Lipocalin-2: A Master Mediator of Intestinal and Metabolic Inflammation. (May 2017)

• Record Type: Journal Article
• Authors: Moschen, Alexander R.; Adolph, Timon E.; Gerner, Romana R.; Wieser, Verena; Tilg, Herbert
• Is Part Of: Trends in endocrinology and metabolism. Volume 28:Number 5(2017)
• Page Start: 388
• Page End: 397
• Publication Date: 2017-05
• Subjects: Endocrinology -- Periodicals; Metabolism -- Periodicals; Metabolism; 616.4
• DOI: 10.1016/j.tem.2017.01.003
• Languages: English
• ISSNs: 1043-2760

Abstract

Abstract : 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. Trends: LCN2 limits bacterial growth by iron sequestration and suppresses intestinal dysbiosis in the inflamed gut. LCN2 may promote sterile inflammation by the modulation of immune responses. Neutralization of LCN2 controls neutrophilic inflammation in experimental disease models of psoriasis, cardiovascular diseases, alcoholic steatohepatitis, and NASH. LCN2 is a biomarker in human inflammatory diseases that can be easily measured in urine, blood, and feces.