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The Escherichia coli O157:H7 EhaB autotransporter protein binds to laminin and collagen I and induces a serum IgA response in O157:H7 challenged cattle
Authors:Timothy J Wells  Tom N McNeilly  Makrina Totsika  Arvind Mahajan  David L Gally  Mark A Schembri
Institution:School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane Queensland 4072, Australia.;
Moredun Research Institute, Pentlands Science Park, Bush Loan, Penicuik EH26 OPZ, UK.;
Cellular Microbiology Group, Division of Infection and Immunity, The Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush Veterinary Centre, Easter Bush, Midlothian EH25 9RG, UK.;
Zoonotic and Animal Pathogens Research Laboratory, Division of Immunity and Infection, Roslin Institute and R(D)SVS, Chancellor's Building, University of Edinburgh, Edinburgh, EH16 4SB, UK.
Abstract:Enterohaemorrhagic Escherichia coli (EHEC) are a subgroup of Shiga toxin-producing E. coli that cause gastrointestinal disease with the potential for life-threatening sequelae. Cattle serve as the natural reservoir for EHEC and outbreaks occur sporadically as a result of contaminated beef and other farming products. While certain EHEC virulence mechanisms have been extensively studied, the factors that mediate host colonization are poorly defined. Previously, we identified four proteins (EhaA,B,C,D) from the prototypic EHEC strain EDL933 that belong to the autotransporter (AT) family. Here we characterize the EhaB AT protein. EhaB was shown to be located at the cell surface and overexpression in E. coli K-12 resulted in significant biofilm formation under continuous flow conditions. Overexpression of EhaB in E. coli K12 and EDL933 backgrounds also promoted adhesion to the extracellular matrix proteins collagen I and laminin. An EhaB-specific antibody revealed that EhaB is expressed in E. coli EDL933 following in vitro growth. EhaB also cross-reacted with serum IgA from cattle challenged with E. coli O157:H7, indicating that EhaB is expressed in vivo and elicits a host IgA immune response.
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