Linked Life Data

6871495

Source:http://linkedlifedata.com/resource/pubmed/id/6871495

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1983-9-9
pubmed:abstractText
Virus infections transiently suppress pulmonary antibacterial defenses by causing dysfunctions in the alveolar macrophage phagocytic system. This impairment of pulmonary bactericidal activity is not associated in time with virus proliferation, but rather with the period of time of rapidly declining virus titers and the expression of the antiviral immune response in the lungs. This temporal relationship suggests that the impairment of pulmonary bactericidal activity might be secondary to the antiviral immune response rather than a direct effect of virus replication. Immune depletion of mice during the course of influenza virus pneumonia ameliorated the virus-induced bactericidal defect and prevented bacterial multiplication in the lungs. In contrast, immune reconstitution reestablished the alveolar macrophage phagocytic defect. These data indicate that virus-induced suppression of pulmonary antibacterial defenses may be, in part, immunologically mediated.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0395-3890
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
173-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:articleTitle
The participation of antiviral immune mechanisms in alveolar macrophage dysfunction during viral pneumonia.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.