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Infection and Immunity, February 2004, p. 988-995, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.988-995.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Enhanced Replication of Leishmania amazonensis Amastigotes in Gamma Interferon-Stimulated Murine Macrophages: Implications for the Pathogenesis of Cutaneous Leishmaniasis

Hai Qi,1 Jiaxiang Ji,2 Nanchaya Wanasen,2 and Lynn Soong1,2*

Department of Pathology,1 Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, Texas 775552

Received 19 May 2003/ Returned for modification 26 July 2003/ Accepted 11 November 2003

During Leishmania major infection in mice, gamma interferon (IFN-{gamma}) plays an essential role in controlling parasite growth and disease progression. In studies designed to ascertain the role of IFN-{gamma} in Leishmania amazonensis infection, we were surprised to find that IFN-{gamma} could promote L. amazonensis amastigote replication in macrophages (M{Phi}s), although it activated M{Phi}s to kill promastigotes. The replication-promoting effect of IFN-{gamma} on amastigotes was independent of the source and genetic background of M{Phi}s, was apparently not affected by surface opsonization of amastigotes, was not mediated by interleukin-10 or transforming growth factor ß, and was observed at different temperatures. Consistent with the different fates of promastigotes and amastigotes in IFN-{gamma}-stimulated M{Phi}s, L. amazonensis-specific Th1 transfer helped recipient mice control L. amazonensis infection established by promastigotes but not L. amazonensis infection established by amastigotes. On the other hand, IFN-{gamma} could stimulate M{Phi}s to limit amastigote replication when it was coupled with lipopolysaccharides but not when it was coupled with tumor necrosis factor alpha. Thus, IFN-{gamma} may play a bidirectional role at the level of parasite-M{Phi} interactions; when it is optimally coupled with other factors, it has a protective effect against infection, and in the absence of such synergy it promotes amastigote growth. These results reveal a quite unexpected aspect of the L. amazonensis parasite and have important implications for understanding the pathogenesis of the disease and for developing vaccines and immunotherapies.

* Corresponding author. Mailing address: 301 University Blvd., Medical Research Building 3.132, Galveston, TX 77555-1070. Phone: (409) 772-8149. Fax: (409) 747-6869. E-mail: lysoong{at}utmb.edu.

Editor: W. A. Petri, Jr.

Infection and Immunity, February 2004, p. 988-995, Vol. 72, No. 2
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.2.988-995.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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