ID | 117227 |
Author |
Miki, Yoshimi
The University of Tokyo|Tokyo Metropolitan Institute of Medical Science
Taketomi, Yoshitaka
The University of Tokyo|Tokyo Metropolitan Institute of Medical Science
Kidoguchi, Yuh
Tokyo Metropolitan Institute of Medical Science|Tokyo Denki University
Yamamoto, Kei
Tokyo Metropolitan Institute of Medical Science|Tokushima University
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Muramatsu, Kazuaki
Tokyo Denki University
Nishito, Yasumasa
Tokyo Metropolitan Institute of Medical Science
Park, Jonguk
National Institutes of Biomedical Innovation, Health and Nutrition
Hosomi, Koji
National Institutes of Biomedical Innovation, Health and Nutrition
Mizuguchi, Kenji
National Institutes of Biomedical Innovation, Health and Nutrition|Osaka University
Kunisawa, Jun
National Institutes of Biomedical Innovation, Health and Nutrition
Soga, Tomoyoshi
Keio University
Boilard, Eric
Université Laval
Gowda, Siddabasave Gowda B.
RIKEN
Ikeda, Kazutaka
RIKEN
Arita, Makoto
RIKEN|Keio University
Murakami, Makoto
The University of Tokyo|Tokyo Metropolitan Institute of Medical Science
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Content Type |
Journal Article
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Description | Besides promoting inflammation by mobilizing lipid mediators, group IIA secreted phospholipase A2 (sPLA2-IIA) prevents bacterial infection by degrading bacterial membranes. Here, we show that, despite the restricted intestinal expression of sPLA2-IIA in BALB/c mice, its genetic deletion leads to amelioration of cancer and exacerbation of psoriasis in distal skin. Intestinal expression of sPLA2-IIA is reduced after treatment with antibiotics or under germ-free conditions, suggesting its upregulation by gut microbiota. Metagenome, transcriptome, and metabolome analyses have revealed that sPLA2-IIA deficiency alters the gut microbiota, accompanied by notable changes in the intestinal expression of genes related to immunity and metabolism, as well as in the levels of various blood metabolites and fecal bacterial lipids, suggesting that sPLA2-IIA contributes to shaping of the gut microbiota. The skin phenotypes in Pla2g2a–/– mice are lost (a) when they are cohoused with littermate WT mice, resulting in the mixing of the microbiota between the genotypes, or (b) when they are housed in a more stringent pathogen-free facility, where Pla2g2a expression in WT mice is low and the gut microbial compositions in both genotypes are nearly identical. Thus, our results highlight a potentially new aspect of sPLA2-IIA as a modulator of gut microbiota, perturbation of which affects distal skin responses.
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Journal Title |
JCI Insight
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ISSN | 23793708
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Publisher | American Society for Clinical Investigation
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Volume | 7
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Issue | 2
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Start Page | e152611
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Published Date | 2022-01-25
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Rights | This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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DOI (Published Version) | |
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language |
eng
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TextVersion |
Publisher
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departments |
Bioscience and Bioindustry
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