Abstract
Colonization of the gut by Clostridium difficile requires the adhesion of the bacterium to host cells. A range of cell surface located factors have been linked to adhesion including the S‐layer protein LMW SLP and the related protein Cwp66. As well as these proteins, the S‐layer of C. difficile may contain many others. One such protein is Cwp2. Here, we demonstrate the production of a C. difficile strain 630 cwp2 knockout mutant and assess the effect on the bacterium. The mutant results in increased TcdA (toxin A) release and impaired cellular adherence in vitro. We also present the extended three domain structure of the ‘functional’ region of Cwp2, consisting of residues 29–318 at 1.9 Å, which is compared to that of LMW SLP and Cwp8. The adhesive properties of Cwp2 and LMW SLP, which are likely to be shared by Cwp8, are predicted to be mediated by the variable loop regions in domain 2.DatabasesStructural data are available in the PDB under the accession number 5NJL.
Highlights
Clostridium difficile is the primary causative agent of antibiotic associated diarrhoea
Cwp2 is constitutively expressed and found on the surface of C. difficile during normal growth [16,20]; it is found in the C. difficile 630 spore coat [17]
The presence of Cwp2 on the cell surface during normal growth does, suggest that it is required for some cellular process(s)
Summary
Clostridium difficile is the primary causative agent of antibiotic associated diarrhoea. The pathogenic strains of C. difficile produce two potent exotoxins, TcdA and TcdB ( known as Toxin A and Toxin B), which induce mucosal inflammation and diarrhoea [3,4] Another important factor that has been identified is the paracrystalline protein array on the surface of C. difficile cells known as an Slayer. The structure and adhesive properties of Cwp possess a ‘functional’ region One such protein is Cwp, the gene for which was first identified in 2001 as part of a cluster of S-layer-associated genes surrounding slpA [8,9]. The altered Slayer caused by the lack of Cwp in strain 167, may be negated by changes in other virulence-associated factors such as increased adhesion, increased toxin production or the presence of a glycosylation gene cluster [13]. The mutant showed an impaired ability to adhere to Caco-2 cells, indicating a potential role for Cwp as an adhesin
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