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Infection and Immunity, February 2004, p. 958-965, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.958-965.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Differential Production of Systemic and Intralesional Gamma Interferon and Interleukin-10 in Nodular and Ulcerative Forms of Buruli Disease

Ghislaine Prévot,1,2 Eliane Bourreau,1 Herve Pascalis,1,2 Roger Pradinaud,3 Audrey Tanghe,4 Kris Huygen,4* and Pascal Launois1,{dagger}

Immunologie des Leishmanies, Institut Pasteur de la Guyane,1 Institut d'Etudes Supérieures de la Guyane, Université Antilles-Guyane,2 Institut Guyanais de Dermatologie Tropicale, Centre Hospitalier Andrée Rosemon, Cayenne, French Guyana,3 Mycobacterial Immunology, Pasteur Institute of Brussels, Brussels, Belgium4

Received 7 July 2003/ Returned for modification 8 September 2003/ Accepted 14 November 2003

Buruli disease, caused by Mycobacterium ulcerans, is the third most important mycobacterial disease in humans besides tuberculosis and leprosy. We have compared systemic and intralesional cytokine production in patients presenting with a nodular form and a necrotizing, ulcerative form of the disease. Gamma interferon (IFN-{gamma}) levels in response to whole M. ulcerans and Mycobacterium bovis BCG bacilli and in response to purified Ag85 protein from BCG were lower in peripheral blood mononuclear cells (PBMC) cultures from Buruli disease patients than in PBMC from healthy purified protein derivative-positive contacts. Interleukin-4 (IL-4) and IL-13 content was below the detection threshold in these PBMC cultures. IFN-{gamma} production after stimulation with M. ulcerans was significantly lower (P < 0.05) in PBMC cultures from patients with ulcers than in those from patients with nodules. On the other hand, PBMC from Buruli disease patients produced significant levels of IL-10 in response to M. ulcerans (but not to M. bovis BCG) and production was highest in patients with the ulcerative form. Third, semiquantitative reverse transcription-PCR analysis demonstrated a similar difference in the local, intralesional cytokine profile for the two forms of the disease: high IFN-{gamma} but low IL-10 mRNA levels in nodular lesions and high IL-10 but low IFN-{gamma} mRNA levels in ulcerative lesions. Intralesional IL-4 and IL-13 mRNA levels were low and only detected in patients with the ulcerative form. Our results indicate, although they do not formally prove, that production of IL-10 rather than production of IL-4 or IL-13 by Th2-type T cells may be involved in the low M. ulcerans-specific IFN-{gamma} response in Buruli disease patients.

* Corresponding author. Mailing address: Mycobacterial Immunology, Pasteur Institute of Brussels, 642 Engelandstraat, B 1180 Brussels, Belgium. Phone: 32 2 373 33 70. Fax: 32 2 373 33 67. E-mail: khuygen{at}pasteur.be.

Editor: S. H. E. Kaufmann

{dagger} Present address: WHO-IRTC, Institut de Biochimie, Université de Lausanne, 1066 Epalinges, Switzerland.

Infection and Immunity, February 2004, p. 958-965, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.958-965.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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