2.50
Hdl Handle:
http://hdl.handle.net/10033/621291
Title:
Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency.
Authors:
Heine, Wiebke; Beckstette, Michael; Heroven, Ann Kathrin; Thiemann, Sophie; Heise, Ulrike; Nuss, Aaron Mischa; Pisano, Fabio; Strowig, Till; Dersch, Petra ( 0000-0001-8177-3280 )
Abstract:
Gastrointestinal infections caused by enteric yersiniae can become persistent and complicated by relapsing enteritis and severe autoimmune disorders. To establish a persistent infection, the bacteria have to cope with hostile surroundings when they transmigrate through the intestinal epithelium and colonize underlying gut-associated lymphatic tissues. How the bacteria gain a foothold in the face of host immune responses is poorly understood. Here, we show that the CNFY toxin, which enhances translocation of the antiphagocytic Yop effectors, induces inflammatory responses. This results in extensive tissue destruction, alteration of the intestinal microbiota and bacterial clearance. Suppression of CNFY function, however, increases interferon-γ-mediated responses, comprising non-inflammatory antimicrobial activities and tolerogenesis. This process is accompanied by a preterm reprogramming of the pathogen's transcriptional response towards persistence, which gives the bacteria a fitness edge against host responses and facilitates establishment of a commensal-type life style.
Affiliation:
Helmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7, 38124 Braunschweig, Germany.
Citation:
Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency. 2018, 14 (2):e1006858 PLoS Pathog.
Journal:
PLoS pathogens
Issue Date:
Feb-2018
URI:
http://hdl.handle.net/10033/621291
DOI:
10.1371/journal.ppat.1006858
PubMed ID:
29390040
Type:
Article
Language:
en
ISSN:
1553-7374
Appears in Collections:
publications of the research group microbial immune regulation (MIKI); publications of the department of molecular Infectionbiology (MIBI)

Full metadata record

DC FieldValue Language
dc.contributor.authorHeine, Wiebkeen
dc.contributor.authorBeckstette, Michaelen
dc.contributor.authorHeroven, Ann Kathrinen
dc.contributor.authorThiemann, Sophieen
dc.contributor.authorHeise, Ulrikeen
dc.contributor.authorNuss, Aaron Mischaen
dc.contributor.authorPisano, Fabioen
dc.contributor.authorStrowig, Tillen
dc.contributor.authorDersch, Petraen
dc.date.accessioned2018-02-21T12:55:05Z-
dc.date.available2018-02-21T12:55:05Z-
dc.date.issued2018-02-
dc.identifier.citationLoss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency. 2018, 14 (2):e1006858 PLoS Pathog.en
dc.identifier.issn1553-7374-
dc.identifier.pmid29390040-
dc.identifier.doi10.1371/journal.ppat.1006858-
dc.identifier.urihttp://hdl.handle.net/10033/621291-
dc.description.abstractGastrointestinal infections caused by enteric yersiniae can become persistent and complicated by relapsing enteritis and severe autoimmune disorders. To establish a persistent infection, the bacteria have to cope with hostile surroundings when they transmigrate through the intestinal epithelium and colonize underlying gut-associated lymphatic tissues. How the bacteria gain a foothold in the face of host immune responses is poorly understood. Here, we show that the CNFY toxin, which enhances translocation of the antiphagocytic Yop effectors, induces inflammatory responses. This results in extensive tissue destruction, alteration of the intestinal microbiota and bacterial clearance. Suppression of CNFY function, however, increases interferon-γ-mediated responses, comprising non-inflammatory antimicrobial activities and tolerogenesis. This process is accompanied by a preterm reprogramming of the pathogen's transcriptional response towards persistence, which gives the bacteria a fitness edge against host responses and facilitates establishment of a commensal-type life style.en
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleLoss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency.en
dc.typeArticleen
dc.contributor.departmentHelmholtz-Zentrum für Infektionsforschung GmbH, Inhoffenstr. 7, 38124 Braunschweig, Germany.en
dc.identifier.journalPLoS pathogensen
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