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Infection and Immunity, June 2001, p. 3605-3610, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3605-3610.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Differential Induction of Gamma Interferon in Legionella pneumophila- Infected Macrophages from BALB/c and A/J Mice

Sheldon Salins, Catherine Newton,* Ray Widen, Thomas W. Klein, and Herman Friedman

Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa, Florida 33612

Received 9 August 2000/Returned for modification 22 November 2000/Accepted 6 March 2001

Gamma interferon (IFN-gamma ), a pleiotropic cytokine, is now known to be produced by macrophages as well as by NK cells, gamma delta cells, and activated T cells. The autocrine biological functions of IFN-gamma on the macrophage include the upregulation of major histocompatibility complex MHC class II and the activation to an antiviral state. In this study, the production of IFN-gamma by macrophages was demonstrated to correspond to antibacterial activity. Legionella pneumophila replicates intracellularly in thioglycolate (TG)-elicited macrophages (TG-macrophages) from A/J mice, while TG-macrophages from BALB/c mice restrict bacterial growth after an initial period of growth. BALB/c TG-macrophages were shown to express IFN-gamma mRNA at 24 and 28 h, which corresponded to the initiation of anti-L. pneumophila activity. Moreover, IFN-gamma neutralization by antibody treatment of the cultures resulted in increased L. pneumophila growth in the macrophages. In contrast, no IFN-gamma mRNA was expressed in TG-macrophages from A/J mice, where L. pneumophila grew unrestricted. As would be expected, IFN-gamma treatment decreased bacterial growth. An IFN-gamma -mediated antibacterial activity was, however, inducible in A/J macrophages by the addition of interleukin-12 following L. pneumophila infection. Thus, autocrine IFN-gamma is involved in anti-L. pneumophila activity associated with different growth patterns and appears to be important during intracellular infection.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, University of South Florida, 12901 Bruce B. Downs Blvd., Tampa, FL 33612. Phone: (813) 974-4017. Fax: (813) 974-4151. E-mail: cnewton{at}hsc.usf.edu.

Infection and Immunity, June 2001, p. 3605-3610, Vol. 69, No. 6
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.6.3605-3610.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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