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The Journal of Immunology, 2000, 164: 3755-3763.
Copyright © 2000 by The American Association of Immunologists

Isolated Pneumocystis carinii Cell Wall Glucan Provokes Lower Respiratory Tract Inflammatory Responses1

Robert Vassallo*, Joseph E. Standing* and Andrew H. Limper2,*,{dagger}

* Thoracic Diseases Research Unit, Division of Pulmonary, Critical Care and Internal Medicine, and {dagger} Department of Biochemistry and Molecular Biology, Mayo Clinic and Foundation, Rochester, MN 55905

Macrophage-induced lung inflammation contributes substantially to respiratory failure during Pneumocystis carinii pneumonia. We isolated a P. carinii cell wall fraction rich in glucan carbohydrate, which potently induces TNF-{alpha} and macrophage-inflammatory protein-2 generation from alveolar macrophages. Instillation of this purified P. carinii carbohydrate cell wall fraction into healthy rodents is accompanied by substantial increases in whole lung TNF-{alpha} generation and is associated with neutrophilic infiltration of the lungs. Digestion of the P. carinii cell wall isolate with zymolyase, a preparation containing predominantly ß-1,3 glucanase, substantially reduces the ability of this P. carinii cell wall fraction to activate alveolar macrophages, thus suggesting that ß-glucan components of the P. carinii cell wall largely mediate TNF-{alpha} release. Furthermore, the soluble carbohydrate ß-glucan receptor antagonists laminariheptaose and laminarin also substantially reduce the ability of the P. carinii cell wall isolate to stimulate macrophage-inflammatory activation. In contrast, soluble {alpha}-mannan, a preparation that antagonizes macrophage mannose receptors, had minimal effect on TNF-{alpha} release induced by the P. carinii cell wall fraction. P. carinii ß-glucan-induced TNF-{alpha} release from alveolar macrophages was also inhibited by both dexamethasone and pentoxifylline, two pharmacological agents with potential activity in controlling P. carinii-induced lung inflammation. These data demonstrate that P. carinii ß-glucan cell wall components can directly stimulate alveolar macrophages to release proinflammatory cytokines mainly through interaction with cognate ß-glucan receptors on the phagocyte.




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