ABSTRACT
Changes in eosinophil counts after intrathoracic (it) injection of endotoxin (LPS) were investigated in Wistar rats (150 - 180 g). Increasing doses of endotoxin (62.5 - 500 ng/cavity) induced a dose-dependent increase in the number of eosinophils recovered from the rat pleural cavity 24 h later. The eosinophilia was apparent within 24 h, peaked within 48 h (from 0.76 ñ 0.12 to 3.68 ñ 0.51 eosinophils x 10**6/cavity, P < 0.001) and returned to basal levels 120h after the it inection of endotoxin (250 ng/cavity). Endotoxin (3 ng - 4 µg/ml) failed to attract eosinophilis in vitro under conditions in which PAF-acether induced a dose-related response. These findings indicate that endotoxin-induced eosinophil migration in vivo is mediated by a secondary mechanism
Subject(s)
Animals , Female , Rats , Endotoxins/administration & dosage , Eosinophils/physiology , Pleurisy/chemically induced , Leukocyte CountABSTRACT
The potential participation of PAF-acether (PAF) on the paw oedema triggered by enterolobin was investigated. Intraplantar injections of enterolobin )5-20 µg/paw) yielded a dose response curve for edema which appeared after 30 min, peaked in the interval between 2-4 h and faded after 24h. The pre-treatment with BN 52021, but not with other PAF antagonists such as PCA 4248 or WEB 2086, significantly blocked enterolobin-induced oedema. To clarify better the discrepant results obtained with the PAF antagonists, desensitization to PAF was performed. The oedema triggered by enterolobin was not modified in paf desensitized animals. It was concluded that the paw inflammation induced by enterolobin does not require PAF mechanism.
Subject(s)
Animals , Male , Rats , Plant Proteins/antagonists & inhibitors , Plant Proteins/toxicity , Azepines/pharmacology , Triazoles/pharmacology , Dihydropyridines/pharmacology , Platelet Activating Factor/antagonists & inhibitors , Platelet Activating Factor/physiology , Rats, Wistar , Ginkgolides , DiterpenesABSTRACT
This study investigated the effect of successive daily intrathoracic (it) injections of PAF-acether upon its demonstrated ability to generate eosinochemotaxin(s). Repeated administration of PAF-acether led to a selective state of desensitization, characterized by a gradual reduction of its ability to induce exudation. Concomitantly, however, there was a progressive pleural accumulation of eosinophilis leading to a 7-fold increase in the eosinophil counts after the 4th restimulation. The generation of eosinochemotaxin(s) elicited by PAF-acether was not modified by desensitization, as detected by transferring the cell-free pleural fluid from donor to recipient animals. We conclude that, in contrast to exudation, eosinophil tissue infiltration induced by PAF-acether is not a desensitizable phenomenon