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C M Pacheco

Publications and source records attributed to C M Pacheco.

3 recordsLinked to original sources
PubMed1998

Pharmacological evidence supporting a role for IL-1, IL-2 and serotonin in the inflammation induced by Schistosoma mansoni soluble egg antigen (SEA) in rat paws.

THIS study intended to characterize pharmacologically the mediator(s) released in the inflammation induced by Soluble Egg Antigen (SEA), the main antigen released from eggs of Schistosoma mansoni, in rat hindpaws. A single intraplantar injection of 0.1-100 microg SEA at day zero induced a dose-dependent increase in the volume of rat hindpaws characterizing an oedema of quick onset (within 15 min) and 4h-duration, which was confirmed by histopathological analysis of the paws. A second injection of SEA in the same paw (1-10 microg) 28 days later induced an increased dose-dependent oedematogenic response. The early oedematogenic response following SEA sensitization was derived from serotonin release and interleukin-1 (IL-1), since treatment with either pizotifen or an antibody against IL-1, reduced the response by 60% and 48%, respectively. The increased oedematogenic response derived from SEA-challenge (10 microg) of rat paws derived from a local rather than systemic reaction, since it was not observed if the sensitization was in the contralateral paw or the peritoneal cavity of the animals. Chronic treatment with inhibitors of IL-2 synthesis/release such as cyclosporin or dexamethasone during the sensitization phase reduced the oedematogenic response due to SEA challenge by 51% and 55%, respectively. These data suggested that SEA-challenge was immune-derived and dependent of IL-2 release. It is discussed the association between cytokine release and the resistance of rats to S. mansoni infection.

Animals↗
PubMed1996

Pharmacological characterization of Sephadex-induced oedema in rat paws: predominant role of serotonin and platelet-activating factor.

An intravenous injection of Sephadex beads has been used to induce lung inflammation and bronchial hyperreactivity in small animals. In the present study, we injected Sephadex beads (0.3-5.5 mg/paw) into rat paws and followed the resulting inflammation plethysmometrically. Our results show that Sephadex beads induced a significant and dose-dependent increase in the hindpaw volume at 5 min; it was maximal at 30-60 min and declined at 4 h. However, the paw volume remained significantly increased for up to 21 days. The initial 4-hour-oedema was confirmed by histopathology of the paw tissues, but the persistent increase in paw volume was related to a chronic inflammatory (granulomatous) response. The Sephadex-induced oedema was predominantly due to serotonin (5-HT) release since specific antagonists such as methysergide (1 mg/kg) and pizotifen (0.1-2 mg/kg) administered both systemically and locally were able to inhibit the oedema (10-100 microgram/paw) as could pretreatment with compound 48/80. In addition, platelet-activating factor (PAF) was also shown to be involved, since systemic pretreatment using the specific PAF antagonist BN 52021 (1 mg/kg) was able to inhibit the increase in paw volume induced by Sephadex. Effective doses of indomethacin (2 mg/kg), L-NAME (1 mg/kg), pyrilamine (1-2 mg/kg), ondansetron (1 mg/kg) and HOE 140 (1 mg/kg) did not affect the Sephadex-induced oedema, thus ruling out the participation of prostaglandins, nitric oxide, histamine, 5-HT3 receptors and bradykinin in its development. Since the late increases in paw volume induced by Sephadex were reduced by pretreatment of the animals with the immunosuppressive drugs rapamycin and dexamethasone but not cyclosporin, our results also suggested that distinct immunological pathways may be involved in the modulation of the chronic phase of inflammation induced by Sephadex beads in rat paws.

Animals↗