| Regulation of bronchoalveolar macrophage proinflammatory cytokine production by dexamethasone and granulocyte-macrophage colony-stimulating factor after stimulation by Aspergillus conidia or lipopolysaccharide. | |
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MedLine Citation:
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PMID: 12200108 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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There is substantial evidence that local production of proinflammatory cytokines are very important in host resistance to aspergillosis. Dexamethasone (DEX) down-regulates production of these cytokines by stimulated bronchoalveolar macrophages (BAM) and constitutes a risk factor for aspergillosis. Granulocyte-macrophage colony-stimulating factor (GM-CSF) antagonizes DEX suppression of antifungal activity by BAM. Here we investigated the possibility that GM-CSF could antagonize DEX down-regulation of interleukin (IL)-1alpha and tumour necrosis factor (TNF)-alpha production by stimulated BAM. Control BAM responded to increasing numbers of conidia of Aspergillus fumigatus with increasing production of IL-1 and TNF. DEX (10(-7)M) significantly suppressed IL-1 and TNF production by BAM+conidia. Although GM-CSF did not enhance IL-1 or TNF production by BAM+conidia, GM-CSF significantly antagonized DEX suppression of IL-1 cytokine production. For comparative purposes, lipopolysaccharide (LPS, 1 microg/ml) was used to stimulate BAM in experiments similar to the above. In contrast to the findings with conidia, GM-CSF enhanced the production of IL-1 (5-fold) and TNF (1.5-fold) by LPS treated BAM. DEX suppression of cytokine production by BAM+LPS was modestly but significantly antagonized by GM-CSF. Moreover, differences between regulation of IL-1 and TNF production by BAM+conidia or LPS and peritoneal macrophages (PM)+conidia or LPS were documented. Finally, the anti-inflammatory cytokine IL-10 was minimally produced by BAM + conidia or LPS, but IL-10 was produced by PM + conidia or LPS. In summary, these data indicate that the risk factor for aspergillosis associated with DEX could be lessened in the pulmonary compartment with GM-CSF. On the other hand, desired effects of DEX could be maintained in other compartments. |
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Authors:
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Marika Kamberi; Elmer Brummer; David A Stevens |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Cytokine Volume: 19 ISSN: 1043-4666 ISO Abbreviation: Cytokine Publication Date: 2002 Jul |
Date Detail:
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Created Date: 2002-08-29 Completed Date: 2003-02-25 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 9005353 Medline TA: Cytokine Country: United States |
Other Details:
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Languages: eng Pagination: 14-20 Citation Subset: IM |
Affiliation:
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Division of Infectious Diseases, Department of Medicine, Santa Clara Valley Medical Center, San Jose, CA 95128-2699, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Aspergillus / metabolism* Cytokines / biosynthesis* Dexamethasone / pharmacology* Enzyme-Linked Immunosorbent Assay Glucocorticoids / pharmacology Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology* Humans Interleukin-1 / metabolism Interleukin-10 / biosynthesis Lipopolysaccharides / metabolism* Lung / cytology* Macrophages / metabolism* Male Mice Tumor Necrosis Factor-alpha / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Glucocorticoids; 0/Interleukin-1; 0/Lipopolysaccharides; 0/Tumor Necrosis Factor-alpha; 130068-27-8/Interleukin-10; 50-02-2/Dexamethasone; 83869-56-1/Granulocyte-Macrophage Colony-Stimulating Factor |
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