Increased virulence of Yersinia pseudotuberculosis by two independent mutations

Rosqvist, Roland; Skurnik, Mikael; Wolf‐Watz, Hans

doi:10.1038/334522a0

Cited by 241 publications

(180 citation statements)

References 20 publications

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“…Of three genes (inv, yadA and ail) associated with these processes in enteropathogenic Yersinia, yadA (Rosqvist et al, 1988) and inv (Simonet et al, 1996) are inactive in Y. pestis. Experiments are ongoing to investigate other roles of OmpX in pathogenesis and its potential application as a vaccine candidate.…”

Section: Discussionmentioning

confidence: 99%

Phenotypic characterization of OmpX, an Ail homologue of Yersinia pestis KIM

et al. 2007

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The goal of this study was to characterize the Yersinia pestis KIM OmpX protein. Yersinia spp. provide a model for studying several virulence processes including attachment to, and internalization by, host cells. For Yersinia enterocolitica and Yersinia pseudotuberculosis, Ail, YadA and Inv, have been implicated in these processes. In Y. pestis, YadA and Inv are inactivated. Genomic analysis of two Y. pestis strains revealed four loci with sequence homology to Ail. One of these genes, designated y1324 in the Y. pestis KIM database, encodes a protein designated OmpX. The mature protein has a predicted molecular mass of 17.47 kDa, shares approximately 70 % sequence identity with Y. enterocolitica Ail, and has an identical homologue, designated Ail, in the Y. pestis CO92 database. The present study compared the Y. pestis KIM6 + parental strain with a mutant derivative having an engineered disruption of the OmpX structural gene. The parental strain (and a merodiploid control strain) expressed OmpX at 28 and 37 6C, and the protein was detectable throughout all phases of growth. OmpX was required for efficient adherence to, and internalization by, cultured HEp-2 cell monolayers and conferred resistance to the bactericidal effect of human serum. Deletion of ompX resulted in a significantly reduced autoaggregation phenotype and loss of pellicle formation in vitro. These results suggest that Y. pestis OmpX shares functional homology with Y. enterocolitica Ail in adherence, internalization into epithelial cells and serum resistance.

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Section: Discussionmentioning

confidence: 99%

Phenotypic characterization of OmpX, an Ail homologue of Yersinia pestis KIM

et al. 2007

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“…In C. jejuni NCTC11168, more than 20 contingency genes have been observed to carry G/C hypervariable HTs with eight or more nucleotides (Parkhill et al, 2000). Contingency genes are also found in other bacteria, such as Yersinia pestis (Rosqvist et al, 1988), Bordetella pertussis (Willems et al, 1990) and Haemophilus influenzae (van Ham et al, 1993). Many bacterial contingency genes, including most of those in C. jejuni, encode enzymes involved in the synthesis or modification of surface structures such as lipooligosaccharide (LOS), pilus, flagella and capsule, suggesting that they play important roles in host interaction and virulence (Moxon et al, 2006;Parkhill et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Passage of Campylobacter jejuni through the chicken reservoir or mice promotes phase variation in contingency genes Cj0045 and Cj0170 that strongly associates with colonization and disease in a mouse model

et al. 2012

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Human illness due to Camplyobacter jejuni infection is closely associated with consumption of poultry products. We previously demonstrated a 50 % shift in allele frequency (phase variation) in contingency gene Cj1139 (wlaN) during passage of C. jejuni NCTC11168 populations through Ross 308 broiler chickens. We hypothesized that phase variation in contingency genes during chicken passage could promote subsequent colonization and disease in humans. To test this hypothesis, we passaged C. jejuni strains NCTC11168, 33292, 81-176, KanR4 and CamR2 through broiler chickens and analysed the ability of passaged and non-passaged populations to colonize C57BL6 IL-10-deficient mice, our model for human colonization and disease. We utilized fragment analysis and nucleotide sequence analysis to measure phase variation in contingency genes. Passage through the chicken reservoir promoted phase variation in five specific contingency genes, and these 'successful' populations colonized mice. When phase variation did not occur in these same five contingency genes during chicken passage, these 'unsuccessful' populations failed to colonize mice. Phase variation during chicken passage generated small insertions or deletions (indels) in the homopolymeric tract (HT) in contingency genes. Singlecolony isolates of C. jejuni strain KanR4 carrying an allele of contingency gene Cj0170 with a 3These authors contributed equally to this work. Two supplementary tables, listing PCR primer sequences for fragment and sequence analysis used in this study, and results of sequence and fragment analysis to confirm large shifts in allele frequency, with a supplementary reference, are available with the online version of this paper. 10G HT colonized mice at high frequency and caused disease symptoms, whereas single-colony isolates carrying the 9G allele failed to colonize mice. Supporting results were observed for the successful 9G allele of Cj0045 in strain 33292. These data suggest that phase variation in Cj0170 and Cj0045 is strongly associated with mouse colonization and disease, and that the chicken reservoir can play an active role in natural selection, phase variation and disease.

