The goblet cell-derived mediator RELM-β drives spontaneous colitis in Muc2-deficient mice by promoting commensal microbial dysbiosis

@article{Morampudi2016TheGC,
  title={The goblet cell-derived mediator RELM-β drives spontaneous colitis in Muc2-deficient mice by promoting commensal microbial dysbiosis},
  author={Vijay Morampudi and Udit Dalwadi and Ganive Bhinder and Ho Pan Sham and Sharonjit K. Gill and Justin Chan and Kirk S. B. Bergstrom and Tina I-T Huang and C. C. H. Ma and Kevan Jacobson and Deanna Lynn Gibson and Bruce A Vallance},
  journal={Mucosal Immunology},
  year={2016},
  volume={9},
  pages={1218-1233}
}
Intestinal goblet cells are potentially key players in controlling susceptibility to ulcerative colitis (UC). Although impaired mucin (Muc2) production by goblet cells increases microbial stimulation of the colonic mucosa, goblet cells secrete other mediators that may influence or promote UC development. Correspondingly, Muc2-deficient (−/−) mice develop spontaneous colitis, concurrent with the dramatic upregulation of the goblet cell mediator, resistin-like molecule-beta (RELM-β). Testing RELM… CONTINUE READING
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implications for inflammatory bowel diseases

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