Journal
JOURNAL OF INNATE IMMUNITY
Volume 4, Issue 2, Pages 149-158Publisher
KARGER
DOI: 10.1159/000332946
Keywords
Glucosylating toxin; Binary toxin; Clostridium difficile infection; Hypervirulence
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Funding
- NIH National Institutes of General Medical Sciences [R00GM092934]
- National Center of Research Resources [P20-RR021905]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR021905] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R00GM092934, P20GM103496] Funding Source: NIH RePORTER
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Clostridium difficile is a significant problem in hospital settings as the most common cause of nosocomial diarrhea worldwide. C. difficile infections (CDIs) are characterized by an acute intestinal inflammatory response with neutrophil infiltration. These symptoms are primarily caused by the glucosylating toxins, TcdA and TcdB. In the past decade, the frequency and severity of CDIs have increased markedly due to the emergence of so-called hypervirulent strains that overproduce cytotoxic glucosylating toxins relative to historical strains. In addition, these strains produce a third toxin, binary toxin or C. difficile transferase (CDT), that may contribute to hypervirulence. Both the glucosylating toxins and CDT covalently modify target cell proteins to cause disassembly of the actin cytoskeleton and induce severe inflammation. This review summarizes our current knowledge of the mechanisms by which glucosylating toxins and CDT disrupt target cell function, alter host physiology and stimulate immune responses. Copyright (C) 2012 S. Karger AG, Basel
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