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Adhesive factor/rabbit 2, a new fimbrial adhesin and a virulence factor from Escherichia coli O103, a serogroup enteropathogenic for rabbits.

ABSTRACT: Enteropathogenic Escherichia coli-like E. coli strains belonging to serovar O103:K-:H2 and rhamnose-negative biotypes are highly pathogenic diarrhea-inducing strains for weaned European rabbits. We describe here the cloning and sequencing of the major subunit gene of a new fimbrial adhesin, adhesive factor/rabbit 2 (AF/R2), which confers on these strains the ability to attach to rabbit enterocytes and to HeLa cells in a diffuse manner and which is associated with in vivo virulence. The chromosomal operon that encodes functional AF/R2 has been cloned from strain B10. The major subunit gene afr2G, as well as an adjacent open reading frame, afr2H, has been sequenced. The Afr2G protein shows homologies with FaeG and ClpG, which are the respective major subunits of fimbrial adhesin K88 (F4) and afimbrial adhesin CS31A. Plasmid carrying the operon transcomplements an AF/R2-negative TnphoA mutant for its ability to express AF/R2. As a whole, AF/R2 is a new member of the E. coli K88 adhesin family which is associated with virulence and which may serve in the design of vaccines.

SUBMITTER: Fiederling F

PROVIDER: S-EPMC176139 | biostudies-other | 1997 Feb

REPOSITORIES: biostudies-other

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Adhesive factor/rabbit 2, a new fimbrial adhesin and a virulence factor from Escherichia coli O103, a serogroup enteropathogenic for rabbits.

Fiederling F F Boury M M Petit C C Milon A A

Infection and immunity 19970201 2

Enteropathogenic Escherichia coli-like E. coli strains belonging to serovar O103:K-:H2 and rhamnose-negative biotypes are highly pathogenic diarrhea-inducing strains for weaned European rabbits. We describe here the cloning and sequencing of the major subunit gene of a new fimbrial adhesin, adhesive factor/rabbit 2 (AF/R2), which confers on these strains the ability to attach to rabbit enterocytes and to HeLa cells in a diffuse manner and which is associated with in vivo virulence. The chromosom ...[more]

PMID: 9009356

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Project description:Attaching and effacing (A/E) rabbit enteropathogenic Escherichia coli (REPEC) strains belonging to serogroup O103 are an important cause of diarrhea in weaned rabbits. Like human EPEC strains, they possess the locus of enterocyte effacement clustering the genes involved in the formation of the A/E lesions. In addition, pathogenic REPEC O103 strains produce an Esp-dependent but Eae (intimin)-independent alteration of the host cell cytoskeleton characterized by the formation of focal adhesion complexes and the reorganization of the actin cytoskeleton into bundles of stress fibers. To investigate the role of intimin and its translocated coreceptor (Tir) in the pathogenicity of REPEC, we have used a newly constructed isogenic tir null mutant together with a previously described eae null mutant. When human HeLa epithelial cells were infected, the tir mutant was still able to induce the formation of stress fibers as previously reported for the eae null mutant. When the rabbit epithelial cell line RK13 was used, REPEC O103 produced a classical fluorescent actin staining (FAS) effect, whereas both the eae and tir mutants were FAS negative. In a rabbit ligated ileal loop model, neither mutant was able to induce A/E lesions. In contrast to the parental strain, which intimately adhered to the enterocytes and destroyed the brush border microvilli, bacteria of both mutants were clustered in the mucus without reaching and damaging the microvilli. The role of intimin and Tir was then analyzed in vivo by oral inoculation of weaned rabbits. Although both mutants were still present in the intestinal flora of the rabbits 3 weeks after oral inoculation, neither mutant strain induced any clinical signs or significant weight loss in the inoculated rabbits whereas the parental strain caused the death of 90% of the inoculated rabbits. Nevertheless, an inflammatory infiltrate was present in the lamina propria of the rabbits infected with both mutants, with an inflammatory response greater for the eae null mutant. In conclusion, we have confirmed the role of intimin in virulence, and we have shown, for the first time, that Tir is also a key factor in vivo for pathogenicity.

Project description:Attaching and effacing (A/E) pathogens adhere intimately to intestinal enterocytes and efface brush border microvilli. A key virulence strategy of A/E pathogens is the type III secretion system (T3SS)-mediated delivery of effector proteins into host cells. The secreted protein EspZ is postulated to promote enterocyte survival by regulating the T3SS and/or by modulating epithelial signaling pathways. To explore the role of EspZ in A/E pathogen virulence, we generated an isogenic espZ deletion strain (?espZ) and corresponding cis-complemented derivatives of rabbit enteropathogenic Escherichia coli and compared their abilities to regulate the T3SS and influence host cell survival in vitro. For virulence studies, rabbits infected with these strains were monitored for bacterial colonization, clinical signs, and intestinal tissue alterations. Consistent with data from previous reports, espZ-transfected epithelial cells were refractory to infection-dependent effector translocation. Also, the ?espZ strain induced greater host cell death than did the parent and complemented strains. In rabbit infections, fecal ?espZ strain levels were 10-fold lower than those of the parent strain at 1 day postinfection, while the complemented strain was recovered at intermediate levels. In contrast to the parent and complemented mutants, ?espZ mutant fecal carriage progressively decreased on subsequent days. ?espZ mutant-infected animals gained weight steadily over the infection period, failed to show characteristic disease symptoms, and displayed minimal infection-induced histological alterations. Terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) staining of intestinal sections revealed increased epithelial cell apoptosis on day 1 after infection with the ?espZ strain compared to animals infected with the parent or complemented strains. Thus, EspZ-dependent host cell cytoprotection likely prevents epithelial cell death and sloughing and thereby promotes bacterial colonization.

Dataset Information

Adhesive factor/rabbit 2, a new fimbrial adhesin and a virulence factor from Escherichia coli O103, a serogroup enteropathogenic for rabbits.

Publications

Adhesive factor/rabbit 2, a new fimbrial adhesin and a virulence factor from Escherichia coli O103, a serogroup enteropathogenic for rabbits.

Similar Datasets

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