Bronchial Interleukin-5 and Eotaxin Expression in Nasal Polyposis

Abstract

An eosinophilic bronchial inflammation was previously demonstrated in patients with nasal polyposis (NP) and asymptomatic bronchial hyperresponsiveness (BHR) similar to that observed in asthmatic patients with NP, whereas patients with NP without BHR did not. The aim of the study was to investigate the contribution of interleukin 5 (IL-5) and eotaxin to the pathogenesis of BHR associated with NP. Eleven patients with NP without BHR (Group A), 8 patients with NP and asymptomatic BHR (Group B), and 9 patients with NP and asthma (Group C) were included. Bronchial biopsies were studied for IL-5 and eotaxin immunoreactivity and IL-5 mRNA expression. IL-5 levels were determined in bronchial lavage (BL). Compared with Groups A and B, Group C patients exhibited higher numbers of IL-5 protein(+) cells, IL-5 mRNA(+) cells, and eotaxin(+) cells in bronchial submucosa. Compared with Group A, Group B patients showed an increased number of IL-5 protein(+) cells, whereas the number of IL-5 mRNA(+) cells and eotaxin(+) cells was similar. IL-5 levels in BL were increased only in Group C. Our study provides evidence of IL-5 involvement in bronchial eosinophilia and in the pathogenesis of asymptomatic BHR associated with NP, whereas both IL-5 and eotaxin are involved in asthma associated with NP.

Exhaled Nitric Oxide Levels and Airway Responsiveness to Adenosine 5′-Monophosphate in Subjects with Nasal Polyposis

“…One possibility is that it reflects the presence of subclinical inflammation within the lower airways. This explanation is supported by data from histopathological studies that demonstrate the presence of bronchial inflammation in nonasthmatic subjects with nasal polyposis [3, 4]. However, the relationship between ENO levels and histologic markers of bronchial inflammation has not been studied in subjects with nasal polyposis.…”

“…Nasal polyposis and asthma are related diseases [2], and studies have identified that nasal polyposis may be a risk factor for subsequent development of asthma [37]. Subclinical inflammation in the lower airways has been reported in some nonasthmatic subjects with nasal polyposis [3, 4]. If ENO measurement is a sensitive method of monitoring airway inflammation, it is tempting to speculate that the presence of increased ENO concentrations in subjects with nasal polyposis represents a latent phase of asthma.…”

“…Although the association between nasal polyposis and asthma is well established [2], the pathophysiology of this disease remains poorly understood. However, recent investigations have indicated that some patients with nasal polyposis, but no history of asthma, exhibit inflammation in bronchial lavage fluid and bronchial biopsy specimens [3, 4]. These findings suggest that nasal polyposis and asthma are linked by a common process that is mainly inflammatory in nature.…”

Water-soluble chitosan-based antisense oligodeoxynucleotide of interleukin-5 for treatment of allergic rhinitis

“…According to previous studies, cytokines derived from Th2 cells, which include IL-5 are involved in IgE synthesis and allergic inflammation. Recently, IL-5 has been shown to be involved in allergic inflammation and airway hypersensitiveness [26,38]. In addition, IgE has also been implicated in development of allergic disease and recruitment or accumulation of inflammatory cells such as eosinophils [39,40].…”

The Role of CC Chemokines in Chronic Sinusitis

“…Atopic and nonatopic asthma seem to be associated with combined bronchial mucosal expression of CC chemokines (RANTES, eotaxin), together with eosinophilactive cytokines (IL-5, GM-CSF, IL-3) [29,58]. These cytokines may contribute either to the nasal or to the bronchial mucosal accumulation of eosinophils.…”