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.
journal_name
PLoS Pathogjournal_title
PLoS pathogensauthors
Heine W,Beckstette M,Heroven AK,Thiemann S,Heise U,Nuss AM,Pisano F,Strowig T,Dersch Pdoi
10.1371/journal.ppat.1006858subject
Has Abstractpub_date
2018-02-01 00:00:00pages
e1006858issue
2eissn
1553-7366issn
1553-7374pii
PPATHOGENS-D-17-01330journal_volume
14pub_type
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