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Published ahead of print on February 13, 2003, doi:10.1164/rccm.200206-563OC
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American Journal of Respiratory and Critical Care Medicine Vol 167. pp. 1279-1282, (2003)
© 2003 American Thoracic Society

Histoplasmosis after Treatment with Anti–Tumor Necrosis Factor-{alpha} Therapy

Karen L. Wood, Chadi A. Hage, Kenneth S. Knox, Martin B. Kleiman, Aruna Sannuti, Richard B. Day, L. Joseph Wheat and Homer L. Twigg, III

Divisions of Pulmonary and Critical Care, and Infectious Disease, Department of Medicine and Department of Pediatrics, Infectious Disease, Indiana University School of Medicine, Indianapolis, Indiana

Correspondence and requests for reprints should be addressed to Homer L. Twigg III, M.D., 1001 West Tenth Street, OPW 425 Indianapolis, IN 46202. E-mail: htwig{at}iupui.edu

Anti–tumor necrosis factor-{alpha} (TNF-{alpha}) antibodies are frequently used to treat inflammatory diseases. However, these drugs also have immunosuppressive effects. We report on three patients who developed disseminated histoplasmosis on therapy with TNF-{alpha} inhibitors. In vitro assays were used to characterize the role of these agents in host defense against Histoplasma capsulatum. Intracellular proliferation of H. capsulatum was measured in alveolar macrophages and peripheral monocytes of normal volunteers in the presence and absence of the TNF-{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. The production of H. capsulatum–induced interferon-{gamma} and TNF-{alpha} 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–TNF-{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 • tumor necrosis factor-{alpha} • anti–tumor necrosis factor-{alpha} antibodies • interferon-{gamma}




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