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 Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Background   Campylobacter jejuni  causes acute disease characterized by severe diarrhea containing blood and leukocytes, fever, and abdominal cramping. Disease caused by  C. jejuni  is dependent on numerous bacterial and host factors.  C. jejuni  invasion of the intestinal epithelial cells is seen in both clinical samples and animal models indicating that host cell invasion is, in part, necessary for disease.  C. jejuni  utilizes a flagellar Type III Secretion System (T3SS) to deliver the  Campylobacter  invasion antigens (Cia) to host cells. The Cia proteins modulate host cell signaling leading to actin cytoskeleton rearrangement necessary for  C. jejuni  host cell invasion, and are required for the development of disease.    Results  This study was based on the hypothesis that the  C. jejuni  CiaD effector protein mediates Erk 1/2 dependent cytoskeleton rearrangement. We showed that CiaD was required for the maximal phosphorylation of Erk 1/2 by performing an immunoblot with a p-Erk 1/2 specific antibody and that Erk 1/2 participates in  C. jejuni  invasion of host cells by performing the gentamicin protection assay in the presence and absence of the PD98059 (a potent inhibitor of Erk 1/2 activation). CiaD was also found to be required for the maximal phosphorylation of cortactin S405 and S418, as judged by immunoblot analysis. The response of human INT 407 epithelial cells to infection with  C. jejuni  was evaluated by confocal microscopy and scanning electron microscopy to determine the extent of membrane ruffling. This analysis revealed that CiaD ,  Erk 1/2, and cortactin participate in  C. jejuni -induced membrane ruffling. Finally, cortactin and N-WASP were found to be involved in  C. jejuni  invasion of host cells using siRNA to N-WASP, and siRNA to cortactin, coupled with the gentamicin protection assay.    Conclusion  We conclude that CiaD is involved in the activation of Erk 1/2 and that activated Erk 1/2 facilitates  C. jejuni  invasion by phosphorylation of cortactin on serine 405 and 418. This is the first time that cortactin and N-WASP have been shown to be involved in  C. jejuni  invasion of host cells. These data also provide a mechanistic basis for the requirement of Erk 1/2 in  C. jejuni- mediated cytoskeletal rearrangement.

Serine phosphorylation of cortactin is required for maximal host cell invasion by Campylobacter jejuni