Abstract

IntroductionIn teenagers with perennial allergic rhinitis, exposure to tobacco cigarette smoke increases the count of eosinophils in the nasal mucosa; the recruitment of eosinophils arises from the combined action of a number of cellular and molecular signals, including eotaxin. ObjectiveTo assess the effect of exposure to tobacco cigarette smoke on the count of immunoreactive cells to eotaxin-1 and eosinophils on the nasal mucosa of children and teenagers with perennial allergic rhinitis. MethodsIn a cross-sectional study, forty-four patients were evaluated (aged 7–19 years old): 22 with and 22 with no exposure to tobacco cigarette smoke. After replying to 2 validated questionnaires, on Asthma and Allergies in Childhood and on the severity of nasal symptoms, nasal mucosal samples were obtained by scraping the middle one-third of the inferior turbinates. Then counts of immunoreactive cells to eotaxin-1 and eosinophils were assessed by immunohistochemistry. ResultsPatients with exposure to tobacco cigarette smoke showed higher cell counts of both eotaxin-1 and eosinophils than patients with no exposure to the smoke, with no correlation between the two variables. However, both counts, of eotaxin-1 and eosinophils, were related to the cotinine/creatinine ratio. ConclusionsExposure to tobacco cigarette smoke can increase eotaxin-1 and the count of eosinophils in the nasal mucosa of young patients with perennial allergic rhinitis.

Highlights

  • In teenagers with perennial allergic rhinitis, exposure to tobacco cigarette smoke increases the count of eosinophils in the nasal mucosa; the recruitment of eosinophils arises from the combined action of a number of cellular and molecular signals, including eotaxin

  • Eotaxin-1 binds with high affinity to CC chemokine receptor 3, which is expressed by a variety of inflammatory cells.4---6

  • The results of this study show evidence that compared to children and teenagers with no exposure to tobacco cigarette smoke, those with perennial allergic rhinitis

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Summary

Introduction

In teenagers with perennial allergic rhinitis, exposure to tobacco cigarette smoke increases the count of eosinophils in the nasal mucosa; the recruitment of eosinophils arises from the combined action of a number of cellular and molecular signals, including eotaxin. Allergic diseases, such as allergic asthma, allergic rhinitis and atopic dermatitis are characterized by an increased number of eosinophils in the circulating blood, and degranulation in the target tissue is considered the major pathogenic event.[1] The recruitment of eosinophils arises from the combined action of a number of cellular and molecular signals, including eotaxin.[2,3] Eotaxin-1 binds with high affinity to CC chemokine receptor 3, which is expressed by a variety of inflammatory cells.4---6. In natural conditions of disease, without nasal challenge, compared with controls, eotaxin-1 concentration in nasal lavage fluid from patients with allergic rhinitis is increased in both, the perennial and seasonal forms, and it is related to the percentage of lavage eosinophils and the severity of symptom expression.[11]

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