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Complement is a rat natural resistance factor to amoebic liver infection
Amoebiasis is a parasitic disease caused by Entamoeba histolytica. This illness is prevalent in poor countries causing 100,000 deaths worldwide. Knowledge of the natural resistance mechanisms of rats to amoebic liver abscess (ALA) development may help to discover new pathogenic factors and to design...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6167500/ https://www.ncbi.nlm.nih.gov/pubmed/30201693 http://dx.doi.org/10.1042/BSR20180713 |
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author | Olivos-García, Alfonso Nequiz, Mario Liceaga, Scarlet Mendoza, Edith Zúñiga, Porfirio Cortes, Azucena López-Velázquez, Gabriel Enríquez-Flores, Sergio Saavedra, Emma Pérez-Tamayo, Ruy |
author_facet | Olivos-García, Alfonso Nequiz, Mario Liceaga, Scarlet Mendoza, Edith Zúñiga, Porfirio Cortes, Azucena López-Velázquez, Gabriel Enríquez-Flores, Sergio Saavedra, Emma Pérez-Tamayo, Ruy |
author_sort | Olivos-García, Alfonso |
collection | PubMed |
description | Amoebiasis is a parasitic disease caused by Entamoeba histolytica. This illness is prevalent in poor countries causing 100,000 deaths worldwide. Knowledge of the natural resistance mechanisms of rats to amoebic liver abscess (ALA) development may help to discover new pathogenic factors and to design novel therapeutic strategies against amoebiasis. In this work, histologic analyses suggested that the complement system may play a central role in rat natural resistance to ALA. E. histolytica trophozoites disappeared from rat liver within 6 h post-infection with minimal or no inflammatory infiltrate. In vitro findings indicate that rat complement was lethal for the parasite. Furthermore, hamsters became resistant to ALA by intravenous administration of fresh rat serum before infection. The amoebicidal potency of rat complement was 10 times higher than hamster complement and was not related to their respective CH50 levels. The alternative pathway of complement plays a central role in its toxicity to E. histolytica since trypan blue, which is a C3b receptor inhibitor, blocks its amoebicidal activity. These results suggest that amoebic membrane affinity, high for C3b and/or low for Factor H, in comparison with the hamster ones, may result in higher deposition of membrane complex attack on parasite surface and death. |
format | Online Article Text |
id | pubmed-6167500 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-61675002018-10-18 Complement is a rat natural resistance factor to amoebic liver infection Olivos-García, Alfonso Nequiz, Mario Liceaga, Scarlet Mendoza, Edith Zúñiga, Porfirio Cortes, Azucena López-Velázquez, Gabriel Enríquez-Flores, Sergio Saavedra, Emma Pérez-Tamayo, Ruy Biosci Rep Research Articles Amoebiasis is a parasitic disease caused by Entamoeba histolytica. This illness is prevalent in poor countries causing 100,000 deaths worldwide. Knowledge of the natural resistance mechanisms of rats to amoebic liver abscess (ALA) development may help to discover new pathogenic factors and to design novel therapeutic strategies against amoebiasis. In this work, histologic analyses suggested that the complement system may play a central role in rat natural resistance to ALA. E. histolytica trophozoites disappeared from rat liver within 6 h post-infection with minimal or no inflammatory infiltrate. In vitro findings indicate that rat complement was lethal for the parasite. Furthermore, hamsters became resistant to ALA by intravenous administration of fresh rat serum before infection. The amoebicidal potency of rat complement was 10 times higher than hamster complement and was not related to their respective CH50 levels. The alternative pathway of complement plays a central role in its toxicity to E. histolytica since trypan blue, which is a C3b receptor inhibitor, blocks its amoebicidal activity. These results suggest that amoebic membrane affinity, high for C3b and/or low for Factor H, in comparison with the hamster ones, may result in higher deposition of membrane complex attack on parasite surface and death. Portland Press Ltd. 2018-10-02 /pmc/articles/PMC6167500/ /pubmed/30201693 http://dx.doi.org/10.1042/BSR20180713 Text en © 2018 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Articles Olivos-García, Alfonso Nequiz, Mario Liceaga, Scarlet Mendoza, Edith Zúñiga, Porfirio Cortes, Azucena López-Velázquez, Gabriel Enríquez-Flores, Sergio Saavedra, Emma Pérez-Tamayo, Ruy Complement is a rat natural resistance factor to amoebic liver infection |
title | Complement is a rat natural resistance factor to amoebic liver infection |
title_full | Complement is a rat natural resistance factor to amoebic liver infection |
title_fullStr | Complement is a rat natural resistance factor to amoebic liver infection |
title_full_unstemmed | Complement is a rat natural resistance factor to amoebic liver infection |
title_short | Complement is a rat natural resistance factor to amoebic liver infection |
title_sort | complement is a rat natural resistance factor to amoebic liver infection |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6167500/ https://www.ncbi.nlm.nih.gov/pubmed/30201693 http://dx.doi.org/10.1042/BSR20180713 |
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