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“…S. typhimurium PhoPc strain transformed with the pKKGFP plasmid was kindly provided by F. Niedergang (24,25). Further, GFP-expressing Yersinia pseudotuberculosis, Escherichia coli-invasin, and E. coli were prepared by the method described (26,27). Mice were anesthetized by i.p.…”

Section: Cell Stainingmentioning

confidence: 99%

Intestinal villous M cells: An antigen entry site in the mucosal epithelium

Jang

Kweon

Iwatani

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

416

323

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T he huge intestinal surface area is physically protected by a layer of tightly joined epithelial cells, which prevent most enteric environmental antigens from penetrating the host (1). However, entry into the host is made possible by a special gateway, comprised of M cells, located over organized mucosal lymphoid follicles such as Peyer's patches (PP). The M cells, characterized by an irregular brush border and reduced glycocalyx, efficiently take up and transport a wide variety of macromolecules and microorganisms from the gut lumen to the inside of the PP (2-6), which contain all of the necessary lymphoid cells for the induction and regulation of antigen-specific IgA responses (7). However, the origin of M cells and the regulation of their development are not understood. A previous study (8) The common mucosal immune system (CMIS), which connects the inductive (e.g., PP) and effector (e.g., lamina propria; LP) sites, has been shown to be a central pathway for the induction of antigen-specific IgA immune responses in the gastrointestinal tract (7). For example, oral administration of Salmonella typhimurium leads to the transport of the bacterial antigen from the lumen of the intestinal tract into the PP by means of M cells for the initial priming of antigen-specific CD4 ϩ T cells and IgA-committed B cells (12). These antigen-sensitized cells leave the PP and contribute to the subsequent induction of Salmonella-specific IgA response in the distant intestinal LP by means of CMIS. In addition to the wellcharacterized CMIS-dependent IgA induction pathway, recent evidence suggests the presence of an additional IgA induction pathway that is independently operated from the PP-originated CMIS (13-15). Interestingly, it also has been reported that induction of intestinal mucosal IgA against the commensal bacteria was independent from T cell help and organized lymphoid tissue (16). Further, our recent study (17) has demonstrated that antigenspecific IgA antibody responses can be induced in the absence of PP. These studies imply the existence of a PP-independent mucosal immune pathway for dietary antigen and bacteria uptake.A recent study (18) has suggested that the invasion gene (SPI1)-deficient S. typhimurium can be disseminated from the intestinal epithelium to the systemic compartment in the absence of PPassociated M cells by means of the CD18-dependent pathway. Further, dendritic cells in the lamina propria of the small intestine expressing tight junction protein offer another possible antigen uptake site (19). Thus, intestinal DCs are capable of extending dendrites to the lumen side by opening the tight junction. However, the exact mechanism for inducing Ag-specific immune responses independently of PP requires further elucidation.In this study, we have discovered intestinal villous M cells, which serve as an antigen gateway for the sampling of gut bacteria and subsequent induction of Ag-specific immune responses in a PPindependent manner. These lines of study are crucial for understanding the mechanisms of antige...

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Increased virulence of Yersinia pseudotuberculosis by two independent mutations

Cited by 241 publications

References 20 publications

Phenotypic characterization of OmpX, an Ail homologue of Yersinia pestis KIM

Phenotypic characterization of OmpX, an Ail homologue of Yersinia pestis KIM

Passage of Campylobacter jejuni through the chicken reservoir or mice promotes phase variation in contingency genes Cj0045 and Cj0170 that strongly associates with colonization and disease in a mouse model

Intestinal villous M cells: An antigen entry site in the mucosal epithelium

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