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The tripeptide feG ameliorates systemic inflammatory responses to rat intestinal anaphylaxis
BACKGROUND: Food allergies are generally associated with gastrointestinal upset, but in many patients systemic reactions occur. However, the systemic effects of food allergies are poorly understood in experimental animals, which also offer the opportunity to explore the actions of anti-allergic drug...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2002
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC126222/ https://www.ncbi.nlm.nih.gov/pubmed/12199907 |
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author | Turesin, Fusun Sadr, Aida Davison, Joseph S Mathison, Ronald |
author_facet | Turesin, Fusun Sadr, Aida Davison, Joseph S Mathison, Ronald |
author_sort | Turesin, Fusun |
collection | PubMed |
description | BACKGROUND: Food allergies are generally associated with gastrointestinal upset, but in many patients systemic reactions occur. However, the systemic effects of food allergies are poorly understood in experimental animals, which also offer the opportunity to explore the actions of anti-allergic drugs. The tripeptide D-phenylalanine-D-glutamate-Glycine (feG), which potentially alleviates the symptoms of systemic anaphylactic reactions, was tested to determine if it also reduced systemic inflammatory responses provoked by a gastric allergic reaction. RESULTS: Optimal inhibition of intestinal anaphylaxis was obtained when 100 μg/kg of feG was given 20 min before the rats were challenged with antigen. The increase in total circulating neutrophils and accumulation of neutrophils in the heart, developing 3 h and 24 h, respectively, after antigen challenge were reduced by both feG and dexamethasone. Both anti-inflammatory agents reduced the increase in vascular permeability induced by antigen in the intestine and the peripheral skin (pinna), albeit with different time courses. Dexamethasone prevented increases in vascular permeability when given 12 h before antigen challenge, whereas feG was effective when given 20 min before ingestion of antigen. The tripeptide prevented the anaphylaxis induced up regulation of specific antibody binding of a cell adhesion molecule related to neutrophil activation, namely CD49d (α4 integrin). CONCLUSIONS: Aside from showing that intestinal anaphylaxis produces significant systemic inflammatory responses in non-intestinal tissues, our results indicate that the tripeptide feG is a potent inhibitor of extra-gastrointestinal allergic reactions preventing both acute (30 min) and chronic (3 h or greater) inflammatory responses. |
format | Text |
id | pubmed-126222 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-1262222002-09-19 The tripeptide feG ameliorates systemic inflammatory responses to rat intestinal anaphylaxis Turesin, Fusun Sadr, Aida Davison, Joseph S Mathison, Ronald BMC Physiol Research Article BACKGROUND: Food allergies are generally associated with gastrointestinal upset, but in many patients systemic reactions occur. However, the systemic effects of food allergies are poorly understood in experimental animals, which also offer the opportunity to explore the actions of anti-allergic drugs. The tripeptide D-phenylalanine-D-glutamate-Glycine (feG), which potentially alleviates the symptoms of systemic anaphylactic reactions, was tested to determine if it also reduced systemic inflammatory responses provoked by a gastric allergic reaction. RESULTS: Optimal inhibition of intestinal anaphylaxis was obtained when 100 μg/kg of feG was given 20 min before the rats were challenged with antigen. The increase in total circulating neutrophils and accumulation of neutrophils in the heart, developing 3 h and 24 h, respectively, after antigen challenge were reduced by both feG and dexamethasone. Both anti-inflammatory agents reduced the increase in vascular permeability induced by antigen in the intestine and the peripheral skin (pinna), albeit with different time courses. Dexamethasone prevented increases in vascular permeability when given 12 h before antigen challenge, whereas feG was effective when given 20 min before ingestion of antigen. The tripeptide prevented the anaphylaxis induced up regulation of specific antibody binding of a cell adhesion molecule related to neutrophil activation, namely CD49d (α4 integrin). CONCLUSIONS: Aside from showing that intestinal anaphylaxis produces significant systemic inflammatory responses in non-intestinal tissues, our results indicate that the tripeptide feG is a potent inhibitor of extra-gastrointestinal allergic reactions preventing both acute (30 min) and chronic (3 h or greater) inflammatory responses. BioMed Central 2002-08-19 /pmc/articles/PMC126222/ /pubmed/12199907 Text en Copyright © 2002 Turesin et al; licensee BioMed Central Ltd. This article is published in Open Access: verbatim copying and redistribution of this article are permitted in all media for any non-commercial purpose, provided this notice is preserved along with the article's original URL. |
spellingShingle | Research Article Turesin, Fusun Sadr, Aida Davison, Joseph S Mathison, Ronald The tripeptide feG ameliorates systemic inflammatory responses to rat intestinal anaphylaxis |
title | The tripeptide feG ameliorates systemic inflammatory responses to rat intestinal anaphylaxis |
title_full | The tripeptide feG ameliorates systemic inflammatory responses to rat intestinal anaphylaxis |
title_fullStr | The tripeptide feG ameliorates systemic inflammatory responses to rat intestinal anaphylaxis |
title_full_unstemmed | The tripeptide feG ameliorates systemic inflammatory responses to rat intestinal anaphylaxis |
title_short | The tripeptide feG ameliorates systemic inflammatory responses to rat intestinal anaphylaxis |
title_sort | tripeptide feg ameliorates systemic inflammatory responses to rat intestinal anaphylaxis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC126222/ https://www.ncbi.nlm.nih.gov/pubmed/12199907 |
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