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Intestinal epithelial endocytosis of commensal bacteria is dependent on IFNγ‐induced terminal web myosin phosphorylation and brush border fanning
Author(s) -
Wu LiLing,
Kuo WeiTing,
Peng WeiHao,
Lu KuoShyan,
Ni YenHsuan,
Yu Linda ChiaHui
Publication year - 2013
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.27.1_supplement.1148.21
Subject(s) - endocytosis , paracellular transport , myosin light chain kinase , microbiology and biotechnology , myosin , enterocyte , phosphorylation , biology , chemistry , small intestine , biochemistry , cell , permeability (electromagnetism) , membrane
Bacterial dissemination is commonly seen in intestinal obstruction (IO). Paracellular influx was mediated by ROCK signaling for phosphorylated myosin light chain (pMLC) and tight junctional disruption. Myosin phosphorylation in terminal web (TW) is associated with brush border (BB) fanning. The mechanism of bacterial endocytosis in enterocytes remains unclear. Aim To investigate the role of IFNγ in TW pMLC for bacterial endocytosis. Methods Mouse intestines were obstructed by loop ligation in which inhibitors were luminally administered. Next, mice were injected i.p. with anti‐IFNγ. Bacterial endocytosis in isolated enterocytes was measured by gentamycin resistance assay and fluorescence in situ hybridization. Epithelial Ca2+/ATP‐dependent TW contraction and BB fanning were visualized using TEM. Results Bacterial endocytosis was observed without paracellular permeability change at 3–6 h of IO. Enterocytic pMLC localized to TW was associated with BB fanning, which may be inhibited by ML‐7 but not Y27632. IO‐induced bacterial endocytosis through intermicrovillus space was reduced by ML‐7 or anti‐IFNγ. Caco‐2 cells treated with IFNγ showed MLCK‐dependent TW contraction and E. coli endocytosis and translocation. Conclusions IFNγ‐induced epithelial MLCK‐dependent TW contraction and BB fanning is involved in bacterial endocytosis. Funding support by National Science Council and NTU.