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Increased expression of VEGF, iNOS, IL-1β, and IL-17 in a rabbit model of gastric content-induced middle ear inflammation

Abstract Objective To investigate the histopathological changes and the expression of vascular endothelial growth factor (VEGF), inducible NO-synthase (iNOS), endothelial NO-synthase (eNOS), interleukin (IL)-1β, and IL-17 in the rabbit middle ear mucosa after direct gastric content exposure. Methods...

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Published in:International journal of pediatric otorhinolaryngology 2012-01, Vol.76 (1), p.64-69
Main Authors: Başoğlu, M. Sinan, Eren, Erdem, Aslan, Hale, Kolatan, H. Efsun, Özbay, Can, İnan, Sevinç, Karaca, Fatma, Öztürkcan, Sedat, Katılmış, Hüseyin
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Language:English
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Summary:Abstract Objective To investigate the histopathological changes and the expression of vascular endothelial growth factor (VEGF), inducible NO-synthase (iNOS), endothelial NO-synthase (eNOS), interleukin (IL)-1β, and IL-17 in the rabbit middle ear mucosa after direct gastric content exposure. Methods Exploratory controlled study in which histological and immunochemical features were studied after gastric content-induced inflammation was established in rabbits. Sixteen healthy rabbits were divided into two equal groups. Gastric contents of an animal were injected into the middle ear of the same animal for 20 days. Saline was injected into the middle ear of the animals in the control group. The rabbits were humanely killed on day 27. Inflammation was assayed by light microscopy. Immunochemical staining was performed for VEGF, iNOS, eNOS, IL-1β, and IL-17 expression. Experimental and control animals were examined using the same protocol. Results The expression levels of VEGF, iNOS, IL-1β, and IL-17 differed significantly between the experimental and control groups ( p = 0.018, p = 0.010, p = 0.002, and p = 0.002, respectively). The expression level of eNOS was not significantly different between the two groups ( p = 0.132). Conclusion This study demonstrates that gastroesophagial reflux induced middle ear inflammation is associated with increased expression of VEGF, IL-1β, IL-17, and iNOS.
ISSN:0165-5876
1872-8464
DOI:10.1016/j.ijporl.2011.10.001