Open AccessContact with enterocyte‐like Caco‐2 cells induces rapid upregulation of toxin production by Clostridium perfringens type C isolates
Author(s) -
Vidal Jorge E.,
Ohtani Kaori,
Shimizu Tohru,
McClane Bruce A.
Publication year - 2009
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2009.01332.x
Subject(s) - clostridium perfringens , toxin , enterocyte , microbiology and biotechnology , biology , downregulation and upregulation , quorum sensing , in vivo , enteritis , in vitro , caco 2 , virulence , gene , bacteria , small intestine , biochemistry , genetics
Summary Clostridium perfringens type C isolates cause necrotizing enteritis in humans and domestic animals. In vitro , type C isolates often produce β toxin (CPB), β2 toxin (CPB2), α toxin (CPA), perfringolysin O (PFO) and TpeL during (or after) late log‐phase growth. In contrast, the current study found that many type C isolates respond to close contact with enterocyte‐like Caco‐2 cells by producing all toxins, except TpeL, much more rapidly than occurs during in vitro growth. This in vivo effect involves rapid transcriptional upregulation of the cpb , cpb 2, pfo A and plc toxin genes. Rapid Caco‐2 cell‐induced upregulation of CPB and PFO production involves the VirS/VirR two‐component system, since upregulated in vivo transcription of the pfo A and cpb genes was blocked by inactivating the vir R gene and was reversible by complementation to restore VirR expression. However, the lux S quorum‐sensing system is not required for the rapid upregulation of type C toxin production induced by contact with Caco‐2 cells. These results provide the first indication of host cell:pathogen cross‐talk affecting toxin production kinetics by any pathogenic Clostridium spp., identify in vivo versus in vitro differences in C. perfringens toxin expression, and implicate VirS/VirR as a possible contributor to some C. perfringens enteric diseases.