Evidence that the Agr-like quorum sensing system regulates the toxin production, cytotoxicity and pathogenicity of Clostridium perfringens type C isolate CN3685

• Type of Material: Article
• Authors: Jorge Vidal Graniel, Emory University; Menglin Ma, University of Pittsburgh; Julian Saputo, University of California, Davis; Jorge Garcia, University of California, Davis; Francisco A. Uzal, University of California, Davis; Bruce A. McClane, University of Pittsburgh
• Language: English
• Date: 2012-01-01
• Publisher: Wiley: 12 months
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2011 Blackwell Publishing Ltd.
• Final Published Version (URL): http://dx.doi.org/10.1111/j.1365-2958.2011.07925.x
• Title of Journal or Parent Work: Molecular Microbiology
• ISSN: 0950-382X
• Volume: 83
• Issue: 1
• Start Page: 179
• End Page: 194
• Grant/Funding Information: This research was generously supported by grant R01 AI-056177-08 from the National Institute of Allergy and Infectious Disease.
• Keywords: EXPRESSION; SPORULATION; Life Sciences & Biomedicine; BETA-TOXIN; BACTERIAL VIRULENCE; Science & Technology; GENE; LOCUS; MODEL; DETERMINANTS; Biochemistry & Molecular Biology; ESCHERICHIA-COLI; ALPHA-TOXIN; Microbiology
• Research Categories: Health Sciences, Public Health; Biology, Microbiology

Abstract

Clostridium perfringens possesses at least two functional quorum sensing (QS) systems, i.e. an Agr-like system and a LuxS-dependent AI-2 system. Both of those QS systems can reportedly control in vitro toxin production by C. perfringens but their importance for virulence has not been evaluated. Therefore, the current study assessed whether these QS systems might regulate the pathogenicity of CN3685, a C. perfringens type C strain. Since type C isolates cause both haemorrhagic necrotic enteritis and fatal enterotoxemias (where toxins produced in the intestines are absorbed into the circulation to target other internal organs), the ability of isogenic agrB or luxS mutants to cause necrotizing enteritis in rabbit small intestinal loops or enterotoxemic lethality in mice was evaluated. Results obtained strongly suggest that the Agr-like QS system, but not the LuxS-dependent AI-2 QS system, is required for CN3685 to cause haemorrhagic necrotizing enteritis, apparently because the Agr-like system regulates the production of beta toxin, which is essential for causing this pathology. The Agr-like system, but not the LuxS-mediated AI-2 system, was also important for CN3685 to cause fatal enterotoxemia. These results provide the first direct evidence supporting a role for any QS system in clostridial infections.