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Updated: Jun 10, 2026
Isolation of Adipose Tissue Immune Cells
Published on: May 22, 2013
Interleukin-33 induces protective effects in adipose tissue inflammation during obesity in mice
Ashley M Miller1, Darren L Asquith, Axel J Hueber
1Division of Immunology, Infection and Inflammation, GBRC, University of Glasgow, Glasgow, United Kingdom. a.miller@clinmed.gla.ac.uk
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.
