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Clinical and Diagnostic Laboratory Immunology, May 2002, p. 727-730, Vol. 9, No. 3
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.3.727-730.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Infection with the Helminth Nippostrongylus brasiliensis Does Not Interfere with Efficient Elimination of Mycobacterium bovis BCG from the Lungs of Mice

Klaus J. Erb,^1* Claudia Trujillo,¹ Mike Fugate,¹ and Heidrun Moll²

Zentrum für Infektionsforschung,¹ Institut für Molekulare Infektionsbiologie, Universität Würzburg, 97070 Würzburg, Germany²

Received 25 July 2001/ Returned for modification 13 September 2001/ Accepted 5 March 2002

Infection with Mycobacterium tuberculosis continues to be one of the major global health threats. Strong mycobacterium-specific Th1 immune responses correlate with protection, and decreased Th1 responses correlate with disease progression. In contrast, the impact of Th2 responses on the development of protective immune responses to mycobacteria remains unclear. To analyze whether ongoing Th2 responses present in the lung influence the development of a protective Th1 immune response to mycobacteria, we coinfected mice with the helminth Nippostrongylus brasiliensis and Mycobacterium bovis BCG. We found that the T cells from the lymph nodes of coinfected mice secreted significantly less gamma interferon than did the T cells from mice infected with M. bovis BCG after in vitro stimulation with purified protein from M. tuberculosis when 10⁸ CFU of M. bovis BCG were used for the infection. This result indicates that the helminth infection reduced the Th1 immune response to the mycobacteria in the lung. However, mycobacterial clearance was not delayed in the coinfected animals. Importantly, the infection with BCG after the helminth infection did not reduce the helminth-induced Th2 response in the lung, ruling out the possibility that the lack of a reduction in bacterial clearance in the coinfected mice was due to a downmodulation of the helminth-induced Th2 response. Taken together, our results suggest that ongoing Th2 responses in the lung do not necessarily lead to increased susceptibility to mycobacterial infection.

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* Corresponding author. Mailing address: Zentrum für Infektionsforschung, Universität Würzburg, Röntgenring 11, 97070 Würzburg, Germany. Phone: (49) 931 31 2174/2133. Fax: (49) 931 31 2578. E-mail: klaus.erb{at}mail.uni-wuerzburg.de.

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Clinical and Diagnostic Laboratory Immunology, May 2002, p. 727-730, Vol. 9, No. 3
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.3.727-730.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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