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

There is increasing evidence that members of the gut microbiota, especially  Fusobacterium nucleatum  ( F. nucleatum ), are associated with Crohn’s disease (CD), but the specific mechanism by which  F. nucleatum  promotes CD development is unclear. Here, we first examined the abundance of  F. nucleatum  and its effects on CD disease activity and explored whether  F. nucleatum  aggravated intestinal inflammation and promoted intestinal mucosal barrier damage  in vitro  and  in vivo . Our data showed that  F. nucleatum  was enriched in 41.21% of CD tissues from patients and was correlated with the clinical course, clinical activity, and refractory behavior of CD  (P  < 0.05). In addition, we found that  F. nucleatum  infection is involved in activating the endoplasmic reticulum stress (ERS) pathway during CD development to promote intestinal mucosal barrier destruction. Mechanistically,  F. nucleatum  targeted caspase activation and recruitment domain 3 (CARD3) to activate the ERS pathway and promote  F. nucleatum -mediated mucosal barrier damage  in vivo  and  in vitro . Thus,  F. nucleatum  coordinates a molecular network involving CARD3 and ERS to control the CD process. Measuring and targeting  F. nucleatum  and its associated pathways will provide valuable insight into the prevention and treatment of CD.

Fusobacterium nucleatum Activates Endoplasmic Reticulum Stress to Promote Crohn’s Disease Development via the Upregulation of CARD3 Expression