Hc. Castrofarianeto et al., A ROLE FOR LYMPHOCYTES AND CYTOKINES ON THE EOSINOPHIL MIGRATION INDUCED BY LPS, Memorias do Instituto Oswaldo Cruz, 92, 1997, pp. 197-200
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.