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Commensal bacteria promote intestinal epithelial restitution by regulating FAK phosphorylation
Author(s) -
Kumar Amrita,
Babbin Brian A.,
Nusrat Asma,
Neish Andrew S.
Publication year - 2008
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.22.1_supplement.464.10
Subject(s) - focal adhesion , paxillin , lactobacillus rhamnosus , microbiology and biotechnology , phosphorylation , motility , cell migration , biology , chemistry , bacteria , cell , lactobacillus , biochemistry , genetics
Commensal enteric bacteria, which are often used as probiotics, positively influence epithelial barrier recovery after injury. Restoration of epithelial barrier following injury (restitution) requires intestinal epithelial cell (IEC) migration‐ a process that is dependent on dynamic turnover of focal cell‐matrix adhesions (FAC). The mechanism(s) by which commensal bacteria regulate IEC migration and restitution after injury are however not understood. Thus, our objectives were to explore the signaling pathways by which commensal bacteria influence IEC migration and restitution. We show that in vitro interaction of model IECs with the commensal bacterial strain Lactobacillus rhamnosus, resulted in a significant increase in cell adhesion, spreading and wound closure. This was associated with phosphorylation/activation of key FAC proteins, focal adhesion kinase (FAK) and paxillin within 5 minutes of bacterial contact. Furthermore, bacterial colonization of cultured epithelial cells resulted in rapid and reversible generation of reactive oxygen species (ROS), which induced sustained FAK activation by oxidative inactivation of a FAK phosphatase, PTEN. These observations demonstrate that commensal/probiotic bacteria facilitate epithelial barrier recovery by stimulating ROS, FAK phosphorylation and IEC restitution. This research was supported by a NIH grant AI064462 and DK55679.