Literature DB >> 35819460

IL-25 directly modulates adipocyte function and inflammation through the regulation of adiponectin.

Siranart Jeerawattanawart1,2, Pilaiwan Siripurkpong1, Sittiruk Roytrakul3, Pornpimon Angkasekwinai4.   

Abstract

OBJECTIVE: This study aimed to investigate the direct role of IL-25 in modulating adipocyte function during homeostasis and low-grade inflammation induced by lipopolysaccharide (LPS).
METHODS: The 3T3-L1 preadipocyte cell lines and primary cultures of adipose-derived stromal vascular precursor cells of wild-type and IL-17RB-deficient mice were used to determine the direct function of IL-25. The expression of IL-17RB in differentiating adipocyte was determined using real-time PCR and flow cytometry analysis. The effect of IL-25 on lipid accumulation, triglyceride content, lipolysis, glucose uptake, and adipokine expression in the mature adipocytes was evaluated. IL-25 modulating the expression of inflammatory cytokines in adipocytes induced by low dose LPS was determined using real-time PCR and ELISA.
RESULTS: The receptor for IL-25 was up-regulated during adipocyte differentiation and IL-25 directly modulated adipocyte function by reducing lipid accumulation and triglyceride concentration and enhancing lipolysis without affecting an insulin-stimulated glucose uptake. Interestingly, IL-25 induced adiponectin secretion through the PI3K/AKT signaling pathway. In 3T3-L1 adipocytes under low-grade inflammation, IL-25 attenuated the expression of IL-6 and CCL5 through the induction of adiponectin.
CONCLUSION: Our studies suggest that IL-25 directly regulates adipocyte function by maintaining the adiponectin level during homeostasis and by alleviating inflammatory response through the regulation of adiponectin during low-grade inflammation in adipocytes.
© 2022. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

Entities:  

Keywords:  Adipocyte; Adipocyte inflammation; Adiponectin; IL-17RB; IL-25; Metabolic homeostasis

Year:  2022        PMID: 35819460     DOI: 10.1007/s00011-022-01606-x

Source DB:  PubMed          Journal:  Inflamm Res        ISSN: 1023-3830            Impact factor:   6.986


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