IL-5 accounts for the mouse pleural eosinophil accumulation triggered by antigen but not by LPS.

The involvement of interleukin-5 (IL-5) in the pleural eosinophilia induced by LPS or allergen was investigated. The number of pleural eosinophils in actively sensitized mice increased 24 h after the intrathoracic (i.t.) injection of ovalbumin (12 mg/cavity), peaked within 72 h, and persisted significantly increased for at least 120 h. Despite being less intense, the i.t. injection of LPS (250 ng/cavity) also increased the number of pleural eosinophils at 24 h, returning to basal levels within 72 h. Intraperitoneal pretreatment with monoclonal antibody to IL-5 (TRFK-4 and TRFK-5, 500 mg/kg) suppressed the eosinophil accumulation induced by IL-5 (200 units/cavity) or ovalbumin, but had no effect on the LPS-induced eosinophilia. Transfer of the cell-free pleural washing from LPS-treated donor mice to naive recipient animals led to a selective increase in the eosinophil counts. The co-incubation of the pleural washing from LPS-treated animals with monoclonal antibody to IL-5 failed to modify the phenomenon. The results indicate that IL-5 plays an important role in the antigen-induced accumulation of eosinophils in vivo, but not in the eosinophilia triggered by LPS.