title: The IbeA invasin of adherent-invasive Escherichia coli mediates interaction with intestinal epithelia and macrophages.
abstract: Adherent-invasive Escherichia coli (AIEC) pathogroup isolates are a group of isolates from the intestinal mucosa of Crohn's disease patients that can invade intestinal epithelial cells (IECs) or macrophages and survive and/or replicate within. We have identified the ibeA gene in the genome of AIEC strain NRG857c and report the contribution of IbeA to the interaction of AIEC with IECs and macrophages and colonization of the mouse intestine. An ibeA deletion mutant strain (NRG857cΔibeA) was constructed, and the in vitro effect on AIEC adhesion and invasion of nonpolarized and polarized Caco-2 cells, the adhesion and transcytosis of M-like cells, the intracellular survival in THP-1 macrophages, and the contribution to intestinal colonization of the CD-1 murine model of infection were evaluated. A significant reduction in invasion was observed with the ibeA mutant in Caco-2 and M-like cells, whereas adhesion was not affected. Complementation of the mutant reestablished Caco-2 invasive phenotype to wild-type levels. Reduction in invasion did not significantly affect transcytosis through M-like cells at early time points. The absence of ibeA significantly affected AIEC intramacrophage survival up to 24 h postinfection. No significant changes associated with IbeA were found in AIEC colonization across the murine gastrointestinal tract, but a slight reduction of gamma interferon was observed in the ceca of mice infected with the ibeA mutant. In addition, a decrease in the pathology scores was observed in the ilea and ceca of mice infected with the ibeA mutant. Our data support the function of IbeA in the AIEC invasion process, macrophage survival, and inflammatory response in the murine intestine.
authors.affiliation: Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA.
authors.forename: Roberto J
authors.initials: RJ
authors.lastname: Cieza
authors.affiliation: Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA.
authors.forename: Jia
authors.initials: J
authors.lastname: Hu
authors.affiliation: Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA.
authors.forename: Brittany N
authors.initials: BN
authors.lastname: Ross
authors.affiliation: Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA.
authors.forename: Elena
authors.initials: E
authors.lastname: Sbrana
authors.affiliation: Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas, USA Department of Pathology, University of Texas Medical Branch, Galveston, Texas, USA altorres@utmb.edu.
authors.forename: Alfredo G
authors.initials: AG
authors.lastname: Torres
mesh_terms: D000818:Animals; D002432:Cecum / Q000473:pathology; D002460:Cell Line; D004195:Disease Models, Animal; D004705:Endocytosis; D004847:Epithelial Cells / Q000382:microbiology*; D004926:Escherichia coli / Q000235:genetics / Q000502:physiology*; D004927:Escherichia coli Infections / Q000382:microbiology; D029968:Escherichia coli Proteins / Q000235:genetics / Q000378:metabolism*; D005260:Female; D017353:Gene Deletion; D005816:Genetic Complementation Test; D006801:Humans; D007082:Ileum / Q000473:pathology; D007422:Intestines / Q000382:microbiology; D008264:Macrophages / Q000382:microbiology*; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D008813:Mice, Inbred ICR; D012720:Severity of Illness Index; D037521:Virulence Factors / Q000235:genetics / Q000378:metabolism*
chemical_list: C096350:CusC protein, E coli; D029968:Escherichia coli Proteins; D008565:Membrane Proteins; D037521:Virulence Factors