Adiponectin and adiponectin receptor 1 overexpression enhance inflammatory bowel disease
Journal
Journal of Biomedical Science
Journal Volume
25
Journal Issue
1
Date Issued
2018
Author(s)
Abstract
Background: Adiponectin (ADN) is an adipokine derived from adipocytes. It binds to adiponectin receptor 1 and 2 (AdipoR1 and R2) to exert its function in regulating whole-body energy homeostasis and inflammatory responses. However, the role of ADN-AdipoR1 signaling in intestinal inflammation is controversial, and its role in the regulation of neutrophils is still unclear. Our goal was to clarify the role of AdipoR1 signaling in colitis and the effects on neutrophils. Methods: We generated porcine AdipoR1 transgenic mice (pAdipoR1 mice) and induced murine colitis using dextran sulfate sodium (DSS) to study the potential role of AdipoR1 in inflammatory bowel disease. We also treated a THP-1 macrophage and a HT-29 colon epithelial cell line with ADN recombinant protein to study the effects of ADN on inflammation. Results: After inducing murine colitis, pAdipoR1 mice developed more severe symptoms than wild-type (WT) mice. Treatment with ADN increased the expression of pro-inflammatory factors in THP-1 and HT-29 cells. Moreover, we also observed that the expression of cyclooxygenase2 (cox2), neutrophil chemokines (CXCL1, CXCL2 and CXCL5), and the infiltration of neutrophils were increased in the colon of pAdipoR1 mice. Conclusions: Our study showed that ADN-AdipoR1 signaling exacerbated colonic inflammation through two possible mechanisms. First, ADN-AdipoR1 signaling increased pro-inflammatory factors. Second, AdipoR1 enhanced neutrophil chemokine expression and recruited neutrophils into the colonic tissue to increase inflammation. ? 2018 The Author(s).
SDGs
Other Subjects
adiponectin; adiponectin receptor 1; CXCL1 chemokine; CXCL2 chemokine; CXCL3 chemokine; cyclooxygenase 2; interleukin 6; interleukin 8; prostaglandin E2; recombinant protein; tumor necrosis factor; adiponectin; adiponectin receptor; ADIPOQ protein, human; dextran sulfate; animal cell; animal experiment; animal model; animal tissue; Article; colon tissue; controlled study; dextran sulfate sodium-induced colitis; disease severity; enteritis; female; gene overexpression; HT-29 cell line; human; human cell; immunohistochemistry; inflammatory bowel disease; macrophage; mouse; neutrophil; neutrophil chemotaxis; nonhuman; priority journal; protein expression; protein function; signal transduction; THP-1 cell line; transgenic mouse; wild type mouse; animal; colitis; gene expression; genetics; inflammatory bowel disease; metabolism; pig; signal transduction; Adiponectin; Animals; Colitis; Dextran Sulfate; Female; Gene Expression; HT29 Cells; Humans; Inflammatory Bowel Diseases; Mice, Transgenic; Receptors, Adiponectin; Recombinant Proteins; Signal Transduction; Sus scrofa; THP-1 Cells
Type
journal article