| Streptomyces spores from mouldy houses induce nitric oxide, TNFα and IL-6 secretion from RAW264.7 macrophage cell line without causing subsequent cell death. | |
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MedLine Citation:
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PMID: 21781759 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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The current view is that only bacterial lipopolysaccharide (LPS) and gamma interferon (IFNγ) are able to alone activate macrophages to secrete nitric oxide (NO), probably a causative agent of cell death. Moreover, some cytokines and gram positive pathogens together with IFNγ induce NO-production. Surprisingly, spores of Streptomyces sp., which are mesophilic gram-positive bacteria found in mouldy houses, stimulated RAW264.7 macrophages to produce pro-inflammatory cytokines, tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6), and induced the expression of inducible NO-synthase (iNOS) with a subsequent NO-production. However, the Streptomyces spores did not kill NO-producing macrophages, as did both LPS and gram negative bacteria Pseudomonas fluorescens, strong inducers of cytokine- and NO-production. These results imply that Streptomyces sp., induced cytokine and NO-secretion, may play a role in the responses evoked by exposure to these microbes. Moreover, factors other than, or in addition to NO, are necessary for cytotoxicity in murine macrophages. |
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Authors:
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M R Hirvonen; A Nevalainen; N Makkonen; J Mönkkönen; K Savolainen |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Environmental toxicology and pharmacology Volume: 3 ISSN: 1382-6689 ISO Abbreviation: Environ. Toxicol. Pharmacol. Publication Date: 1997 Feb |
Date Detail:
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Created Date: 2011-07-25 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9612020 Medline TA: Environ Toxicol Pharmacol Country: Netherlands |
Other Details:
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Languages: eng Pagination: 57-63 Citation Subset: - |
Affiliation:
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Division of Environmental Health, National Public Health Institute, P.O. Box 95, FIN-70701 Kuopio, Finland. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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