Workgroup Campylobacter and Tularemia
Institute of Bacterial Infections and Zoonoses
Research Areas / Projects Campylobacter
- Investigations of host-pathogen interactions by Campylobacter to identificate the virulence mechanisms of enteric Campylobacter infection
- Mechanisms of colonization and adhesion on chicken intestinal epithelial cells by Campylobacter jejuni (Project description see below)
Mechanisms of colonization and adhesion on chicken intestinal epithelial cells by Campylobacter (C.) jejuni
Project duration: 01/2010 – 12/2011
The main source of human campylobacteriosis is assumed to be the consumption or handling of contaminated poultry meat products. Poultry such as chicken are frequently highly colonized with Campylobacter in an asymptomatic, commensal association. The reason for this pathological difference, whereby Campylobacter (C.). jejuni is pathogenic to humans but exists as commensal in chickens, is still unknown. Cell adherence and invasion are essential for the pathogenesis of human Campylobacter diarrhoea. The mechanisms by which Campylobacter adhere to the epithelium of the human intestine or asymptomatically colonize the avian gut are not well defined. Moreover, little is known about the host cell surface receptors that may be involved in the initial adherence of Campylobacter.
The focus of this work will be the investigation of differences in C. jejuni colonization/adhesion when grown in conditions which model human or chicken intestinal tract environments, reflecting pathogenic and non-pathogenic situations, respectively. Based on a recently in our laboratory established chicken intestinal epithelial cell line we will identify factors that account for the divergent disease outcome following Campylobacter infection to better understand why Campylobacter colonizes the avian gut asymptomatically but causes enteric disease in humans. A better insight into host factors will allow a more complete understanding of the interaction between Campylobacter and the host and, eventually, may lead to improved strategies for controlling this zoonotic disease. We hypothesize that different mechanisms exist for binding to intestinal cell membranes from humans and chicken, thereby inducing differences in signal transduction of the respective eukaryotic cell.