First Author | Miller AM | Year | 2010 |
Journal | Circ Res | Volume | 107 |
Issue | 5 | Pages | 650-8 |
PubMed ID | 20634488 | Mgi Jnum | J:175027 |
Mgi Id | MGI:5142182 | Doi | 10.1161/CIRCRESAHA.110.218867 |
Citation | Miller AM, et al. (2010) Interleukin-33 induces protective effects in adipose tissue inflammation during obesity in mice. Circ Res 107(5):650-8 |
abstractText | RATIONALE: Chronic low-grade inflammation involving adipose tissue likely contributes to the metabolic consequences of obesity. The cytokine interleukin (IL)-33 and its receptor ST2 are expressed in adipose tissue, but their role in adipose tissue inflammation during obesity is unclear. OBJECTIVE: To examine the functional role of IL-33 in adipose tissues and investigate the effects on adipose tissue inflammation and obesity in vivo. METHODS AND RESULTS: We demonstrate that treatment of adipose tissue cultures in vitro with IL-33 induced production of Th2 cytokines (IL-5, IL-13, IL-10) and reduced expression of adipogenic and metabolic genes. Administration of recombinant IL-33 to genetically obese diabetic (ob/ob) mice led to reduced adiposity, reduced fasting glucose and improved glucose and insulin tolerance. IL-33 also induced accumulation of Th2 cells in adipose tissue and polarization of adipose tissue macrophages toward an M2 alternatively activated phenotype (CD206(+)), a lineage associated with protection against obesity-related metabolic events. Furthermore, mice lacking endogenous ST2 fed high-fat diet had increased body weight and fat mass and impaired insulin secretion and glucose regulation compared to WT controls fed high-fat diet. CONCLUSIONS: In conclusion, IL-33 may play a protective role in the development of adipose tissue inflammation during obesity. |