期刊
CELLULAR AND MOLECULAR GASTROENTEROLOGY AND HEPATOLOGY
卷 7, 期 1, 页码 135-156出版社
ELSEVIER INC
DOI: 10.1016/j.jcmgh.2018.09.010
关键词
Inflammatory Bowel Disease; Dermatitis; Gut Microbiome
资金
- Japanese Society for the Promotion of Science [17K19668, 17H05082, 17K15966, 15H02534]
- Japan Agency for Medical Research and Development [17929894, Crest-16813798]
- Applied Enzyme Foundation
- Yakult Bioscience Research Foundation
- Keio University Medical Science Fund (Sakaguchi Memorial)
- Takeda Science Foundation
- Mochida Memorial Foundation
- Astellas Foundation
- Grants-in-Aid for Scientific Research [17H05082, 15H02534, 17K19668, 17K15966] Funding Source: KAKEN
Dermatitis induced by Toll-like receptor 7 agonist accelerates dextran sulfate sodium colitis accompanied with decreased naive B cells and a perturbed microbiome with reduced Lactobacillus species in the gut. We show the skingut axis is associated with the gut microbiome. BACKGROUND & AIMS: Psoriasis and inflammatory bowel disease (IBD) are both chronic inflammatory diseases occurring in the skin and gut, respectively. It is well established that psoriasis and IBD have high concordance rates, and similar changes in immune cells and microbiome composition have been reported in both conditions. To study this connection, we used a combination murine model of psoriatic dermatitis and colitis in which mice were treated topically with the Toll-like receptor 7 agonist imiquimod (IMQ) and fed dextran sulfate sodium (DSS). METHODS: We applied IMQ topically to B6 mice (IMQ mice) and subsequently fed them 2% DSS in their drinking water. Disease activity and immune cell phenotypes were analyzed, and the microbial composition of fecal samples was investigated using 16S ribosomal RNA sequencing. We transplanted feces from IMQ mice to germ-free IQI/Jic (IQI) mice and fed them DSS to assess the effect of the gut microbiome on disease. RESULTS: We first confirmed that IMQ mice showed accelerated DSS colitis. IMQ mice had decreased numbers of IgD thorn and IgM(+) B cells and increased numbers of non-cytokine-producing macrophages in the gut. Moreover, the gut microbiomes of IMQ mice were perturbed, with significant reductions of Lactobacillus johnsonii and Lactobacillus reuteri populations. Germ-free mice transplanted with feces from IMQ mice, but not with feces from untreated mice, also developed exacerbated DSS colitis. CONCLUSIONS: These results suggest that skin inflammation may contribute to pathogenic conditions in the gut via immunologic and microbiological changes. Our finding of a novel potential skin-gut interaction provides new insights into the coincidence of psoriasis and IBD.
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