Interleukin 17A: A Potential Target for Its Plausible Roles in the Pathogenesis of Idiopathic Epistaxis

Document Type : Original

Authors

1 Department of Medical Immunology, Afzalipour Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.

2 Department of Otolaryngology, Faculty of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

3 Immunology of Infectious Diseases Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

4 Neuroscience Research Center, Institute of Neuropharmacology, and Department of Biochemistry, Afzalipour Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.

5 Department of Laboratory Sciences, Faculty of Paramedicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

Abstract

Introduction:
It has been reported that inflammation may be a potential risk factor for the progression of epistaxis. Due to the major roles played by Th17 in the induction of inflammation, the present study aimed to assess the serum levels of Interleukin 17A (IL-17A) and IL-23, as the most important cytokines in the Th17 pathway, as well as IFN-g, IL-4, and IL-10 serum levels, as regulatory cytokines for Th17 cells in patients with idiopathic epistaxis. 
 
Materials and Methods:
The serum levels of IL-4, IL-10, IL-17A, IL-23, and IFN-g were evaluated in 90 patients with idiopathic epistaxis and 90 healthy controls using enzyme-linked immunosorbent assay (ELISA) technique.
 
Results:
The obtained results pointed out that the serum levels of IL-17A and IL-10, but not IL-4 and IL-23, were significantly up-regulated, and IFN-g serum levels were significantly down-regulated in patients with idiopathic epistaxis. Furthermore, female patients with epistaxis had higher IL-10 serum levels. 
Conclusions:
As evidenced by the results of the present study, IL-17A is the main cytokine which participates in the pathogenesis of idiopathic epistaxis; moreover, in association with IL-10, it can be regarded as the suppressor of IFN-g in patients. 

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