English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Campylobacter jejuni  infections have a high prevalence worldwide and represent a significant socioeconomic burden.  C. jejuni  can cross the intestinal epithelial barrier as visualized in biopsies derived from human patients and animal models, however, the underlying molecular mechanisms and associated immunopathology are still not well understood. We have recently shown that the secreted serine protease HtrA (high temperature requirement A) plays a key role in  C. jejuni  cellular invasion and transmigration across polarized epithelial cells  in vitro . In the present  in vivo  study we investigated the role of HtrA during  C. jejuni  infection of mice. We used the gnotobiotic IL-10 −/−  mouse model to study campylobacteriosis following peroral infection with the  C. jejuni  wild-type (WT) strain NCTC11168 and the isogenic, non-polar NCTC11168Δ htrA  deletion mutant. Six days post infection (p.i.) with either strain mice harbored comparable intestinal  C. jejuni  loads, whereas ulcerative enterocolitis was less pronounced in mice infected with the Δ htrA  mutant strain. Moreover, Δ htrA  mutant infected mice displayed lower apoptotic cell numbers in the large intestinal mucosa, less colonic accumulation of neutrophils, macrophages and monocytes, lower large intestinal nitric oxide, IFN-γ, and IL-6 as well as lower TNF-α and IL-6 serum concentrations as compared to WT strain infected mice at day 6 p.i. Notably, immunopathological responses were not restricted to the intestinal tract given that liver and kidneys exhibited mild histopathological changes 6 days p.i. with either  C. jejuni  strain. We also found that hepatic and renal nitric oxide levels or renal TNF-α concentrations were lower in the Δ htrA  mutant as compared to WT strain infected mice. In conclusion, we show here that the  C. jejuni  HtrA protein plays a pivotal role in inducing host cell apoptosis and immunopathology during murine campylobacteriosis in the gut  in vivo .

frontiers in cellular and infection microbiology

The role of serine protease HtrA in acute ulcerative enterocolitis and extra-intestinal immune responses during Campylobacter jejuni infection of gnotobiotic IL-10 deficient mice