Format

Send to

Choose Destination
Circ Res. 2010 Sep 3;107(5):650-8. doi: 10.1161/CIRCRESAHA.110.218867. Epub 2010 Jul 15.

Interleukin-33 induces protective effects in adipose tissue inflammation during obesity in mice.

Author information

1
Division of Immunology, Infection and Inflammation, GBRC, University of Glasgow, Glasgow, United Kingdom. a.miller@clinmed.gla.ac.uk

Abstract

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.

PMID:
20634488
PMCID:
PMC4254700
DOI:
10.1161/CIRCRESAHA.110.218867
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Atypon Icon for PubMed Central
Loading ...
Support Center