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Obesity predisposes to Th17 bias
Shawn Winer1, Geoff Paltser, Yin Chan
1Neuroscience and Mental Health program, Research Institute, The Hospital for Sick Children, University of Toronto Departments of Pediatrics & Immunology, Toronto, Ontario Canada.
European Journal of Immunology
|August 8, 2009
Summary
Obesity promotes the expansion of pro-inflammatory Th17 cells, a process dependent on Interleukin-6 (IL-6). This Th17 bias exacerbates autoimmune diseases, linking obesity to inflammation.
Area of Science:
- Immunology
- Metabolic disorders
Background:
- Obesity is linked to inflammatory conditions like atherosclerosis, autoimmune disease, and cancer.
- Obesity-associated increases in TNF-alpha, IL-6, and TGF-beta are suspected contributors.
Purpose of the Study:
- To investigate the mechanistic link between obesity and inflammatory/autoimmune diseases.
- To determine if obesity influences specific T-cell subsets involved in inflammation.
Main Methods:
- Utilized diet-induced obesity models in mice.
- Analyzed T-cell populations and cytokine production (IL-17).
- Assessed disease severity in experimental autoimmune encephalomyelitis (EAE) and trinitrobenzene sulfonic acid (TNBS) colitis models.
Main Results:
- Obesity selectively expanded Th17 cell populations.
- Obese mice showed increased IL-17 production in an IL-6-dependent manner.
- Obesity exacerbated autoimmune disease severity and associated Th17 infiltration in target tissues.
Conclusions:
- Obesity promotes a pro-inflammatory Th17 cell bias.
- This Th17 bias is mechanistically linked to the heightened risk of autoimmune diseases in obesity.
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