Open AccessLoss of CNFY toxin-induced inflammation drives Yersinia pseudotuberculosis into persistency
Author(s) -
Wiebke Heine,
Michael Beckstette,
Ann Kathrin Heroven,
Sophie Thiemann,
Ulrike Heise,
Aaron M. Nuss,
Fabrizio Pisano,
Till Strowig,
Petra Dersch
Publication year - 2018
Publication title -
plos pathogens
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.719
H-Index - 206
eISSN - 1553-7374
pISSN - 1553-7366
DOI - 10.1371/journal.ppat.1006858
Subject(s) - yersinia pseudotuberculosis , biology , microbiology and biotechnology , immune system , yersinia , inflammation , yersinia enterocolitica , pathogen , immunology , intestinal epithelium , effector , yersinia infections , bacteria , lymphatic system , epithelium , virulence , enterobacteriaceae , escherichia coli , biochemistry , genetics , gene
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.