Contributions of neutrophils to resolution of mucosal inflammation

被引:17
作者
Colgan, Sean P. [1 ,2 ,3 ]
Ehrentraut, Stefan F. [1 ,2 ,3 ]
Glover, Louise E. [1 ,2 ,3 ]
Kominsky, Douglas J. [1 ,2 ,3 ]
Campbell, Eric L. [1 ,2 ,3 ]
机构
[1] Univ Colorado, Sch Med, Dept Med, Aurora, CO 80045 USA
[2] Univ Colorado, Sch Med, Dept Anesthesiol, Aurora, CO 80045 USA
[3] Univ Colorado, Sch 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; Nucleotide; Nucleoside; Nucleotidase; Mucosa; Colitis; Neutrophil; Epithelium; Endothelium; Murine model; INDUCIBLE FACTOR-I; N-3; FATTY-ACIDS; FIND-ME SIGNAL; KAPPA-B; ANTIINFLAMMATORY PROPERTIES; EXPERIMENTAL COLITIS; ADENOSINE RECEPTORS; BARRIER FUNCTION; LIPID MEDIATORS; ATP RELEASE;
D O I
10.1007/s12026-012-8350-2
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Neutrophil (PMN) recruitment from the blood stream into surrounding tissues involves a regulated series of events central to acute responses in host defense. Accumulation of PMN within mucosal tissues has historically been considered pathognomonic features of both acute and chronic inflammatory conditions. Historically, PMNs have been deemed necessary but detrimental when recruited, given the potential for tissue damage that results from a variety of mechanisms. Recent work, however, has altered our preconceived notions of PMN contributions to inflammatory processes. In particular, significant evidence implicates a central role for the PMN in triggering inflammatory resolution. Such mechanisms involve both metabolic and biochemical crosstalk pathways during the intimate interactions of PMN with other cell types at inflammatory sites. Here, we highlight several recent examples of how PMN coordinate the resolution of ongoing inflammation, with a particular focus on the gastrointestinal mucosa.
引用
收藏
页码:75 / 82
页数:8
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