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Infection and Immunity, November 2005, p. 7281-7289, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7281-7289.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Intestinal Innate Immunity to Campylobacter jejuni Results in Induction of Bactericidal Human Beta-Defensins 2 and 3

Matthias Zilbauer,1 Nick Dorrell,2* Parjeet K. Boughan,1 Andrew Harris,3 Brendan W. Wren,2 Nigel J. Klein,1 and Mona Bajaj-Elliott1*

Department of Infectious Diseases and Microbiology, Institute of Child Health, London,1 Department of Infections and Tropical Diseases, London School of Hygiene and Tropical Medicine, London,2 MRC Molecular Pathogenesis Centre for Infectious Disease, Institute for Cell and Molecular Science, Barts' and the London, Queen Mary's School of Medicine and Dentistry, London, United Kingdom3

Received 8 March 2005/ Returned for modification 26 April 2005/ Accepted 8 July 2005

Campylobacter jejuni is the most prevalent cause of bacterial diarrhea worldwide. Despite the serious health problems caused by this bacterium, human innate immune responses to C. jejuni infection remain poorly defined. Human ß-defensins, a family of epithelial antimicrobial peptides, are a major component of host innate defense at the gastrointestinal mucosal surface. In this study, the effect of two different C. jejuni wild-type strains on human intestinal epithelial innate responses was investigated. Up-regulation of ß-defensin gene and peptide expression during infection was observed and recombinant ß-defensins were shown to have a direct bactericidal effect against C. jejuni through disruption of cell wall integrity. Further studies using an isogenic capsule-deficient mutant showed that, surprisingly, the absence of the bacterial polysaccharide capsule did not change the innate immune responses induced by C. jejuni or the ability of C. jejuni to survive exposure to recombinant ß-defensins. This study suggests a major role for this family of antimicrobial peptides in the innate immune defense against this human pathogen.

* Corresponding author. Mailing address for Mona Bajaj-Elliott: Department of Infectious Diseases and Microbiology, Institute of Child Health, London WC1N 1EH, United Kingdom. Phone: 44-20-7907-2215. Fax: 44-20-7813-8494. E-mail: m.bajaj-elliott{at}ich.ucl.ac.uk. Mailing address for Nick Dorrell: Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London WC1E 7HT, United Kingdom. Phone: 44-20-7927-2838. Fax: 44-20-7637-4314. E-mail: nick.dorrell{at}lshtm.ac.uk.

Editor: V. J. DiRita

Infection and Immunity, November 2005, p. 7281-7289, Vol. 73, No. 11
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.11.7281-7289.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Friis, L. M., Keelan, M., Taylor, D. E. (2009). Campylobacter jejuni Drives MyD88-Independent Interleukin-6 Secretion via Toll-Like Receptor 2. Infect. Immun. 77: 1553-1560 [Abstract] [Full Text]  
  • Llobet, E., Tomas, J. M., Bengoechea, J. A (2008). Capsule polysaccharide is a bacterial decoy for antimicrobial peptides. Microbiology 154: 3877-3886 [Abstract] [Full Text]  
  • Boughan, P. K., Argent, R. H., Body-Malapel, M., Park, J.-H., Ewings, K. E., Bowie, A. G., Ong, S. J., Cook, S. J., Sorensen, O. E., Manzo, B. A., Inohara, N., Klein, N. J., Nunez, G., Atherton, J. C., Bajaj-Elliott, M. (2006). Nucleotide-binding Oligomerization Domain-1 and Epidermal Growth Factor Receptor: CRITICAL REGULATORS OF beta-DEFENSINS DURING HELICOBACTER PYLORI INFECTION. J. Biol. Chem. 281: 11637-11648 [Abstract] [Full Text]  


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