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Loss of CNF(Y) toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency
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...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5811047/ https://www.ncbi.nlm.nih.gov/pubmed/29390040 http://dx.doi.org/10.1371/journal.ppat.1006858 |
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author | Heine, Wiebke Beckstette, Michael Heroven, Ann Kathrin Thiemann, Sophie Heise, Ulrike Nuss, Aaron Mischa Pisano, Fabio Strowig, Till Dersch, Petra |
author_facet | Heine, Wiebke Beckstette, Michael Heroven, Ann Kathrin Thiemann, Sophie Heise, Ulrike Nuss, Aaron Mischa Pisano, Fabio Strowig, Till Dersch, Petra |
author_sort | Heine, Wiebke |
collection | PubMed |
description | 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 CNF(Y) 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 CNF(Y) 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. |
format | Online Article Text |
id | pubmed-5811047 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-58110472018-02-28 Loss of CNF(Y) toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency Heine, Wiebke Beckstette, Michael Heroven, Ann Kathrin Thiemann, Sophie Heise, Ulrike Nuss, Aaron Mischa Pisano, Fabio Strowig, Till Dersch, Petra PLoS Pathog Research Article 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 CNF(Y) 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 CNF(Y) 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. Public Library of Science 2018-02-01 /pmc/articles/PMC5811047/ /pubmed/29390040 http://dx.doi.org/10.1371/journal.ppat.1006858 Text en © 2018 Heine et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Heine, Wiebke Beckstette, Michael Heroven, Ann Kathrin Thiemann, Sophie Heise, Ulrike Nuss, Aaron Mischa Pisano, Fabio Strowig, Till Dersch, Petra Loss of CNF(Y) toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency |
title | Loss of CNF(Y) toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency |
title_full | Loss of CNF(Y) toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency |
title_fullStr | Loss of CNF(Y) toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency |
title_full_unstemmed | Loss of CNF(Y) toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency |
title_short | Loss of CNF(Y) toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency |
title_sort | loss of cnf(y) toxin-induced inflammation drives yersinia pseudotuberculosis into persistency |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5811047/ https://www.ncbi.nlm.nih.gov/pubmed/29390040 http://dx.doi.org/10.1371/journal.ppat.1006858 |
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