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
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
Subject(s)
Rats , Animals , Male , Female , Eosinophils/physiology , Eosinophilia/chemically induced , Platelet Activating Factor/pharmacology , Pleural Effusion/chemically induced , Platelet Activating Factor/administration & dosage , Rats, WistarABSTRACT
Subcutaneous injection of PAF-acether into rat's paw to a local inflammatory response (edema) followed by desensitization after repeated injections of the substance. The desensitizing effect was not modified by previous adrenalectomy, whereas the inflammatory response observed after the first injection of PAF-acether was exacerbated. This finding suggests that adrenal hormones may act as modulators of PAF-induced inflammatory reactions. Because LY 171883, an LTD4 blocker, inhibited the edema which follows the first injection of PAF-acether, we suggest that leukotrienes may play an important role in the phenomenon