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J Med Microbiol 37 (1992), 319-325; DOI: 10.1099/00222615-37-5-319
© 1992 Society for General Microbiology
ISSN 0022-2615
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Differentiated Caco-2 cells as a model for enteric invasion by Campylobacter jejuni and C. coli

P. H. Everest3, H. Goossens*, J.-P. Butzler*, D. Lloyd{dagger}, S. Knutton{dagger}, J. M. Ketley3 and P. H. Williams{dagger},*

3Department of Genetics, University of Leicester, Leicester LE1 7RH

*WHO Collaborating Centre for Enteric Campylobacter, Department of Microbiology, St Pieters University Hospital, B-1000 Brussels, Belgium

{dagger}Institute of Child Health, University of Birmingham, Birmingham B16 8ET

{ddagger}Correspondence should be sent to Dr P. H. Williams.

Received December 31, 1991
Accepted February 5, 1992

SUMMARY: A collection of 44 Campylobacter isolates (37 C. jejuni and seven C. coli) from children with colitis (21 strains) or watery diarrhoea (23 strains) was analysed for toxin production, association with HeLa cells, and invasion of differentiated Caco-2 cell cultures. There was no obvious association of clinical symptoms with species, biotype or enterotoxin production. All colitis strains and most of the isolates from watery diarrhoea were cytotoxic for Chinese hamster ovary cells. Measurements of bacterial association indices with HeLa cells varied with time, and were considered to be unreliable for discriminating between isolates from the two diagnostic groups. Statistically significant differences were observed between the two groups (all colitis strains and 65% of strains from non-inflammatory diarrhoea) with respect to invasion of both HeLa and Caco-2 cell monolayers. However, among the strains from non-inflammatory diarrhoea that did invade, numbers of internalised bacteria were similar to the range observed for colitis strains. Of the colitis strains, 86% were able to transcytose through polarised Caco-2 monolayers grown on filters, compared with 48% of isolates from non-inflammatory disease. We propose the use of Caco-2 cells as a model for studying invasion of intestinal epithelia by C. jejuni and C. coli.




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