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Published ahead of print on February 13, 2003, doi:10.1164/rccm.200206-563OC

Am. J. Respir. Crit. Care Med., Volume 167, Number 9, May 2003, 1279-1282

A more recent version of this article appeared on May 1, 2003
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Submitted on July 10, 2002
Accepted on February 10, 2003

Histoplasmosis after Treatment with Anti-TNF-{alpha} Therapy

Karen L Wood1, Chadi A Hage2, Kenneth S Knox1, Martin B Kleiman3, Aruna Sannuti1, Richard B Day1, L. Joseph Wheat2, and Homer L Twigg1*

1 Medicine, Pulmonary Division, Indiana University School of Medicine, Indianapolis, IN, USA, 2 Medicine, Infectious Disease, Indiana University School of Medicine, Indianapolis, IN, USA, 3 Pediatrics, Infectious Disease, Indiana University School of Medicine, Indianapolis, IN, USA

* To whom correspondence should be addressed. E-mail: htwig{at}iupui.edu.

Anti-tumor necrosis factor-{alpha} antibodies are frequently used to treat inflammatory diseases. However, these drugs also have immunosuppressive effects. We report three patients who developed disseminated histoplasmosis on therapy with tumor necrosis factor-{alpha} inhibitors. In vitro assays were utilized to characterize the role of these agents in host defense against H. capsulatum. Intracellular proliferation of H. capsulatum was measured in alveolar macrophages and peripheral monocytes of normal volunteers in the presence and absence of the tumor necrosis factor-{alpha} antibody, infliximab. Both infliximab and control antibody enhanced fungal growth in monocytes and alveolar macrophages suggesting this was a nonspecific antibody response. Despite similar intracellular fungal loads in the presence of both antibodies, lymphocyte proliferation in response to blood monocytes and alveolar macrophages infected with H. capsulatum was inhibited by the addition of physiologic doses of infliximab whereas control antibody had no effect. H. capsulatum-induced interferon-{gamma} and tumor necrosis factor-{alpha} production was assessed in 5-day cultures containing lymphocytes and alveolar macrophages or monocytes. Interferon-{gamma} secretion was significantly reduced in the presence of infliximab. In summary, patients receiving anti-tumor necrosis factor-{alpha} therapy are at risk for developing disseminated histoplasmosis. This may be due to a defect in the TH1 arm of cellular immunity.
Key words: Histoplasmosis, TNF-alpha, anti-TNF-alpha antibodies, Interferon-gamma




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