FAM3D is essential for colon homeostasis and host defense against inflammation associated carcinogenesis

Weiwei Liang, Xinjian Peng, Qingqing Li, Pingzhang Wang, Ping Lv, Quansheng Song, Shaoping She, Shiyang Huang, Keqiang Chen, Wanghua Gong, Wuxing Yuan, Vishal Thovarai, Teizo Yoshimura, Colm O’huigin, Giorgio Trinchieri, Jiaqiang Huang, Shuye Lin, Xiaohong Yao, Xiuwu Bian, Wei Kong, Jianzhong Xi, Ji Ming Wang () and Ying Wang ()
Additional contact information
Weiwei Liang: School of Basic Medical Sciences and NHC Key Laboratory of Medical Immunology, Peking University
Xinjian Peng: School of Basic Medical Sciences and NHC Key Laboratory of Medical Immunology, Peking University
Qingqing Li: School of Basic Medical Sciences and NHC Key Laboratory of Medical Immunology, Peking University
Pingzhang Wang: School of Basic Medical Sciences and NHC Key Laboratory of Medical Immunology, Peking University
Ping Lv: School of Basic Medical Sciences and NHC Key Laboratory of Medical Immunology, Peking University
Quansheng Song: School of Basic Medical Sciences and NHC Key Laboratory of Medical Immunology, Peking University
Shaoping She: School of Basic Medical Sciences and NHC Key Laboratory of Medical Immunology, Peking University
Shiyang Huang: School of Basic Medical Sciences and NHC Key Laboratory of Medical Immunology, Peking University
Keqiang Chen: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick
Wanghua Gong: Basic Research Program, Leidos Biomedical Research, Inc
Wuxing Yuan: Microbiome Sequencing Core, Leidos Biomedical Research, Inc
Vishal Thovarai: Basic Science Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research
Teizo Yoshimura: Okayama University
Colm O’huigin: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick
Giorgio Trinchieri: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick
Jiaqiang Huang: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick
Shuye Lin: Cancer Research Center, Beijing Chest Hospital affiliated to Capital Medical University, Beijing Tuberculosis & Thoracic Tumor Research Institute
Xiaohong Yao: Institute of Pathology, South-west Hospital and Cancer Center
Xiuwu Bian: Institute of Pathology, South-west Hospital and Cancer Center
Wei Kong: Peking University
Jianzhong Xi: Peking University
Ji Ming Wang: Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick
Ying Wang: School of Basic Medical Sciences and NHC Key Laboratory of Medical Immunology, Peking University

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract The physiological homeostasis of gut mucosal barrier is maintained by both genetic and environmental factors and its impairment leads to pathogenesis such as inflammatory bowel disease. A cytokine like molecule, FAM3D (mouse Fam3D), is highly expressed in mouse gastrointestinal tract. Here, we demonstrate that deficiency in Fam3D is associated with impaired integrity of colonic mucosa, increased epithelial hyper-proliferation, reduced anti-microbial peptide production and increased sensitivity to chemically induced colitis associated with high incidence of cancer. Pretreatment of Fam3D−/− mice with antibiotics significantly reduces the severity of chemically induced colitis and wild type (WT) mice co-housed with Fam3D−/− mice phenocopy Fam3D-deficiency showing increased sensitivity to colitis and skewed composition of fecal microbiota. An initial equilibrium of microbiota in cohoused WT and Fam3D−/− mice is followed by an increasing divergence of the bacterial composition after separation. These results demonstrate the essential role of Fam3D in colon homeostasis, protection against inflammation associated cancer and normal microbiota composition.

Date: 2020
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DOI: 10.1038/s41467-020-19691-z

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