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• W2105289323 abstract "Over the past two decades, Pneumocystis carinii pneumonia has emerged as a major cause of mortality and morbidity in immunocompromised patients. Although P. carinii pneumonia predominantly affects patients with the acquired immunodeficiency syndrome (AIDS), individuals with hematologic and solid malignancies, organ transplantation, or those receiving intensive immunosuppression for inflammatory conditions also have enhanced risk for acquiring this infection (I). Despite apparently effective treatment regimens, the mortality of an individual episode of P. carinii pneumonia ranges between 15% and 40% (2). Even followingsuccessful treatment, P. carinii infection may relapse, making lifelong chemoprophylaxis necessary in chronically immunosuppressed patients. Recent investigations have begun to unravel the mechanisms of native host defense against P. carinii and the manner in which these systems are altered during various states of immunosuppression. Host response against Pneumocystis centers around CD4 T-lymphocytes, whose depletion or impairment is the prominent risk factor promoting infection in most patients (I). In addition to lymphocytic defense, recent work indicates that alveolar macrophages provide key functions mediating uptake and clearance of organisms from the lung (3-6). Upon challenge with P. carinii, alveolar macrophages bind and phagocytize P. carinii (3, 4). In addition, macrophages are stimulated by these organisms to release inflammatory substances including reactive oxidants, eicosanoid metabolites, and cytokines, most notably tumor necrosis factor a (TNFa) (4-7). In the current issue of the Journal, Kolls and colleagues provide evidence supporting a central role for TNFa in host defense against P. carinii (8). This report extends prior investigations implicating increased TNFa activity during this infection. Alveolar macrophages derived from AIDS patients with P. carinii pneumonia exhibit strongly enhanced TNFa release when maintained in tissue culture (9). Furthermore, alveolar macrophages challenged with P. carinii organisms both in vitro and in whole animal models respond" @default.
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• W2105289323 date "1997-02-01" @default.
• W2105289323 modified "2023-09-23" @default.
• W2105289323 title "Tumor necrosis factor alpha-mediated host defense against Pneumocystis carinii." @default.
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• W2105289323 doi "https://doi.org/10.1165/ajrcmb.16.2.9032116" @default.
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