Studying the Serum as Well as Serous Level of IL-17 and IL-23 in Patients with Serous Otitis Media

  • Ahmad Yeghaneh Moghaddam Department of ENT, Kashan University of Medical Sciences, Kashan, Iran
  • Rezvan Talaei Autoimmune Research Center, Kashan University of Medical Sciences, Kashan, Iran
  • Hassan Nikoueinejad Department of Immunology, Baqiyatallah University of Medical Sciences, Tehran, Iran AND Nephrology and Urology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
  • Hossein Akbari Trauma Research center, Kashan University of Medical Sciences, Kashan, Iran
Keywords: Interleukin 17, Interleukin 23, Otitis media with effusion

Abstract

Serous otitis media with effusion (OME) is a middle ear inflammatory response to allergens and microbes which stimulate leukocytes to produce different inflammatory mediators after obstruction of Eustachian tube. Here, we investigated the levels of these mediators, IL-17 and IL-23, in serum and middle ear fluids of children with OME. 75 patients with otitis media and 75 age and sex-matched healthy controls were enrolled in this study. IL-17 and IL-23 levels in serous secretion of the patients and their serum levels were measured in both groups by ELISA. Serum IL-17 levels were significantly higher in the patients than controls (p=0.001). There was no significant difference between serum IL-23 levels in patients and controls. Patients’ serous levels of both cytokines of IL-17 and IL-23 were higher than those in serum according to different parameters of sex, age, and duration of the disease. This study shows an elevated presence of IL-17 and IL-23, as pro inflammatory cytokines, in OME. These finding may represent the contribution of such cytokines in the pathogenesis of OME. Blocking such molecules may yield new non-surgical therapeutics. 

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Published
2017-12-23
How to Cite
1.
Yeghaneh Moghaddam A, Talaei R, Nikoueinejad H, Akbari H. Studying the Serum as Well as Serous Level of IL-17 and IL-23 in Patients with Serous Otitis Media. ijaai. 16(6):520-4.
Section
Original Article(s)