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Modulation of tight junction barrier function by outer membrane proteins of enteropathogenic Escherichia coli : Role of F‐actin and junctional adhesion molecule‐1
Author(s) -
Puthenedam Manjula,
Williams Peter H.,
Lakshmi B.S.,
Balakrishnan Arun
Publication year - 2007
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2007.01.036
Subject(s) - microbiology and biotechnology , enteropathogenic escherichia coli , barrier function , actin , tight junction , cytoskeleton , bacterial outer membrane , actin cytoskeleton , adhesion , chemistry , signal transduction , cadherin , cell adhesion molecule , biology , mutant , escherichia coli , biochemistry , cell , organic chemistry , gene
Abstract Enteropathogenic Escherichia coli (EPEC) is a major cause of infantile diarrhea. In this work we investigated the effect of outer membrane proteins (OMP) of EPEC on barrier integrity and the role of actin, junctional adhesion molecule (JAM) and signaling pathways contributing to these changes. Barrier function was assessed by transepithelial electrical resistance (TER). OMP of wild type EPEC, eaeA and maltoporin mutants decreased TER levels of Caco‐2 cells. The OMP of espB mutant was deficient in decreasing TER of Caco‐2 cells. The proteinase K‐digested wild type OMP and EAF mutant OMP did not cause any change in barrier function. Our previous studies have demonstrated that EPEC OMP induced changes in cadherin junctions of Caco‐2 cells. Immunofluorescence revealed disruption in actin cytoskeleton by EPEC OMP. However, no change in expression of junctional adhesion molecule‐1 was observed. NF‐κB inhibitor slightly blocked the decrease in TER and protected against actin disruption while ERK1/2 inhibitor had no effect in blocking these changes. In conclusion, our data suggest that the OMP of EPEC alter intestinal barrier function by disrupting actin cytoskeleton and signaling pathways like NF‐κB may have a role in regulating barrier changes.