Bozza P T, Castro-Faria-Neto H C, Penido C, Larangeira A P, das Graças M, Henriques M O, Silva P M, Martins M A, dos Santos R R, Cordeiro R S
Departamento de Fisiologia e Farmacodinâmica, Instituto Oswaldo Cruz/FIOCRUZ, Rio de Janeiro, Brazil.
J Leukoc Biol. 1994 Aug;56(2):151-8. doi: 10.1002/jlb.56.2.151.
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.
在本研究中，我们调查了炎症细胞在脂多糖（LPS）诱导的嗜酸性粒细胞胸膜积聚中的作用。向大鼠胸腔内注射LPS（250 ng/腔）可诱导显著的嗜酸性粒细胞积聚，该积聚在24小时内开始出现，48小时时达到峰值，并在120小时内恢复至对照值。在这种嗜酸性粒细胞流入之前，4小时内有大量中性粒细胞流入，并伴有24至48小时的单核细胞积聚。用抗中性粒细胞单克隆抗体（RP-3，每只动物2 ml）预处理可在8小时内选择性减少循环中性粒细胞的数量，但未能改变LPS诱导的嗜酸性粒细胞增多。同样，用抗大鼠血小板抗血清使血小板耗竭也未改变LPS诱导的嗜酸性粒细胞积聚。环孢素（50 mg/kg，提前12小时和2小时）部分抑制（51%）LPS诱导的胸膜嗜酸性粒细胞增多，而用多粘菌素B（10 μg/腔，提前24小时）使胸膜肥大细胞预先脱颗粒并未改变嗜酸性粒细胞增多。此外，使用抗Thy 1.0单克隆抗体选择性清除T淋巴细胞可显著抑制LPS引发的嗜酸性粒细胞增多。胸腔内注射含二氯亚甲基二膦酸盐的脂质体5天后可显著减少（65%）驻留巨噬细胞的数量。在这种情况下，LPS诱导的嗜酸性粒细胞浸润被完全抑制。因此，将从注射LPS的大鼠胸腔获得的巨噬细胞单层上清液注射到未处理的受体动物胸腔内，可使胸膜嗜酸性粒细胞数量增加两倍。总之，我们的数据表明驻留巨噬细胞和T淋巴细胞在LPS诱导的嗜酸性粒细胞积聚中起重要作用。
