Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
1994-9-23
|
pubmed:abstractText |
In this study we investigated the involvement of inflammatory cells in the pleural accumulation of eosinophils induced by lipopolysaccharide (LPS). Intrathoracic (i.t.) injection of LPS (250 ng/cavity) into rats induced a significant eosinophil accumulation that developed within 24 h, was maximal at 48 h, and returned to control values within 120 h. This eosinophil influx was preceded by a huge neutrophil influx within 4 h and accompanied by a mononuclear cell accumulation between 24 and 48 h. Pretreatment with an antineutrophil monoclonal antibody (RP-3, 2 ml per animal) selectively reduced the number of circulating neutrophils within 8 h but failed to alter the LPS-induced eosinophilia. Similarly, platelet depletion with an anti-rat platelet antiserum did not alter the LPS-induced eosinophil accumulation. Cyclosporine (50 mg/kg, 12 and 2 h before) partially inhibited (51%) the LPS-induced pleural eosinophilia, whereas the eosinophilia was not changed by prior degranulation of pleural mast cells with polymyxin B (10 micrograms/cavity, 24 h before). Moreover, selective depletion of T lymphocytes using an anti-Thy 1.0 monoclonal antibody significantly inhibited the eosinophilia triggered by LPS. The i.t. injection of liposomes containing dichloromethylene diphosphonate significantly reduced (65%) the number of resident macrophages after 5 days. Under this condition, the eosinophil infiltration induced by LPS was completely inhibited. Accordingly, the i.t. injection of supernatant from macrophage monolayers, obtained from the pleural cavities of LPS-injected rats, into naive recipient animals led to a twofold increase in the number of pleural eosinophils. In conclusion, our data suggest an important role for resident macrophages and T lymphocytes in the eosinophil accumulation induced by LPS.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0741-5400
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
56
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
151-8
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:8071592-Animals,
pubmed-meshheading:8071592-Cell Degranulation,
pubmed-meshheading:8071592-Chemotactic Factors, Eosinophil,
pubmed-meshheading:8071592-Chemotaxis, Leukocyte,
pubmed-meshheading:8071592-Cyclosporine,
pubmed-meshheading:8071592-Eosinophils,
pubmed-meshheading:8071592-Injections, Spinal,
pubmed-meshheading:8071592-Lipopolysaccharides,
pubmed-meshheading:8071592-Macrophages,
pubmed-meshheading:8071592-Male,
pubmed-meshheading:8071592-Mast Cells,
pubmed-meshheading:8071592-Mice,
pubmed-meshheading:8071592-Pulmonary Eosinophilia,
pubmed-meshheading:8071592-Rats,
pubmed-meshheading:8071592-Rats, Wistar,
pubmed-meshheading:8071592-Stimulation, Chemical,
pubmed-meshheading:8071592-T-Lymphocytes
|
pubmed:year |
1994
|
pubmed:articleTitle |
Requirement for lymphocytes and resident macrophages in LPS-induced pleural eosinophil accumulation.
|
pubmed:affiliation |
Departamento de Fisiologia e Farmacodinâmica, Instituto Oswaldo Cruz/FIOCRUZ, Rio de Janeiro, Brazil.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|