Lipocalin-2: A Master Mediator of Intestinal and Metabolic Inflammation

被引：271

作者：

Moschen, Alexander R. ^{[1
,2
]}

Adolph, Timon E. ^{[1
,2
]}

Gerner, Romana R. ^{[1
,2
]}

Wieser, Verena ^{[1
,2
]}

Tilg, Herbert ^{[1
,2
]}

机构：

[1] Med Univ Innsbruck, Dept Internal Med Gastroenterol Hepatol & Endocri, Innsbruck, Austria

[2] Med Univ Innsbruck, Christian Doppler Lab Mucosal Immunol, Innsbruck, Austria

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2017年 / 28卷 / 05期

关键词：

GELATINASE-ASSOCIATED LIPOCALIN; NECROSIS-FACTOR-ALPHA; SEVERELY OBESE WOMEN; INSULIN-RESISTANCE; GUT MICROBIOTA; ADIPOSE-TISSUE; BACTERIAL-INFECTION; IN-VIVO; EXPRESSION; LIVER;

D O I：

10.1016/j.tem.2017.01.003

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Lipocalin-2 (LCN2), also known as neutrophil gelatinase-associated lipocalin (NGAL), is released by various cell types and is an attractive biomarker of inflammation, ischemia, infection, and kidney damage. Both intestinal and metabolic inflammation, as observed in obesity and related disorders, are associated with increased LCN2 synthesis. While LCN2 in the intestinal tract regulates the composition of the gut microbiota and shows anti-inflammatory activities, it also exhibits proinflammatory activities in other experimental settings. In animal models of metabolic inflammation, type 2 diabetes mellitus (T2DM), or nonalcoholic steatohepatitis (NASH), increased LCN2 expression favors inflammation via the recruitment of inflammatory cells, such as neutrophils, and the induction of proinflammatory cytokines. A better understanding of this crucial marker of innate immunity might pave the way for targeting this pathway in future therapies.

引用

页码：388 / 397

页数：10

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