REQUIREMENT FOR LYMPHOCYTES AND RESIDENT MACROPHAGES IN LPS-INDUCED PLEURAL EOSINOPHIL ACCUMULATION

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 rat s 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 with in 4 h and accompanied by a mononuclear cell accumulation between 24 a nd 48 h. Pretreatment with an antineutrophil monoclonal antibody (RP-3 , 2 ml per animal) selectively reduced the number of circulating neutr ophils within 8 h but failed to alter the LPS-induced eosinophilia. Si milarly, platelet depletion with an anti-rat platelet antiserum did no t alter the LPS-induced eosinophil accumulation. Cyclosporine (50 mg/k g, 12 and 2 h before) partially inhibited (51%) the LPS-induced pleura l eosinophilia, whereas the eosinophilia was not changed by prior degr anulation of pleural mast cells with polymyxin B (10 mu g/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 dichlorom ethylene diphosphonate significantly reduced (65 %) the number of resi dent macrophages after 5 days. Under this condition, the eosinophil in filtration 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 anima ls led to a twofold increase in the number of pleural eosinophils. In conclusion, our data suggest an important role for resident macrophage s and T lymphocytes in the eosinophil accumulation induced by LPS.