Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model
| Autor: | Elsadig Kazzam, Elhadi H. Aburawi, Seth L. Alper, Mohamed Shafiuallah, Suhail Al-Salam, Javed Yasin, Suleiman Al-Hammadi, Aktham Awwad, Manjusha Sudhadevi, Abdelouahab Bellou, Sekhar Dhanasekaran |
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| Rok vydání: | 2019 |
| Předmět: |
Male
Pathology medicine.medical_specialty Ovalbumin Injections Subcutaneous lcsh:QR1-502 cellular changes tryptase Tryptase Spleen Nitric Oxide Biochemistry lcsh:Microbiology Article Nitric oxide 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Enos medicine Animals 030216 legal & forensic medicine Rats Wistar Molecular Biology Anaphylaxis Inflammation Lung biology Chemistry anaphylactic shock Mast cell biology.organism_classification Rats Nitric oxide synthase iNOS Disease Models Animal medicine.anatomical_structure 030228 respiratory system c-kit Injections Intravenous biology.protein eNOS Hypotension |
| Zdroj: | Biomolecules Biomolecules, Vol 9, Iss 3, p 101 (2019) Volume 9 Issue 3 |
| ISSN: | 2218-273X |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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