Abstract

Sinonasal polyps are very common benign lesions of the nasal mucosa. Most of nasal polyps (NP) are idiopathic, and the pathophysiology of this disease is still incompletely understood. Nitric oxide (NO) is a reactive molecule generated by nitric oxide synthase (NOS). NO has been identified as an important mediator in airway function and pathogenesis of several respiratory system diseases. Histological and genetical expression of iNOS was detected to evaluate the role of NO in the pathogenesis of allergic (ANP) and nonallergic nasal polyps (NANP). Forty patients with nasal polyps (20 allergic and 20 nonallergic) were identified by history, clinical examination, and investigation. NPs were obtained from the middle turbinate (MT) during concha bullosa surgery. Twenty normal MT nasal tissues were taken as the control from patients undergoing concha bullosa surgery, without any evidence of allergy or inflammation. A nasal polyp specimen from each patient was subjected for immune-histochemical study followed by histological examination to detect the expression of iNOS. RT-PCR was used to evaluate the iNOS gene expression in isolated tissues. The expression of iNOS in both epithelial and stromal layers was greater in NP than in MT tissues. The ANP group showed more iNOS expression than those of the NANP group. The relative mRNA levels of iNOS gene were significantly higher in ANP (2.5-fold) compared to the normal (1.02-fold, P < 0.001) and NANP (1.5-fold, P < 0.01) groups. NP exhibited a significantly high expression of iNOS at both histological and genetical levels. NO might be an essential factor in the life history of NP. Further studies in a larger sample size are required to explain the probable mechanisms of NO in pathogenesis of NP.

Highlights

  • Nasal polyps (NPs) have been stated to happen in 0.5%-4% of the population, with the presence of popular asymptomatic nasal polyps (NP) in elder patients [1]

  • The Hematoxylin and Eosin (H&E) stain experiment showed that Group A, control group, has normal nasal mucosa with pseudostratified ciliated epithelium with goblet cells resting on thin basal lamina and lamina propria of loose connective tissue containing multiple blood vessels

  • Our study showed that iNOS expression was much more in NPs than normal middle turbinate (MT) tissues in both epithelial and stromal layers

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Summary

Introduction

Nasal polyps (NPs) have been stated to happen in 0.5%-4% of the population, with the presence of popular asymptomatic NPs in elder patients [1]. NPs commonly initiate from the ethmoid cells that comprise an epithelial inside layer adjacent primary edema, glandular hyperplasia, fibrosis, and eosinophilic infiltration. These are the distinguishing histological characters of NPs. The polypoid stroma is extremely edematous with a fluctuating mass of inflammatory cells. The underlying pathophysiology of NPs is left not well understood. They have long been accompanying rhinitis, acetyl salicylic acid (aspirin) sensitivity, cystic fibrosis, Kartagener’s syndrome, and bronchial asthma [2]. In the human air route, mostly the nasal mucosa, all 3 isoforms of NOS are initiated in epithelial cells [4]

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