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. 1995 Apr;63(4):1286-90.
doi: 10.1128/iai.63.4.1286-1290.1995.

Phospholipid composition of Pneumocystis carinii carinii and effects of methylprednisolone immunosuppression on rat lung lipids

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Phospholipid composition of Pneumocystis carinii carinii and effects of methylprednisolone immunosuppression on rat lung lipids

Z Guo et al. Infect Immun. 1995 Apr.

Abstract

The phospholipid class composition of Pneumocystis carinii carinii freshly isolated from infected lungs generally resembled that of the host lung, suggesting that the parasite scavenges lung alveolar lipids. However, subtle quantitative differences were demonstrated, indicating that the pathogen has the metabolic capacity to de novo synthesize, or at least tailor, its lipids. The concentration of phosphatidylcholine, the major lung surfactant lipid, in the organism was lower than that in lungs of normal and immunosuppressed uninfected rats, and the concentration of phosphatidylinositol was higher. Phosphonolipids were not detected in the organism by chemical analysis and nuclear magnetic resonance spectrometry. The immunosuppressive regimen alone caused increases in both surfactant protein A and the lipid content of the whole lung. The lungs of rats that were subjected to corticosteroid immunosuppression and had heavy parasite loads had dramatically elevated surfactant protein A levels, whereas the lipid contents of these lungs were not different from lipid contents in whole lungs of immunosuppressed uninfected rats. P. carinii was found to concentrate lipids, indicating that a large amount of the lipids in the whole infected rat lung was within the parasites residing in the organ. These observations have important implications relevant to the use of corticosteroid therapy for P. carinii pneumonitis.

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