Open AccessThe ability of an attaching and effacing pathogen to trigger localized actin assembly contributes to virulence by promoting mucosal attachment
Author(s) -
Mallick Emily M.,
Garber John J.,
Vanguri Vijay K.,
Balasubramanian Sowmya,
Blood Timothy,
Clark Stacie,
Vingadassalom Didier,
Louissaint Christopher,
McCormick Beth,
Snapper Scott B.,
Leong John M.
Publication year - 2014
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12302
Subject(s) - virulence , biology , pathogen , shiga toxin , microbiology and biotechnology , actin , bacteria , mutant , toxin , escherichia coli , virology , genetics , gene
Summary Enterohaemorrhagic E scherichia coli ( EHEC ) colonizes the intestine and causes bloody diarrhoea and kidney failure by producing S higa toxin. Upon binding intestinal cells, EHEC triggers a change in host cell shape, generating actin ‘pedestals’ beneath bound bacteria. To investigate the importance of pedestal formation to disease, we infected genetically engineered mice incapable of supporting pedestal formation by an EHEC ‐like mouse pathogen, or wild type mice with a mutant of that pathogen incapable of generating pedestals. We found that pedestal formation promotes attachment of bacteria to the intestinal mucosa and vastly increases the severity of S higa toxin‐mediated disease.