Abstract
BackgroundAcute gastroenteritis caused by the food-borne pathogen Campylobacter jejuni is associated with attachment of bacteria to the intestinal epithelium and subsequent invasion of epithelial cells. In C. jejuni, the periplasmic protein HtrA is required for efficient binding to epithelial cells. HtrA has both protease and chaperone activity, and is important for virulence of several bacterial pathogens.ResultsThe aim of this study was to determine the role of the dual activities of HtrA in host cell interaction of C. jejuni by comparing an htrA mutant lacking protease activity, but retaining chaperone activity, with a ΔhtrA mutant and the wild type strain. Binding of C. jejuni to both epithelial cells and macrophages was facilitated mainly by HtrA chaperone activity that may be involved in folding of outer membrane adhesins. In contrast, HtrA protease activity played only a minor role in interaction with host cells.ConclusionWe show that HtrA protease and chaperone activities contribute differently to C. jejuni's interaction with mammalian host cells, with the chaperone activity playing the major role in host cell binding.
Highlights
Acute gastroenteritis caused by the food-borne pathogen Campylobacter jejuni is associated with attachment of bacteria to the intestinal epithelium and subsequent invasion of epithelial cells
Once the bacteria have adhered to the host cells, C. jejuni needs HtrA protease activity for optimal internalization; the exact effect of the chaperone activity on internalization could not be assessed from these results, since no internalized ΔhtrA mutants could be recovered
The results show that the chaperone activity of HtrA plays a significant role in attachment of C. jejuni to host cells
Summary
Acute gastroenteritis caused by the food-borne pathogen Campylobacter jejuni is associated with attachment of bacteria to the intestinal epithelium and subsequent invasion of epithelial cells. Acute gastroenteritis caused by C. jejuni is characterized by watery or bloody diarrhea, abdominal pain, fever, and malaise. While these symptoms typically last 3 - 7 days, serious complications may follow such as the acute autoimmune disease Guillan Barré Syndrome, affecting the peripheral nervous system. The importance of epithelial cell invasion in disease has been demonstrated in infected humans and animals [3,4], and is emphasized by studies showing that C. jejuni mutants attenuated for virulence in animal models are less capable of invading intestinal epithelial cells in vitro [5,6]. Upon invasion by C. jejuni, human epithelial cells respond by secreting cytokines, such as IL-8, which stimulate recruitment of inflammatory cells [2], including macrophages and
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