Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency

Heine W, Beckstette M, Heroven AK, Thiemann S, Heise U, Nuss AM, Pisano F, Strowig T, Dersch P (2018)
PLOS Pathogens 14(2): e1006858.

Zeitschriftenaufsatz | Veröffentlicht | Englisch
 
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Autor*in
Heine, Wiebke; Beckstette, MichaelUniBi; Heroven, Ann Kathrin; Thiemann, Sophie; Heise, Ulrike; Nuss, Aaron Mischa; Pisano, Fabio; Strowig, Till; Dersch, Petra
Abstract / Bemerkung
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.
Erscheinungsjahr
2018
Zeitschriftentitel
PLOS Pathogens
Band
14
Ausgabe
2
Art.-Nr.
e1006858
eISSN
1553-7374
Page URI
https://pub.uni-bielefeld.de/record/2953293

Zitieren

Heine W, Beckstette M, Heroven AK, et al. Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency. PLOS Pathogens. 2018;14(2): e1006858.
Heine, W., Beckstette, M., Heroven, A. K., Thiemann, S., Heise, U., Nuss, A. M., Pisano, F., et al. (2018). Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency. PLOS Pathogens, 14(2), e1006858. https://doi.org/10.1371/journal.ppat.1006858
Heine, W., Beckstette, M., Heroven, A. K., Thiemann, S., Heise, U., Nuss, A. M., Pisano, F., Strowig, T., and Dersch, P. (2018). Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency. PLOS Pathogens 14:e1006858.
Heine, W., et al., 2018. Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency. PLOS Pathogens, 14(2): e1006858.
W. Heine, et al., “Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency”, PLOS Pathogens, vol. 14, 2018, : e1006858.
Heine, W., Beckstette, M., Heroven, A.K., Thiemann, S., Heise, U., Nuss, A.M., Pisano, F., Strowig, T., Dersch, P.: Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency. PLOS Pathogens. 14, : e1006858 (2018).
Heine, Wiebke, Beckstette, Michael, Heroven, Ann Kathrin, Thiemann, Sophie, Heise, Ulrike, Nuss, Aaron Mischa, Pisano, Fabio, Strowig, Till, and Dersch, Petra. “Loss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency”. PLOS Pathogens 14.2 (2018): e1006858.

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