The physiologic consequences of such interactions often determine endpoint organ function, and for this reason, much recent interest has developed in identifying mechanisms and novel targets to promote the resolution of mucosal inflammation. Physiologically-relevant in vitro and in vivo model systems have aided in discovery of novel pathways to define basic inflammatory mechanisms and approaches to defining the concepts of inflammatory resolution. Here, we will review the recent literature regarding the contribution of neutrophils to inflammatory resolution, with an emphasis on the role of the tissue microenvironment, endogenous pathways for promoting resolution and the molecular determinants of neutrophil-epithelial cell interactions during ongoing inflammation. These recent studies highlight the dynamic nature of pro-resolving pathways and lend insight into the complexity of treating mucosal inflammation. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:177 / 183
页数:7
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