Open AccessContributions of O Island 48 to Adherence of Enterohemorrhagic Escherichia coli O157:H7 to Epithelial Cells In Vitro and in Ligated Pig Ileal Loops
Author(s) -
Yin X,
Roger Wheatcroft,
James R. Chambers,
Bianfang Liu,
Jing Zhu,
Carlton Gyles
Publication year - 2009
Publication title -
applied and environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.552
H-Index - 324
eISSN - 1070-6291
pISSN - 0099-2240
DOI - 10.1128/aem.00507-09
Subject(s) - complementation , escherichia coli , microbiology and biotechnology , biology , in vitro , mutant , gene , pathogen , enterobacteriaceae , colonization , in vivo , gene cluster , bacterial adhesin , genetics
O island 48 (OI-48) ofEscherichia coli consists of three functional gene clusters that encode urease, tellurite resistance (Ter ), and putative adhesins Iha and AIDA-1. The functions of these clusters in enterohemorrhagicE. coli (EHEC) O157:H7 infection are unknown. Deletion mutants for these three regions were constructed and evaluated for their ability to adhere to epithelial cells in vitro and in ligated pig ileal loops. Deletion of the Ter gene cluster reduced the ability of the organism to adhere to and form large clusters on IPEC-J2 and HEp-2 cells. Complementation of the mutation by introducing the wild-typeter genes restored adherence and large-cluster formation. Tests in ligated pig ileal loops showed a decrease in colonization by the Ter -negative mutant, but the difference was not significant compared to colonization by the wild type (26.4% ± 21.2% versus 40.1% ± 19.1%;P = 0.168). The OI-48aidA gene deletion had no effect on adherence in vitro or in vivo. Deletion of theiha andureC genes had no effect on adherence in vitro but significantly reduced the colonization of EHEC O157:H7 in the ligated pig intestine. These data suggest that Ter , Iha, and urease may contribute to EHEC O157:H7 pathogenesis by promoting adherence of the pathogen to the host intestinal epithelium.