Linked Life Data

9419186

Source:http://linkedlifedata.com/resource/pubmed/id/9419186

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-1-23
pubmed:abstractText
Pneumocystis carinii pneumonia (PCP) remains a major cause of morbidity in AIDS. The pathogenesis of PCP is poorly understood, but evidence of surfactant abnormalities is mounting. The role of the major surface glycoprotein of P. carinii, gpA, in producing surfactant abnormalities was investigated. Rat type II pneumocytes were incubated with [3H]choline, purified gpA, and modulators. Lipid was extracted, and [3H]dipalmitoyl phosphatidylcholine (DPPC) secretion was calculated. Contaminating endotoxin had no effect on DPPC secretion. gpA inhibited basal and ATP-stimulated DPPC secretion in a dose- and time-dependent manner. An anti-gpA monoclonal antibody attenuated inhibition of DPPC secretion. Unglycosylated recombinant gpA inhibited secretion, suggesting that functional activity resides in the protein moiety of gpA. These results suggest that gpA is a specific trigger for abnormalities of surfactant lipids in PCP. This is a unique role for a microbial product in disease pathogenesis and a potentially exploitable therapeutic target.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1899
pubmed:author
pubmed:issnType
Print
pubmed:volume
177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
182-7
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Pneumocystis carinii glycoprotein A inhibits surfactant phospholipid secretion by rat alveolar type II cells.
pubmed:affiliation
Pulmonary Division, Allegheny University Hospitals-Medical College of Pennsylvania Division, Philadelphia, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't