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The ability of disease and non-disease producing strains of Clostridium perfringens from chickens to adhere to extracellular matrix molecules and Caco-2 cells
Authors:Thomas G. Martin  Joan A. Smyth
Affiliation:1. Animal Biosciences and Biotechnology Laboratory, Beltsville Agricultural Research Center, USDA, ARS, Beltsville, MD 20705, USA;2. Department of Animal Science and Technology, Chung-Ang University, Anseong 456-756, South Korea;3. National Academy of Agricultural Science, Rural Development Administration, Wanju, Jeollabuk-do 565-851, South Korea;4. Department of Pediatrics, University of Maryland School of Medicine, Baltimore, MD 21201, USA;5. InVivo ANH, Talhouët, 56250 St. Nolff, France
Abstract:Clostridium perfringens is a major enteric pathogen that is responsible for causing necrotic enteritis of poultry. The ability to adhere to the host’s intestinal epithelium and to extracellular matrix molecules (ECMM) in the gut, are strategies used by numerous bacterial enteropathogens, however, C. perfringens has received comparatively little attention in this respect. The present study investigated sixteen type A C. perfringens isolates from chickens, with varying disease producing ability with respect to necrotic enteritis in chickens, for their ability to adhere to nine different extracellular matrix molecules (ECMM) and to the intestinal epithelial cell line Caco-2. C. perfringens strains were able to bind to ECMMs and there was strain variation. Strains of C. perfringens that produced severe disease, were capable of binding to collagen type III, IV and V, fibrinogen, laminin and vitronectin at higher levels than less severe disease producing strains, suggesting that the ability to adhere to ECMMs might enhance virulence with respect to induction of necrotic enteritis. In addition, severe disease producing strains also bound better to collagen type III and IV and fibrinogen, than non-disease producing strains. The present study also showed that some strains of C. perfringens possessed the ability to adhere to Caco-2 cells; however no relationship was found between the ability to adhere to Caco-2 cells and disease producing ability.
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