Cytolethal distending toxin upregulates RANKL expression in Jurkat T-cells

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Belibasakis GN, Brage M, Lagergård T, Johansson A. Cytolethal distending toxin upregulates RANKL expression in Jurkat T-cells. APMIS 2008;116:499–506.

Cytolethal distending toxin, a bacterial exotoxin produced by a number of Gram-negative species, causes growth arrest and morphological alterations in host cells. Among these species are Haemophilus ducreyi, the etiological agent of chancroid, and the periodontal pathogen Aggregatibacter actinomycetemcomitans, highly implicated in localized aggressive periodontitis. CDT induces receptor activator of NF-χB ligand (RANKL) expression in periodontal fibroblasts, the key bone-resorbing cytokine. T-cells are actively involved in localized inflammation-induced bone destruction, including periodontitis. The aim of this study was to investigate the effects of purified CDT on the expression of RANKL and its decoy receptor osteoprotegerin (OPG), in the Jurkat T-cell line. Quantitative real-time PCR indicated that 100 pg/ml of purified H. ducreyi CDT upregulated RANKL mRNA expression by 2.2-fold, after 24 h of exposure. This increase was corroborated by a 2.0-fold increase in RANKL protein release, as determined by ELISA. OPG was not detected in this experimental system. In conclusion, CDT enhances RANKL expression in T-cells, denoting that these cells are a potential target for the toxin and strengthening the potential link between this virulence factor and mechanisms associated with localized bone resorption.

Keywords: Aggregatibacter actinomycetemcomitans; RANKL; T-cells; cytolethal distending toxin; periodontitis

Document Type: Research Article


Affiliations: 1: Department of Microbiology and Immunology, Institute of Biomedicine, Göteborg University, Göteborg 2: Division of Periodontology, Institute of Odontology, Umeå University, Umeå, Sweden

Publication date: June 1, 2008

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