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Microbiology (2002), 148, 2753-2763.
© 2002 Society for General Microbiology

Research Paper

Activation of the transcription factor NF-{kappa}B by Campylobacter jejuni

Kenneth H. Mellits1, Joseph Mullen1, Matthew Wand1, Gisèle Armbruster1, Amit Patel1, Phillippa L. Connerton1, Maeve Skelly2 and Ian F. Connerton1

Division of Food Sciences, School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough LE12 5RD, UK1
Division of Gastroenterology, University Hospital Nottingham, Queen’s Medical Centre, Nottingham NG7 2UH, UK2

Author for correspondence: Kenneth H. Mellits. Tel: +44 115 95 16161. Fax: +44 115 95 16162. e-mail: ken.mellits{at}nottingham.ac.uk

Campylobacter jejuni is a food-borne pathogen responsible for infectious enterocolitis. The early-response transcription factor NF-{kappa}B triggers the expression of genes associated with cellular immune and inflammatory responses. Co-incubation of HeLa cells with viable C. jejuni leads to the activation of the transcription factor NF-{kappa}B as determined by specific induction of a cellular luciferase-based reporter. Boiled cell-free extracts of C. jejuni are also potent dose-dependent stimulators of NF-{kappa}B-dependent transcription, the levels of which can reach up to 1000-fold as compared with independent controls. Using both cultured HeLa cells and human colonic epithelial (HCA-7) cells, the activation of NF-{kappa}B by C. jejuni boiled extract has been monitored through the degradation of IKB{alpha} and DNA binding of the nuclear translocated p50/p65 heterodimer of NF-{kappa}B. These events are co-ordinated with elaboration of the pro-inflammatory cytokine interleukin-8. Fractionation of the boiled C. jejuni extract suggests that the majority of the bioactive component has a molecular mass of 3 kDa or less, which is insensitive to proteinase K treatment.

Keywords: transcription, innate immunity, interleukin-8, inflammation, food safety

Abbreviations: BCE, boiled-cell extract; EMS, electrophoretic mobility shift; IL, interleukin; LOS, lipo-oligosaccharide; TNF-{alpha}; tumour necrosis factor-{alpha}




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