@article{oai:air.repo.nii.ac.jp:00002562,
 author = {NAKAMURA, Ryotaro and TAKASUGA, Shunsuke and HORIE, Yasuo and SASAKI, Takehiko},
 issue = {3/4},
 journal = {秋田医学},
 month = {Mar},
 note = {We recently established mice lacking the type III phosphatidylinositol phosphate kinase gene
(PipkIII) in enterocytes, which represent a unique model of intestinal inflammation associated
with extensive fibrosis that closely resembles human Crohn’s disease. These mutant mice
develop spontaneous juvenile colitis with marked inflammatory cytokine expression, but the primary
pathogenic mechanism remains unclear. In the present study, we found that administration
of broad-specific antibiotics effectively ameliorated the colitis of PipkIII-deficient mice, suggesting
the involvement of intestinal bacterial flora in the onset of colitis. Furthermore, we showed
that altered intestinal permeability facilitating commensal bacteria entry putatively caused the
intestinal inflammation and fibrosis observed in these mutant mice.},
 pages = {129--135},
 title = {Alterations in Intestinal Permeability Cause Colonic Inflammation and Fibrosis in Type III Phosphatidylinositol Phosphate Kinase-Deficient Mice},
 volume = {41},
 year = {2015}
}