A ROLE FOR LYMPHOCYTES AND CYTOKINES ON THE EOSINOPHIL MIGRATION INDUCED BY LPS

In the present work we review the existing evidence for a LPS-induced cytokine-mediated eosinophil accumulation in a model of acute inflamma tion. Intrathoracic administration of LPS into rodents (mice, rats or guinea pigs) induces a significant increase in the number of eosinophi ls recovered from the pleural fluid 24 hr later. This phenomenon is pr eceded by a neutrophil influx and accompanied by lymphocyte and monocy te accumulation. The eosinophil accumulation induced by LPS is not aff ected by inhibitors of cyclo or lipoxygenase nor by PAF antagonists bu t can be blocked by dexamethasone or the protein synthesis inhibitor c ycloheximide. Transfer of cell-free pleural wash fr-om LPS injected ra ts (LPS-PW) to naive recipient animals induces a selective eosinophil accumulation within 24 hr. The eosinophilotactic activity present on t he LPS-PW has a molecular weight ranging between 10 and 50 kDa and its effect is abolished by trypsin digestion of the pleural wash indicati ng the proteic nature of this activity. The production of the eosinoph ilotactic activity depends on the interaction between macrophages and T-lymphocytes and its effect can not be blocked by anti-IL-5 monoclona l antibodies. Accumulated evidence suggest that the eosinophil accumul ation induced by LPS is a consequence of a eosinophilotactic cytokine produced through macrophage and T-cell interactions in the site of a L PS-induced inflammatory reaction.