Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl

PL EN


Preferences help
enabled [disable] Abstract
Number of results
2005 | 53 | 3 | 234-244

Article title

Cellular responses to attaching and effacing bacteria: activation and implication of the innate immune system

Title variants

Languages of publication

EN

Abstracts

EN
During the last decade, research on attaching-effacing (A/E) bacteria/host cell interactions has revealed much of the molecular basis of colonization and lesion formation. The colonic mucosa represents the first line of defense against these pathogens, and its integrity is required to avoid translocation of bacteria or bacterial soluble factors into the infected host. Therefore, the cellular immune response to A/E pathogens plays an important role in bacterial pathogenesis since it can clear the bacteria or modulate the inflammatory processes. Data obtained from infected patients demonstrate a correlation between the production of pro-inflammatory cytokines and the severity of the disease. In vitro studies of infected epithelial cells have clearly elucidated A/E bacteria-induced host signal transduction events. However, the identification of the bacterial factors responsible for cellular activation remains a subject of controversy. Experimental studies with knock-out mice infected with Citrobacter rodentium, a rodent A/E pathogen, indicate that innate immunity is an essential component of pathogenesis. This review summarizes in vivo and in vitro evidence for the induction and potential role of the innate immune system during infection with A/E bacteria.

Contributors

author
author
author

References

Document Type

REVIEW

Publication order reference

Alain P. Gobert, Unite de Microbiologie, Institut National de la Recherche Agronomique, Centre de Theix, 63122 Saint-Gencs-Champanelle, France

Identifiers

YADDA identifier

bwmeta1.element.element-from-psjc-24e48bc8-41e6-3297-a742-f96257bcf661
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.