Epithelial cells in fetal intestine produce chemerin to recruit macrophages

Abstract

Macrophages are first seen in the fetal intestine at 11-12 wk and rapidly increase in number during the 12- to 22-wk period of gestation. The development of macrophage populations in the fetal intestine precedes the appearance of lymphocytes and neutrophils and does not require the presence of dietary or microbial antigens. In this study, we investigated the role of chemerin, a recently discovered, relatively selective chemoattractant for macrophages, in the recruitment of macrophage precursors to the fetal intestine. Chemerin mRNA/protein expression was measured in jejunoileal tissue from 10- to 24-wk human fetuses, neonates operated for intestinal obstruction, and adults undergoing bariatric surgery. The expression of chemerin in intestinal epithelial cells (IECs) was confirmed by using cultured primary IECs and IEC-like cell lines in vitro. The regulatory mechanisms involved in chemerin expression were investigated by in silico and immunolocalization techniques. IECs in the fetal, but not mature, intestine express chemerin. Chemerin expression peaked in the fetal intestine at 20-24 wk and then decreased to original low levels by full term. During the 10- to 24-wk period, chemerin accounted for most of the macrophage chemotactic activity of cultured fetal IECs. The maturational changes in chemerin expression correlated with the expression of retinoic acid receptor-beta in the intestine. Chemerin is an important mediator of epithelial-macrophage cross talk in the fetal/premature, but not in the mature, intestine. Understanding the regulation of the gut macrophage pool is an important step in development of novel strategies to boost mucosal immunity in premature infants and other patient populations at risk of microbial translocation.

Circulating levels of chemerin and adiponectin are higher in ulcerative colitis and chemerin is elevated in Crohnʼs disease

“…Adiponectin and chemerin are released from adipocytes, but whereas adiponectin is preferentially produced by these cells, chemerin is also synthesized by other cells like fetal intestinal epithelial cells or hepatocytes [26,27]. Comparison of different fat depots revealed that visceral fat produces higher amounts of adiponectin compared to subcutaneous adipose tissue [28].…”

Chemerin-ChemR23 Signaling in Tooth Development

“…Based on reports of Chemerin signaling in intestinal epithelial cell differentiation (Maheshwari et al, 2009), we hypothesized that Chemerin/ChemR23 signaling might also mediate DE-DM signaling in tooth development. The findings presented here lead to the novel hypothesis that Chemerin/ChemR23 signaling may facilitate proper DE-DM cell interactions during tooth development.…”

Chemerin/ChemR23 signaling axis is involved in the endothelial protection by KATP channel opener iptakalim

“…Chemerin, the endogenous ligand of ChemR23, is a newly discovered adipokine that regulates adipocyte differentiation and modulates chemotaxis and recruitment of NK cells, dendritic cells, and macrophages [8][9][10] . Chemerin is strongly associated with markers of inflammation, metabolic syndrome components, and atherosclerosis [11] , for which endothelial dysfunction is a fundamental etiological factor.…”