Campylobacter-host cell interactions.

K G Wooldridge; J M Ketley

doi:10.1016/s0966-842x(97)01004-4

Home/Archive/PubMed

PubMed · 9080607

Campylobacter-host cell interactions.

K G Wooldridge·J M Ketley

View original source ↗Export metadata ↓

Abstract

The enteric pathogens Campylobacter jejuni and Campylobacter coli are a major cause of infectious diarrhoea. Their ability to adhere to human epithelial cells is ubiquitous and their propensity to invade cells is also well documented and requires motility and de novo protein synthesis, as well as several host factors. The molecular basis of the interaction between campylobacters and host cells is only beginning to be elucidate. The characteristics of this interaction promise to be interesting and may provide new insights into host-pathogen interactions in other enteric diseases.

Explore related subjects

Campylobacter Infections Campylobacter coli Campylobacter jejuni Cell Line Epithelial Cells Humans Macrophages Monocytes Neutrophils Journal Article Research Support, Non-U.S. Gov't Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

K G Wooldridge, J M Ketley. 1997. Campylobacter-host cell interactions.. https://doi.org/10.1016/s0966-842x(97)01004-4

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1998

Campylobacter enteritis: it could happen to you!

Explore the source record for details and available documents.

Campylobacter Infections↗

PubMed1998

Determining the burden of human illness from food borne diseases. CDC's emerging infectious disease program Food Borne Diseases Active Surveillance Network (FoodNet).

Food borne diseases cause a significant burden of illness in the United States. The Food Borne Diseases Active Surveillance Network (FoodNet), established in 1995, continues to monitor the burden and causes of food borne diseases and provide much of the data to address this public health problem.

Campylobacter Infections↗

PubMed1998

HLA and T-cell receptor gene polymorphisms in Guillain-Barré syndrome.

OBJECTIVE: We examined a possible involvement of genetic factors influencing the development of Guillain-Barré syndrome (GBS). METHODS: We studied T-cell receptor (TCR), alpha-chain constant (AC), and beta-chain variable (BV) gene polymorphisms using microsatellite markers and serologic HLA class I antigens, HLA-DRB1, and HLA-DQB1 alleles in 81 Japanese patients with GBS and 87 controls. RESULTS: There were no significant differences in these genetic markers between GBS patients and controls. Subgrouping of GBS patients according to recent Campylobacter jejuni infection, the presence of anti-GM1 antibody in the sera, or their combinations also failed to reveal significant associations with these genetic markers. There was, however, a tendency for an increased frequency of HLA-DRB1*0803 in the C. jejuni + GM1 + GBS group, when compared with controls. CONCLUSIONS: The data suggest that the roles of TCRAC, T-cell receptor beta-chain variable (TCRBV), HLA class I or class II in the development of GBS are not critical, and further research is necessary to clarify other genes encoded within the HLA region for genetic susceptibility to GBS.

Campylobacter Infections↗