title: Requirement for lymphocytes and resident macrophages in LPS-induced pleural eosinophil accumulation.
abstract: 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.
authors.affiliation: Departamento de Fisiologia e Farmacodinâmica, Instituto Oswaldo Cruz/FIOCRUZ, Rio de Janeiro, Brazil.
authors.forename: P T
authors.initials: PT
authors.lastname: Bozza
authors.forename: H C
authors.initials: HC
authors.lastname: Castro-Faria-Neto
authors.forename: C
authors.initials: C
authors.lastname: Penido
authors.forename: A P
authors.initials: AP
authors.lastname: Larangeira
authors.forename: M
authors.initials: M
authors.lastname: das Graças
authors.forename: M O
authors.initials: MO
authors.lastname: Henriques
authors.forename: P M
authors.initials: PM
authors.lastname: Silva
authors.forename: M A
authors.initials: MA
authors.lastname: Martins
authors.forename: R R
authors.initials: RR
authors.lastname: dos Santos
authors.forename: R S
authors.initials: RS
authors.lastname: Cordeiro
mesh_terms: D000818:Animals; D015550:Cell Degranulation / Q000502:physiology; D002631:Chemotactic Factors, Eosinophil / Q000096:biosynthesis; D002634:Chemotaxis, Leukocyte / Q000187:drug effects / Q000502:physiology; D016572:Cyclosporine / Q000494:pharmacology; D004804:Eosinophils / Q000166:cytology* / Q000187:drug effects* / Q000502:physiology; D007278:Injections, Spinal; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology*; D008297:Male; D008407:Mast Cells / Q000502:physiology; D051379:Mice; D011657:Pulmonary Eosinophilia / Q000139:chemically induced; D051381:Rats; D017208:Rats, Wistar; D013268:Stimulation, Chemical; D013601:T-Lymphocytes / Q000187:drug effects* / Q000502:physiology*
chemical_list: D002631:Chemotactic Factors, Eosinophil; D008070:Lipopolysaccharides; D016572:Cyclosporine