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Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro

Eosinophils from the peritoneal cavity of normal rats, in the presence of fresh normal rat serum (NRS), adhered to schistosomula of Schistosoma mansoni in vitro and killed the majority of parasites within 18 h. The reaction differed from the previously described antibody-mediated eosinophil adherenc...

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Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1978
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2184099/
https://www.ncbi.nlm.nih.gov/pubmed/627834
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description Eosinophils from the peritoneal cavity of normal rats, in the presence of fresh normal rat serum (NRS), adhered to schistosomula of Schistosoma mansoni in vitro and killed the majority of parasites within 18 h. The reaction differed from the previously described antibody-mediated eosinophil adherence to schistosomula which occurs in heat-inactivated immune rat serum (IRS) and where adherence is mediated through Fc receptors. Adherence of eosinophils in fresh NRS was shown to be due to the activation of complement at the schistosomular surface by the alternative pathway, and it was effected through C3 receptors. The ability of eosinophils to kill in Fc-mediated adherence. This enhancement of killer activity may be due to the generation by complement activation of eosinophil chemotactic factors which increase the concentration of cells at the target surface. It is suggested that eosinophil adherence mediated through complement activation could be the principla mechanism of destroying schistosomula in the host.
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spelling pubmed-21840992008-04-17 Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro J Exp Med Articles Eosinophils from the peritoneal cavity of normal rats, in the presence of fresh normal rat serum (NRS), adhered to schistosomula of Schistosoma mansoni in vitro and killed the majority of parasites within 18 h. The reaction differed from the previously described antibody-mediated eosinophil adherence to schistosomula which occurs in heat-inactivated immune rat serum (IRS) and where adherence is mediated through Fc receptors. Adherence of eosinophils in fresh NRS was shown to be due to the activation of complement at the schistosomular surface by the alternative pathway, and it was effected through C3 receptors. The ability of eosinophils to kill in Fc-mediated adherence. This enhancement of killer activity may be due to the generation by complement activation of eosinophil chemotactic factors which increase the concentration of cells at the target surface. It is suggested that eosinophil adherence mediated through complement activation could be the principla mechanism of destroying schistosomula in the host. The Rockefeller University Press 1978-01-01 /pmc/articles/PMC2184099/ /pubmed/627834 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Articles
Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro
title Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro
title_full Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro
title_fullStr Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro
title_full_unstemmed Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro
title_short Complement-mediated killing of schistosomula of Schistosoma mansoni by rat eosinophils in vitro
title_sort complement-mediated killing of schistosomula of schistosoma mansoni by rat eosinophils in vitro
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2184099/
https://www.ncbi.nlm.nih.gov/pubmed/627834