Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-8-27
pubmed:abstractText
Pneumocystis carinii is an opportunistic organism that causes severe lung injury in immunocompromised hosts. Macrophage responses to P. carinii are poorly defined. Arachidonic acid (AA) and its metabolites are potent mediators of inflammation and have been implicated in host response to microorganisms. We therefore examined the production of eicosanoids from rat and rabbit alveolar macrophages stimulated with purified P. carinii. [14C]AA-labeled rabbit macrophages released 8.50 +/- 1.33% of the incorporated [14C]AA after 90 min in response to P. carinii (P = 0.0001 compared with unstimulated controls). In contrast, a similar number of rat alveolar macrophages exhibited a smaller but significant response to P. carinii, releasing 3.84 +/- 1.54% of their [14C]AA after 90 min (P = 0.001 compared with control). We further determined that P. carinii stimulated substantial production of prostaglandin E2 and concurrently a small amount of leukotriene B4 release from alveolar macrophages. To further investigate whether serum opsonization of P. carinii enhances these alterations in AA metabolism, we assessed the effect of P. carinii immune serum on P. carinii-induced AA release. P. carinii opsonized with this antiserum caused significantly greater AA release from rat alveolar macrophages than either unopsonized P. carinii or organisms opsonized with nonimmune serum. Previous studies suggest that P. carinii interacts with macrophage beta-glucan and mannose receptors. However, incubation of macrophages with P. carinii in the presence of either soluble beta-glucan or alpha-mannan failed to alter the release of AA from macrophages in response to P. carinii. Macrophage release of eicosanoids represents a potentially important host inflammatory response to P. carinii infection.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acids, http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone, http://linkedlifedata.com/resource/pubmed/chemical/Glucans, http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type, http://linkedlifedata.com/resource/pubmed/chemical/Leukotriene B4, http://linkedlifedata.com/resource/pubmed/chemical/Mannose, http://linkedlifedata.com/resource/pubmed/chemical/Mannose-Binding Lectins, http://linkedlifedata.com/resource/pubmed/chemical/Opsonin Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/beta-glucan receptor, http://linkedlifedata.com/resource/pubmed/chemical/mannose receptor
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
73-81
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:8393326-Animals, pubmed-meshheading:8393326-Arachidonic Acids, pubmed-meshheading:8393326-Dinoprostone, pubmed-meshheading:8393326-Female, pubmed-meshheading:8393326-Glucans, pubmed-meshheading:8393326-Lectins, C-Type, pubmed-meshheading:8393326-Leukotriene B4, pubmed-meshheading:8393326-Macrophages, Alveolar, pubmed-meshheading:8393326-Mannose, pubmed-meshheading:8393326-Mannose-Binding Lectins, pubmed-meshheading:8393326-Opsonin Proteins, pubmed-meshheading:8393326-Phagocytosis, pubmed-meshheading:8393326-Pneumocystis, pubmed-meshheading:8393326-Pneumonia, Pneumocystis, pubmed-meshheading:8393326-Rabbits, pubmed-meshheading:8393326-Rats, pubmed-meshheading:8393326-Rats, Sprague-Dawley, pubmed-meshheading:8393326-Receptors, Cell Surface, pubmed-meshheading:8393326-Receptors, Immunologic, pubmed-meshheading:8393326-Solubility
pubmed:year
1993
pubmed:articleTitle
Pneumocystis carinii induces the release of arachidonic acid and its metabolites from alveolar macrophages.
pubmed:affiliation
Thoracic Diseases Research Unit, Mayo Clinic and Foundation, Rochester, Minnesota 55905.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't