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Sialidases affect the host cell adherence and epsilon toxin-induced cytotoxicity of Clostridium perfringens type D strain CN3718

Li, J and Sayeed, S and Robertson, S and Chen, J and McClane, BA (2011) Sialidases affect the host cell adherence and epsilon toxin-induced cytotoxicity of Clostridium perfringens type D strain CN3718. PLoS Pathogens, 7 (12). ISSN 1553-7366

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Clostridium perfringens type B or D isolates, which cause enterotoxemias or enteritis in livestock, produce epsilon toxin (ETX). ETX is exceptionally potent, earning it a listing as a CDC class B select toxin. Most C. perfringens strains also express up to three different sialidases, although the possible contributions of those enzymes to type B or D pathogenesis remain unclear. Type D isolate CN3718 was found to carry two genes (nanI and nanJ) encoding secreted sialidases and one gene (nanH) encoding a cytoplasmic sialidase. Construction in CN3718 of single nanI, nanJ and nanH null mutants, as well as a nanI/nanJ double null mutant and a triple sialidase null mutant, identified NanI as the major secreted sialidase of this strain. Pretreating MDCK cells with NanI sialidase, or with culture supernatants of BMC206 (an isogenic CN3718 etx null mutant that still produces sialidases) enhanced the subsequent binding and cytotoxic effects of purified ETX. Complementation of BMC207 (an etx/nanH/nanI/nanJ null mutant) showed this effect is mainly attributable to NanI production. Contact between BMC206 and certain mammalian cells (e.g., enterocyte-like Caco-2 cells) resulted in more rapid sialidase production and this effect involved increased transcription of BMC206 nanI gene. BMC206 was shown to adhere to some (e.g. Caco-2 cells), but not all mammalian cells, and this effect was dependent upon sialidase, particularly NanI, expression. Finally, the sialidase activity of NanI (but not NanJ or NanH) could be enhanced by trypsin. Collectively these in vitro findings suggest that, during type D disease originating in the intestines, trypsin may activate NanI, which (in turn) could contribute to intestinal colonization by C. perfringens type D isolates and also increase ETX action. © 2011 Li et al.


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Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Li, Jjihongli@pitt.eduJIHONGLI
Sayeed, Ssas69@pitt.eduSAS69
Robertson, S
Chen, Jjic40@pitt.eduJIC40
McClane, BAbamcc@pitt.eduBAMCC
ContributionContributors NameEmailPitt UsernameORCID
Date: 1 December 2011
Date Type: Publication
Journal or Publication Title: PLoS Pathogens
Volume: 7
Number: 12
DOI or Unique Handle: 10.1371/journal.ppat.1002429
Schools and Programs: School of Public Health > Environmental and Occupational Health
School of Medicine > Microbiology and Molecular Genetics
Refereed: Yes
ISSN: 1553-7366
MeSH Headings: Animals; Bacterial Toxins--genetics; Bacterial Toxins--metabolism; Blotting, Southern; Blotting, Western; Caco-2 Cells; Cell Adhesion; Clostridium Infections--genetics; Clostridium Infections--metabolism; Clostridium perfringens--genetics; Clostridium perfringens--metabolism; Enzyme Activation--genetics; Gene Knockout Techniques; Host-Parasite Interactions--physiology; Humans; Microscopy, Fluorescence; Neuraminidase--genetics; Neuraminidase--metabolism; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction; Trypsin--metabolism
Other ID: NLM PMC3234242
PubMed Central ID: PMC3234242
PubMed ID: 22174687
Date Deposited: 07 Sep 2012 19:42
Last Modified: 02 Feb 2019 16:58


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