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Infection and Immunity, October 2002, p. 5562-5567, Vol. 70, No. 10
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.10.5562-5567.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Cytokine Profiles of Patients Infected with Mycobacterium ulcerans and Unaffected Household Contacts

Travis M. Gooding,1,2 Paul D. R. Johnson,3 May Smith,4 Andrew S. Kemp,2,5,6 and Roy M. Robins-Browne1,2*

Departments of Microbiology and Immunology,1 Paediatrics, University of Melbourne, Melbourne,5 Murdoch Children's Research Institute,2 Department of Immunology, Royal Children's Hospital, Parkville,6 Department of Infectious Diseases, Austin and Repatriation Medical Centre, Heidelberg Victoria,3 Mossman Hospital, Mossman, Queensland, Australia4

Received 18 March 2002/ Returned for modification 15 May 2002/ Accepted 28 June 2002

Mycobacterium ulcerans, the cause of Buruli ulcer, is an environmental mycobacterium with a distinct geographic distribution. The reasons why only some individuals who are exposed to M. ulcerans develop ulcers are not known but are likely to reflect individual differences in the immune response to infections with this bacterium. In this study, we investigated cytokine profiles of peripheral blood mononuclear cells (PBMC) from 23 Buruli ulcer patients and 25 household contacts in a region of Australia where Buruli ulcer is endemic. The results showed that following stimulation with M. ulcerans or Mycobacterium bovis BCG, PBMC from Buruli ulcer patients mounted a Th2-type response, which was manifested by the production of mRNA for interleukin 4 (IL-4), IL-5, IL-6, and IL-10, whereas unaffected contacts responded mainly with the Th1 cytokines gamma interferon (IFN-{gamma}) and IL-12. For example, mRNA for IL-4 was detected in 18 of 23 patients but in only 3 of 25 control subjects (P < 0.0001). By contrast, PBMC from 21 of 25 unaffected individuals produced IFN-{gamma} compared with 3 of 23 patients (P < 0.0001). IFN-{gamma} release following stimulation with mycobacteria was markedly reduced in affected subjects. Frequencies of antibodies to M. ulcerans in serum samples from affected and unaffected subjects were similar, indicating that many of the control subjects had been exposed to this bacterium. Together, these findings suggest that a Th1-type immune response to M. ulcerans may prevent the development of Buruli ulcer in people exposed to M. ulcerans, but a Th-2 response does not.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria 3010, Australia. Phone: 61 3 8344 8275. Fax: 61 3 8344 8276. E-mail: r.browne{at}unimelb.edu.au.

Editor: S. H. E. Kaufmann

Infection and Immunity, October 2002, p. 5562-5567, Vol. 70, No. 10
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.10.5562-5567.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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