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The Novel Roles of Dusp6 in Gut Barrier Modulation and Microbiome Shaping
Author(s) -
KAO CHENG-YUAN,
Chang Cherng-Shyang,
Liao Yi-Chu,
Huang Chih-Ting,
Lin Chiao-Mei,
Ruan Jhen-Wei,
Liao Yu-Chieh
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.09605
Subject(s) - transcriptome , microbiome , dysbiosis , gut–brain axis , gut flora , biology , feces , gene , gene expression , medicine , immunology , bioinformatics , microbiology and biotechnology , genetics
Gut microbiome has been associated with many human disorders and conditions such as allergy, obesity, inflammatory bowel disease and various types of cancers. Many of these diseases have become important health issues worldwide and effective strategies for their treatment and/or prevention are highly desired. We previously have found that dual‐specificity phosphatase 6 (Dusp6)‐deficient mice had reduced body weight gain and alleviated metabolic disorders. Notably, 16S rRNA gene sequencing revealed that the gut/fecal microbiota in Dusp6‐deficient mice was more resistant to high‐fat‐diet‐ induced dysbiosis compared with wild‐type mice. The RNA‐seq gut transcriptome analysis has shown several potential mechanisms driving the microbiota alteration in Dusp6‐deficient mice. We also found that Dusp6 knockout mice compared with wild‐type littermate mice were more resistant to dextran sulfate sodium (DSS)‐induced colitis and the mechanisms of the Dusp6 deficiency in shaping gut microbiome and barrier integrity were investigated. In summary, these findings indicate that Dusp6‐deficiency is a novel host genetic factor that could modulate gut barrier and inhibiting DUSP6 might be a novel strategy to maintain gut microbiome eubiosis. Support or Funding Information This work was supported by the following grants: IM‐108‐PP‐04 from NHRI and 106‐2628‐B‐ 400‐001‐MY3, 106‐2923‐B‐400‐001‐MY3, 108‐2321‐B‐400‐011‐ from MOST.