High-fat diet exacerbates imiquimod-induced psoriasis-like dermatitis in mice

被引:28
作者
Higashi, Yuko [1 ]
Yamakuchi, Munekazu [2 ]
Fukushige, Tomoko [1 ]
Ibusuki, Atsuko [1 ]
Hashiguchi, Teruto [2 ]
Kanekura, Takuro [1 ]
机构
[1] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Dermatol, Kagoshima, Japan
[2] Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Lab & Vasc Med, Kagoshima, Japan
关键词
caspase-1; hyperlipidaemia; IL-1beta; Inflammasome; psoriasis; METABOLIC SYNDROME; SKIN INFLAMMATION; INFLAMMASOMES MECHANISM; CARDIOVASCULAR-DISEASE; NLRP3; INFLAMMASOME; PREVALENCE; CELLS; IL-23; GAMMA; IMMUNOPATHOGENESIS;
D O I
10.1111/exd.13484
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Psoriasis, a chronic inflammatory skin disease, is closely related to systemic metabolism. An elevated body mass index (BMI) is a risk factor for psoriasis; inflammasomes are activated by adipose tissue macrophages in obese subjects. We hypothesized that hyperlipidaemia is involved in the pathogenesis of psoriasis and examined the role of a high-fat diet (HFD) in the development of psoriasis in imiquimod (IMQ)-treated mice. The body weight and serum level of cholesterol were significantly higher in mice fed an HFD than in a regular diet (RD). HFD mice had higher psoriasis skin scores, and the number of neutrophils infiltrating into the lesional skin was elevated. IL-17A mRNA expression was significantly increased in the skin of IMQ-treated HFD mice; the expression of IL-22, IL-23 and TNF- mRNA was not enhanced. Caspase-1 and IL-1 were activated in the skin of IMQ-treated HFD mice, and their serum level of IL-17A, TNF- and IL-1 was significantly upregulated. Our findings strongly suggest that hyperlipidaemia is involved in the development and progression of psoriasis via systemic inflammation and inflammasome activation.
引用
收藏
页码:178 / 184
页数:7
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