Cell Biology of Human Host Cell Entry by Campylobacter jejuni

• Published in: Campylobacter pp. 297 - 313
• Main Authors: Kopecko, Dennis J, Hu, Lan
• Format: Book Chapter
• Language: English
• Published: Washington, DC, USA ASM Press 2008; American Society for Microbiology (ASM)
• Edition: 3rd Edition
• Subjects: Bacterial Pathogenesis; Biochemistry, Biology & Biotechnology; Biology & Microbiology; Campylobacter jejuni; cell biology; Food Safety & Quality; Food Science; host damage; human host cell entry; intestinal epithelial cells
• ISBN: 9781555814373; 1555814379
• DOI: 10.1128/9781555815554.ch17

This chapter presents an overview of the interaction of Campylobacter jejuni with intestinal host cells and focuses on bacterial adherence and invasion into the intestinal epithelium, transcytosis across the epithelial mucosa, and ensuing damage to host cells. Campylobacter invasion into the epithelial mucosa appears to be an essential process leading to colitis. Although many researchers would agree with this general summary of Campylobacter invasion events, there still remains considerable confusion regarding how Campylobacter enter and cross the intestinal mucosa. In fact, researchers concluded, after treating T‐84 cells with EGTA, that CadF‐dependent invasion of epithelial cells occurs preferentially at the basolateral surface, which normally interacts with fibronectin. In the above study, the number of internalized C. jejuni F38011 increased approximately threefold after EGTA treatment and was then reduced ~80% by treating with anti‐fibronectin antibody. A common theme among pathogenic invasive microorganisms is their ability to usurp the eukaryotic cell signaling systems both to allow for invasion and to trigger disease pathogenesis. The current data on signal transduction events involved in C. jejuni invasion suggest that host cell “invasion receptors” reside in filipin III‐sensitive membrane microdomains (i.e., lipid rafts). Clinical infections, experimental infections in humans and animals, and in vitro analyses in cultured human cells have now clearly demonstrated that cell adherence and invasiveness are necessary steps in Campylobacter‐induced inflammatory diarrhea. Much progress has been made in the past 10 years in the understanding of the cell biology of these events.