Atopic Dermatitis: a Short Summary
- Obesity is a public health problem
- It is also associated with psoriasis and the Th17 cell plays a role
- There is a link between Body Mass Index (BMI) and the prevalence of psoriasis: however the pathophysiological reason to this link is unknown…however this study tries to give an explanation
- The authors used a mouse obese model and fed them for 10 weeks
- Methods:
- one group was given a high fat diet (HFD, 35% fat)
- one group was given a normal fat diet (ND, 5%)
- Imiquimod was then applied on ear skin to induce psoriasis
- Results show:
- that ear thickness was higher in HFD mice fed mass versus ND mice
- Il-17a production was higher in HFD and a higher number gamma delta T cells was present
- In Il-17a deficient mice, there was similar ear thickness in the HFD and HD group
- Then the authors:
- Stained the adipose tissue around blood vessels adipocytes was done (bopidy, CD31)
- Adipocytes distributed around vessels in human and mice were found to be greater in number and size of adipocytes in the HFD group
- « CCL20 attracts Th17 cells from adipocytes »: In adipocytes CCL20 expression was found to be higher in perivascular adipose tissue (PAT) vs subcutaneous and visceral fat
- In cell cultures apidocytes enhance gamma-delta T cell proliferation
- PAT would then enhance T cell proliferation and Il-17 release thus resulting in keratinocytes to produce inflammatory cytokines. This then leads then to [neutrophil migration (murine model) and] keratinocyte proliferation
- Methods:
This study although not performed in humans provides a molecular credible explanation about how obesity is causally linked with psoriasis.
Contributors
Dr Christophe Hsu – dermatologist. Geneva, Switzerland
Source of information: Nakamizo Y. et al. High fat diet contributes to cutaneous Il-17 producing delta T cell recruitment and exacerbates imiquimod-induced psoriatric dermatitis. JSID Annual Meeting (Japanese Society of Investigative Dermatology, 日本研究皮膚科学会) 2014 – Osaka, Japan
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