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Psoriasis modulates inflammatory bowel disease risk and intestinal epithelium lipid metabolism via IL-1β-producing
Jiaqi Wu1, Shuangshuang Liu1, Wei Dan1
1Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism & Integrative Biology, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 200438, China.
Abstract:
Patients with psoriasis have an increased risk of developing inflammatory bowel disease, yet the mechanisms underlying this comorbidity remain unclear. In a clinical cohort, we observed an inverse correlation between psoriasis severity and postprandial plasma apolipoprotein B48 levels, a finding recapitulated in experimental psoriasis mouse models, indicating impaired intestinal lipid handling. To directly interrogate this process, we developed a recombinant photoconvertible apolipoprotein B reporter that enables real-time quantification of endogenous chylomicron production in intestinal organoids and in vivo. Using this system, we demonstrate that psoriasis promotes the expansion of interleukin (IL)-1β-producing intestinal macrophages, which accelerate apolipoprotein B degradation, impair chylomicron secretion, drive epithelial lipid accumulation, and exacerbate mucosal inflammation. Integrating human and experimental data, our findings implicate macrophage-driven metabolic dysregulation of the intestinal epithelium as a mechanistic link between psoriasis and gut inflammation and highlight intestinal IL-1β as a potential therapeutic target.
Insights
Psoriasis patients show impaired intestinal lipid handling, linked to inflammation. Interleukin-1β-producing macrophages worsen this by affecting apolipoprotein B, a key protein in lipid transport, potentially offering a new therapeutic target.
Area of Science:
- Gastroenterology
- Immunology
- Dermatology
Background:
- Psoriasis is associated with an increased risk of inflammatory bowel disease (IBD).
- The underlying mechanisms connecting psoriasis and IBD remain largely unknown.
- Impaired intestinal lipid metabolism is suggested by inverse correlations between psoriasis severity and apolipoprotein B48 levels.
Purpose of the Study:
- To investigate the mechanistic link between psoriasis and gut inflammation.
- To elucidate the role of intestinal lipid handling in this comorbidity.
- To identify potential therapeutic targets for psoriasis-associated gut inflammation.
Main Methods:
- Development of a recombinant photoconvertible apolipoprotein B reporter for real-time chylomicron production quantification.
- Analysis of intestinal organoids and in vivo models.
- Integration of human clinical data and experimental mouse models.
Main Results:
- Psoriasis is linked to an expansion of interleukin-1β (IL-1β)-producing intestinal macrophages.
- These macrophages accelerate apolipoprotein B degradation, impairing chylomicron secretion.
- This leads to epithelial lipid accumulation and exacerbated mucosal inflammation.
Conclusions:
- Macrophage-driven metabolic dysregulation of the intestinal epithelium is a key link between psoriasis and gut inflammation.
- Intestinal IL-1β plays a critical role in this process.
- Targeting intestinal IL-1β may offer a therapeutic strategy for managing psoriasis-associated gut inflammation.
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