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 pawsReport as inadecuate




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 - Download this document for free, or read online. Document in PDF available to download.

Mediators of Inflammation - Volume 7 1998, Issue 4, Pages 261-267



Department of Pharmacology, Institute of Federal University of Minas Gerais, Campus da Pampulha, Avenida Antonio Carlos 6627, Belo Horizonte 31270–100, Brazil

Department of Biochemistry, Institute of Federal University of Minas Gerais, Campus da Pampulha, Avenida Antonio Carlos 6627, Belo Horizonte 31270–100, Brazil

Department of Parasitology, Institute of Federal University of Minas Gerais, Campus da Pampulha, Avenida Antonio Carlos 6627, Belo Horizonte 31270–100, Brazil

Department of General Pathology of Biological Science, Institute of Federal University of Minas Gerais, Campus da Pampulha, Avenida Antonio Carlos 6627, Belo Horizonte 31270–100, Brazil



Copyright © 1998 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

This study intended to characterize pharmacologically the mediators 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 μg SEA at day zero induced a dose-dependent increase in the volume of rat hindpaws characterizing an oedema of quick onset within 15 min and4 h-duration, which was confirmed by his topathological analys is of the paws . A second injection of SEAin the same paw 1–10 μg 28 days later induced an increased dose -dependent oedematogenic response.The early oedematogenic response following SEA sensitization was derived from serotonin release andinterleukin-1 IL-1, since treatment with either pizotifen or anantibody against IL-1, reduced theresponse by 60% and 48%, respectively. The increased oedematogenic response derived from SEA-challenge 10 μg of rat paws derived from a local rather than systemic reaction, since it was notobserved if the sensitization was in the contralateral paw or the peritoneal cavity of the animals. Chronictre atment with inhibitors of IL-2 synthesis - release such as cyclosporin or dexamethasone during thesens itization 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. Itis discussed the association between cytokine release and the resistance of rats to S. mans o ni infe ction.





Author: C. M. F. Pacheco, C. A. P. Tavares, P. M. Z. Coelho, O. A. Rocha, J. M. M. Santos, F. R. M. Prado, and J. N. Francischi

Source: https://www.hindawi.com/



DOWNLOAD PDF




Related documents