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Systemic inflammation-induced adipose tissue remodeling drives psoriasis exacerbation in obesity through epigenetic and immunometabolic dysregulation

ABSTRACT: Obesity has been known to be associated with psoriasis, negatively affecting its prevalence, severity, and treatment response. However, a detailed systemic inflammatory microenvironment in obesity-associated psoriasis has not been extensively investigated. To explore this further, we used a mouse model of psoriasis induced by topical application of imiquimod or injection of IL-23. We found that obese mice exhibited systemic inflammatory responses when exposed to imiquimod, with increased expression of inflammatory cytokines in the skin and elevated serum levels of mediators implicated in psoriasis pathogenesis. Notably, imiquimod also caused a significant decrease in body weight and fat, which was more pronounced in obese mice, resulting a thinner subcutaneous fat layer. Further analysis revealed higher macrophage infiltration, upregulated genes relating to the inflammatory response, and increased expression of necrosis-associated molecules in the perigonadal fat of imiquimod-treated obese mice than in lean mice. IL-23 injection induced comparable pathogenic features of psoriatic inflammation in obese and lean mice without causing adipose tissue destruction or systemic increase of inflammatory mediators.

ORGANISM(S): Mus musculus

PROVIDER: GSE246074 | GEO | 2025/07/31

REPOSITORIES: GEO

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Project description:The polyphenol resveratrol has anti-inflammatory effects in various cells, tissues, animals and human settings of low-grade inflammation. Psoriasis is a disease of both localized and systemic low-grade inflammation. The Sirtuin1 enzyme thought to mediate the effects of resveratrol is present in skin and resveratrol is known to downregulate NF-κB; a major contributor in the development of psoriasis. Consequently we investigated whether resveratrol has an effect on an Imiquimod induced psoriasis-like skin inflammation in mice and sought to identify candidate genes, pathways and interleukins mediating the observed effects. The study consisted of three treatment groups: A control group, an Imiquimod group and an Imiquimod+resveratrol group. Psoriasis severity was assessed using elements of the Psoriasis Area Severity Index, actual skin thickness measurements, and histological examination. We performed an RNA microarray from lesional skin and afterwards Ingenuity pathway analysis to identify affected signalling pathways. Our microarray was compared to a previously deposited microarray to determine if gene changes were psoriasis-like, and to a human microarray to determine if findings could be relevant in a human setting. Imiquimod treatment induced a psoriasis-like skin inflammation. Resveratrol significantly diminished the severity of the psoriasis-like skin inflammation. The RNA microarray revealed a psoriasis-like gene expression-profile in the Imiquimod treated group, and highlighted several resveratrol dependent changes in relevant genes, such as increased expression of genes associated with retinoic acid stimulation and reduced expression of genes involved in IL-17 dependent pathways (e.g.IL-17A, IL-17F,IL-23p19 ). Quantitative PCR confirmed a resveratrol dependent decrease in mRNA levels of IL-17A and IL-19; both central in developing psoriasis. In conclusion, resveratrol ameliorates psoriasis, and changes in expression of retinoic acid stimulated genes, IL-17 signalling pathways, IL-17A and IL-19 mRNA levels in a beneficial manner suggests it might have a role in the treatment of psoriasis and should be explored further in a human setting.

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Systemic inflammation-induced adipose tissue remodeling drives psoriasis exacerbation in obesity through epigenetic and immunometabolic dysregulation

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