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Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model

Anaphylactic shock (AS) is a life-threatening, multisystem disorder arising from sudden release of mast cell- and basophil-derived mediators into the circulation. In this study, we have used a Wistar rat model to investigate AS-associated histopathologic changes in various organs. Rats were sensitiz...

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Autores principales: Al-Salam, Suhail, Aburawi, Elhadi H., Al-Hammadi, Suleiman, Dhanasekaran, Sekhar, Shafiuallah, Mohamed, Yasin, Javed, Sudhadevi, Manjusha, Awwad, Aktham, Alper, Seth L., Kazzam, Elsadig E., Bellou, Abdelouahab
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468713/
https://www.ncbi.nlm.nih.gov/pubmed/30871269
http://dx.doi.org/10.3390/biom9030101
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author Al-Salam, Suhail
Aburawi, Elhadi H.
Al-Hammadi, Suleiman
Dhanasekaran, Sekhar
Shafiuallah, Mohamed
Yasin, Javed
Sudhadevi, Manjusha
Awwad, Aktham
Alper, Seth L.
Kazzam, Elsadig E.
Bellou, Abdelouahab
author_facet Al-Salam, Suhail
Aburawi, Elhadi H.
Al-Hammadi, Suleiman
Dhanasekaran, Sekhar
Shafiuallah, Mohamed
Yasin, Javed
Sudhadevi, Manjusha
Awwad, Aktham
Alper, Seth L.
Kazzam, Elsadig E.
Bellou, Abdelouahab
author_sort Al-Salam, Suhail
collection PubMed
description Anaphylactic shock (AS) is a life-threatening, multisystem disorder arising from sudden release of mast cell- and basophil-derived mediators into the circulation. In this study, we have used a Wistar rat model to investigate AS-associated histopathologic changes in various organs. Rats were sensitized with ovalbumin (1 mg s.c), and AS was induced by intravenous injection of ovalbumin (1 mg). Experimental groups included nonallergic rats (n = 6) and allergic rats (n = 6). Heart rate and blood pressure were monitored during one hour. Organs were harvested at the end of the experiment and prepared for histologic and immunohistochemical studies. Lung, small bowel mucosa and spleen were found to undergo heavy infiltration by mast cells and eosinophils, with less prominent mast cell infiltration of cardiac tissue. The mast cells in lung, small bowel and spleen exhibited increased expression of tryptase, c-kit and induced nitric oxide synthase (iNOS). Increased expression of endothelial nitric oxide synthase (eNOS) by vascular endothelial cells was noted principally in lung, heart and small bowel wall. The Wistar rat model of AS exhibited accumulation of mast cells and eosinophils in the lung, small bowel, and spleen to a greater extent than in the heart. We conclude that lung and gut are principal inflammatory targets in AS, and likely contribute to the severe hypotension of AS. Targeting nitric oxide (NO) production may help reduce AS mortality.
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spelling pubmed-64687132019-04-24 Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model Al-Salam, Suhail Aburawi, Elhadi H. Al-Hammadi, Suleiman Dhanasekaran, Sekhar Shafiuallah, Mohamed Yasin, Javed Sudhadevi, Manjusha Awwad, Aktham Alper, Seth L. Kazzam, Elsadig E. Bellou, Abdelouahab Biomolecules Article Anaphylactic shock (AS) is a life-threatening, multisystem disorder arising from sudden release of mast cell- and basophil-derived mediators into the circulation. In this study, we have used a Wistar rat model to investigate AS-associated histopathologic changes in various organs. Rats were sensitized with ovalbumin (1 mg s.c), and AS was induced by intravenous injection of ovalbumin (1 mg). Experimental groups included nonallergic rats (n = 6) and allergic rats (n = 6). Heart rate and blood pressure were monitored during one hour. Organs were harvested at the end of the experiment and prepared for histologic and immunohistochemical studies. Lung, small bowel mucosa and spleen were found to undergo heavy infiltration by mast cells and eosinophils, with less prominent mast cell infiltration of cardiac tissue. The mast cells in lung, small bowel and spleen exhibited increased expression of tryptase, c-kit and induced nitric oxide synthase (iNOS). Increased expression of endothelial nitric oxide synthase (eNOS) by vascular endothelial cells was noted principally in lung, heart and small bowel wall. The Wistar rat model of AS exhibited accumulation of mast cells and eosinophils in the lung, small bowel, and spleen to a greater extent than in the heart. We conclude that lung and gut are principal inflammatory targets in AS, and likely contribute to the severe hypotension of AS. Targeting nitric oxide (NO) production may help reduce AS mortality. MDPI 2019-03-13 /pmc/articles/PMC6468713/ /pubmed/30871269 http://dx.doi.org/10.3390/biom9030101 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Al-Salam, Suhail
Aburawi, Elhadi H.
Al-Hammadi, Suleiman
Dhanasekaran, Sekhar
Shafiuallah, Mohamed
Yasin, Javed
Sudhadevi, Manjusha
Awwad, Aktham
Alper, Seth L.
Kazzam, Elsadig E.
Bellou, Abdelouahab
Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model
title Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model
title_full Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model
title_fullStr Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model
title_full_unstemmed Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model
title_short Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model
title_sort cellular and immunohistochemical changes in anaphylactic shock induced in the ovalbumin-sensitized wistar rat model
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468713/
https://www.ncbi.nlm.nih.gov/pubmed/30871269
http://dx.doi.org/10.3390/biom9030101
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