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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 1
pubmed:dateCreated
1996-11-20
pubmed:abstractText
Surfactant protein A (SP-A) regulates alveolar macrophage function and has been implicated in the mediation of pulmonary host defense. Our goals were to characterize the interaction of SP-A with various pulmonary pathogens, to investigate the mechanism of SP-A-mediated phagocytosis using an assay that distinguishes bound from internalized bacteria by quenching the fluorescence of extracellular bacteria, and to examine further the interactions of SP-A and the structurally homologous protein complement component 1q (C1q) with alveolar macrophages and peripheral blood monocytes. We found that SP-A binds to and increases the phagocytosis of Haemophilus influenzae, Streptococcus pneumoniae, and Group A Streptococcus; SP-A aggregates only H. influenzae. SP-A neither binds to, aggregates, nor stimulates the phagocytosis of Pseudomonas aeruginosa. We have also found that bronchoalveolar lavage stimulates phagocytosis and that this stimulation is reduced by an anti-SP-A antibody. While the enhancement of phagocytosis by SP-A is inhibited in blood monocytes adhered to C1q-coated surfaces, which presumably clusters the C1q receptor on the basal surface of the cell, alveolar macrophages on C1q-coated slides show no significant change in their response to SP-A. In summary, SP-A stimulates the phagocytosis by alveolar macrophages of specific pulmonary pathogens to which it binds, but aggregation is not required for the effect. Additionally, the role of the C1q receptor in the response to SP-A may differ between monocytes and alveolar macrophages.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
270
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
L677-88
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Surfactant protein A stimulates phagocytosis of specific pulmonary pathogens by alveolar macrophages.
pubmed:affiliation
Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.