Resistance of Chemokine Receptor 6-Deficient Mice to Yersinia Enterocolitica Infection

Westphal, Sabine; Lügering, Andreas; Wedel, Julia von; Eiff, Christof von; Maaser, Christian; Spahn, Thomas W.; Heusipp, Gerhard; Schmidt, M. Alexander; Herbst, Hermann; Williams, Ifor R.; Domschke, Wolfram; Kucharzik, Torsten

doi:10.2353/ajpath.2008.070393

Cited by 44 publications

(56 citation statements)

References 38 publications

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“…i.p. inoculation has been used to study other virulence factors of Y. pestis CO92 (12) and has been used specifically to bypass the colonization of the lymphatics in Y. enterocolitica infections (49,54). The i.p.…”

Section: Resultsmentioning

confidence: 99%

Evolution and Virulence Contributions of the Autotransporter Proteins YapJ and YapK of Yersinia pestis CO92 and Their Homologs in Y. pseudotuberculosis IP32953

2012

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ABSTRACTYersinia pestis, the causative agent of plague, evolved from the gastrointestinal pathogenYersinia pseudotuberculosis. Both species have numerous type Va autotransporters, most of which appear to be highly conserved. InY. pestisCO92, the autotransporter genesyapKandyapJshare a high level of sequence identity. By comparingyapKandyapJto three homologous genes inY. pseudotuberculosisIP32953 (YPTB0365, YPTB3285, and YPTB3286), we show thatyapKis conserved inY. pseudotuberculosis, whileyapJis unique toY. pestis. All of these autotransporters exhibit >96% identity in the C terminus of the protein and identities ranging from 58 to 72% in their N termini. By extending this analysis to include homologous sequences from numerousY. pestisandY. pseudotuberculosisstrains, we determined that these autotransporters cluster into a YapK (YPTB3285) class and a YapJ (YPTB3286) class. The YPTB3286-like gene of mostY. pestisstrains appears to be inactivated, perhaps in favor of maintainingyapJ. Since autotransporters are important for virulence in many bacterial pathogens, includingY. pestis, any change in autotransporter content should be considered for its impact on virulence. Using established mouse models ofY. pestisinfection, we demonstrated that despite the high level of sequence identity,yapKis distinct fromyapJin its contribution to disseminatedY. pestisinfection. In addition, a mutant lacking both of these genes exhibits an additive attenuation, suggesting nonredundant roles foryapJandyapKin systemicY. pestisinfection. However, the deletion of the homologous genes inY. pseudotuberculosisdoes not seem to impact the virulence of this organism in orogastric or systemic infection models.

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Section: Resultsmentioning

confidence: 99%

Evolution and Virulence Contributions of the Autotransporter Proteins YapJ and YapK of Yersinia pestis CO92 and Their Homologs in Y. pseudotuberculosis IP32953

2012

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“…CCR6 + T cells are in majority HIV-specific (32), and their permissiveness to productive viral infection may contribute to altered immunity against HIV. In addition, by their ability to migrate into the GALT via integrin b 7 and CCR6 (17,24,25), and also into the brain via CCR6 (59), CCR6 + T cells may significantly contribute to HIV dissemination from the portal site of entry and the establishment of HIV reservoirs in immunoprivileged tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Among gut-homing chemokine receptors, CCR6 is critical for cell migration into Peyer's patches of the distal small intestine (ileum) (17,24,25), whereas CCR9 mediates cell infiltration into lamina propria of the proximal small intestine (20,26,27). In addition to being a homing receptor, CCR6 is a well-established marker for human Th17 cells (28,29).…”

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confidence: 99%

Memory CCR6+CD4+ T Cells Are Preferential Targets for Productive HIV Type 1 Infection Regardless of Their Expression of Integrin β7

Monteiro

Gosselin

Wacleche

et al. 2011

The Journal of Immunology

131

162

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HIV type 1 infection is associated with a rapid depletion of Th17 cells from the GALT. The chemokine receptor CCR6 is a marker for Th17 lineage polarization and HIV permissiveness in memory CD4+ T cells. CCR6+ T cells have the potential to migrate into the GALT via the gut-homing integrin α4β7, a newly identified HIV-gp120 binding receptor. In this study, we investigated whether memory T cells coexpressing CCR6 and integrin β7 are selective HIV targets and whether retinoic acid (RA)-induced imprinting for gut-homing selectively increases CCR6+ T cell permissiveness to infection. We demonstrated that β7−R6+ and β7+R6+ compared with β7−R6− and β7+R6− T cells were highly permissive to HIV, produced Th17 cytokines, and their frequency was decreased in the peripheral blood of HIV-infected subjects. RA upregulated integrin α4 and β7 coexpression in both CCR6+ and CCR6− T cells, but increased HIV permissiveness selectively in CCR6+ T cells via entry (CCR5 upregulation) and postentry mechanisms. In conclusion, these results demonstrate that CCR6, but not the integrin β7, is a discriminative marker for memory T cells imprinted with a transcriptional program favorable to HIV replication. Nevertheless, given the ability of integrin β7 to regulate cell migration into the GALT and bind HIV-gp120, CCR6+ T cells coexpressing integrin β7 and CCR5 might have an extraordinary ability to disseminate HIV from the portal sites of entry. Understanding the molecular mechanisms of memory CCR6+ T cell differentiation is critical for the design of new therapeutic strategies that should interfere with viral permissiveness but not Th17 lineage commitment and gut-homing potential in CCR6+ T cells.

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“…Epithelial cells can produce the chemokine CCL20 in response to flagellated bacterial pathogens including S. typhimurium, S. enteritidis and L. monocytogenes, leading to the recruitment of DCs and lymphocytes [56]. In the absence of CCR6, the cognate receptor for CCL20, M cell differentiation was compromised [57][58][59]. A subset of CCR6+, CD11c-expressing B cells have been shown to be recruited to the FAE and promotes M cell differentiation [57].…”

Section: Antigen Uptake In the Gutmentioning

confidence: 99%

Delivery strategies to enhance oral vaccination against enteric infections

Davitt

Lavelle

2015

Advanced Drug Delivery Reviews

133

102

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Resistance of Chemokine Receptor 6-Deficient Mice to Yersinia Enterocolitica Infection

Cited by 44 publications

References 38 publications

Evolution and Virulence Contributions of the Autotransporter Proteins YapJ and YapK of Yersinia pestis CO92 and Their Homologs in Y. pseudotuberculosis IP32953

Evolution and Virulence Contributions of the Autotransporter Proteins YapJ and YapK of Yersinia pestis CO92 and Their Homologs in Y. pseudotuberculosis IP32953

Memory CCR6+CD4+ T Cells Are Preferential Targets for Productive HIV Type 1 Infection Regardless of Their Expression of Integrin β7

Delivery strategies to enhance oral vaccination against enteric infections

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