Open AccessTranslocation of Vibrio parahaemolyticus across an in vitro M cell model
Author(s) -
Finn Rebecca,
Ahmad Tauseef,
Coffey Eleanor T.,
Brayden David J.,
Baird Alan W.,
Boyd Aoife
Publication year - 2014
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/1574-6968.12323
Subject(s) - vibrio parahaemolyticus , microbiology and biotechnology , biology , chromosomal translocation , type three secretion system , secretion , vibrionaceae , mapk/erk pathway , bacteria , virulence , kinase , biochemistry , gene , genetics
Consumption of V ibrio parahaemolyticus via contaminated shellfish results in inflammatory gastroenteritis characterised by severe diarrhoea, nausea and stomach cramps. This study investigated the translocation of V . parahaemolyticus across a P eyer's patch M cell‐like Caco‐2/Raji B co‐culture model system, as M cells represent a primary site of infection for many pathogenic bacteria. V ibrio parahaemolyticus translocated across co‐culture monolayers in higher numbers as compared to Caco‐2 monolayers. Moreover, the bacteria induced a greater disruption of the transepithelial resistance in M cell‐like co‐cultures than in Caco‐2 monocultures. Virulence factors associated with this pathogen include two type three secretion systems ( TTSS ‐1 and TTSS ‐2). TTSS ‐1 had no effect on translocation efficiency, with TTSS ‐2 exhibiting a modest enhancing effect. ERK activity was required for optimal translocation 1 h postinfection, however, neither ERK nor the JNK and p38 MAPK were required at 2 h pi. Additionally, TER disruption in response to bacterial infection occurred independently of the TTSS and MAPK activation. It was concluded that V. parahaemolyticus causes TER disruption of M cell‐like co‐cultures and translocates in high numbers across the M cell‐like co‐culture monolayer. These data implicate M cells as important sites for V. parahaemolyticus invasion across the intestinal epithelium during infection.