Cellular and Immunohistochemical Changes in Anaphylactic Shock Induced in the Ovalbumin-Sensitized Wistar Rat Model
Suhail Al-Salam,
Elhadi H. Aburawi,
Suleiman Al-Hammadi,
Sekhar Dhanasekaran,
Mohamed Shafiuallah,
Javed Yasin,
Manjusha Sudhadevi,
Aktham Awwad,
Seth L. Alper,
Elsadig E. Kazzam,
Abdelouahab Bellou
Affiliations
Suhail Al-Salam
Department of Pathology, College of Medicine & Health Sciences, United Arab Emirates University, AlAin 17666, Abu Dhabi, UAE
Elhadi H. Aburawi
Department of Paediatrics, College of Medicine & Health Sciences, United Arab Emirates University, AlAin 17666, Abu Dhabi, UAE
Suleiman Al-Hammadi
Department of Paediatrics, College of Medicine & Health Sciences, United Arab Emirates University, AlAin 17666, Abu Dhabi, UAE
Sekhar Dhanasekaran
Renaissance LLC, South Brunswick Dayton, New Jersey 08810, USA
Mohamed Shafiuallah
Department of Pharmacology, College of Medicine & Health Sciences, United Arab Emirates University, AlAin 17666, Abu Dhabi, UAE
Javed Yasin
Department of Internal Medicine, College of Medicine & Health Sciences, United Arab Emirates University, AlAin 17666, Abu Dhabi, UAE
Manjusha Sudhadevi
Department of Pathology, College of Medicine & Health Sciences, United Arab Emirates University, AlAin 17666, Abu Dhabi, UAE
Aktham Awwad
Department of Laboratory Medicine, Tawam Hospital, AlAin 15258, Abu Dhabi, UAE
Seth L. Alper
Division of Nephrology and Vascular Biology Research Center, Beth Israel Deaconess Medical Center, Department of Medicine, Harvard Medical School, Boston, MA 02215, USA
Elsadig E. Kazzam
Department of Internal Medicine, College of Medicine & Health Sciences, United Arab Emirates University, AlAin 17666, Abu Dhabi, UAE
Abdelouahab Bellou
Department of Emergency Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
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.