Colonic Inhibition of Phosphatase and Tensin Homolog Increases Colitogenic Bacteria, Causing Development of Colitis in Il10-/- Mice
Author(s) -
Jonathon Mitchell,
Su Jin Kim,
Γεώργιος Κούκος,
Alexandra Seelmann,
Brendan Veit,
Brooke Shepard,
Sara E. BlumerSchuette,
Harland S. Winter,
Dimitrios Iliopoulos,
Charalabos Pothoulakis,
Eunok Im,
Sang Hoon Rhee
Publication year - 2018
Publication title -
inflammatory bowel diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.932
H-Index - 146
eISSN - 1536-4844
pISSN - 1078-0998
DOI - 10.1093/ibd/izy124
Subject(s) - pten , colitis , tensin , inflammatory bowel disease , ulcerative colitis , intestinal mucosa , biology , cancer research , immunology , medicine , pi3k/akt/mtor pathway , disease , signal transduction , microbiology and biotechnology
Phosphatase and tensin homolog (Pten) is capable of mediating microbe-induced immune responses in the gut. Thus, Pten deficiency in the intestine accelerates colitis development in Il10-/- mice. As some ambient pollutants inhibit Pten function and exposure to ambient pollutants may increase inflammatory bowel disease (IBD) incidence, it is of interest to examine how Pten inhibition could affect colitis development in genetically susceptible hosts.
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