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

Robert Vassallo, Joseph E. Standing and Andrew H. Limper
J Immunol April 1, 2000, 164 (7) 3755-3763; DOI: https://doi.org/10.4049/jimmunol.164.7.3755
Robert Vassallo
*Thoracic Diseases Research Unit, Division of Pulmonary, Critical Care and Internal Medicine, and
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Joseph E. Standing
*Thoracic Diseases Research Unit, Division of Pulmonary, Critical Care and Internal Medicine, and
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Andrew H. Limper
*Thoracic Diseases Research Unit, Division of Pulmonary, Critical Care and Internal Medicine, and
†Department of Biochemistry and Molecular Biology, Mayo Clinic and Foundation, Rochester, MN 55905
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Abstract

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-α 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-α generation and is associated with neutrophilic infiltration of the lungs. Digestion of the P. carinii cell wall isolate with zymolyase, a preparation containing predominantly β-1,3 glucanase, substantially reduces the ability of this P. carinii cell wall fraction to activate alveolar macrophages, thus suggesting that β-glucan components of the P. carinii cell wall largely mediate TNF-α release. Furthermore, the soluble carbohydrate β-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 α-mannan, a preparation that antagonizes macrophage mannose receptors, had minimal effect on TNF-α release induced by the P. carinii cell wall fraction. P. carinii β-glucan-induced TNF-α 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 β-glucan cell wall components can directly stimulate alveolar macrophages to release proinflammatory cytokines mainly through interaction with cognate β-glucan receptors on the phagocyte.

  • Received September 3, 1999.
  • Accepted January 24, 2000.
  • Copyright © 2000 by The American Association of Immunologists
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The Journal of Immunology: 164 (7)
The Journal of Immunology
Vol. 164, Issue 7
1 Apr 2000
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Isolated Pneumocystis carinii Cell Wall Glucan Provokes Lower Respiratory Tract Inflammatory Responses
Robert Vassallo, Joseph E. Standing, Andrew H. Limper
The Journal of Immunology April 1, 2000, 164 (7) 3755-3763; DOI: 10.4049/jimmunol.164.7.3755

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Isolated Pneumocystis carinii Cell Wall Glucan Provokes Lower Respiratory Tract Inflammatory Responses
Robert Vassallo, Joseph E. Standing, Andrew H. Limper
The Journal of Immunology April 1, 2000, 164 (7) 3755-3763; DOI: 10.4049/jimmunol.164.7.3755
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