Abstract

ObjectiveCigarette smoke (CS) exposure reportedly enhances allergic airway inflammation. However, some studies have shown an association between current cigarette smoke exposure and a low risk for allergic rhinitis. Thus, the impact of CS exposure on allergic rhinitis remains poorly understood. The purpose of this study was to investigate the effects of CS on the respiratory mucosa (RM) and the olfactory epithelium (OE) of mice with allergic rhinitis, as the effects may differ depending on the nasal histological compartments.MethodsEight-week-old male BALB/c mice were used for this study. We developed a mouse model of smoking by intranasally administering 10 doses of a CS solution (CSS), and a mouse model of allergic rhinitis by sensitization with intraperitoneal ovalbumin (OVA) injection and intranasal challenge with OVA. We examined the effects of CS on the nasal RM and OE in mice with or without allergic rhinitis using histological, serum, and genetic analyses. First, we examine whether CSS exposure induces allergic responses and then, examined allergic responses in the OVA-sensitized allergic rhinitis mice with or without CSS exposure.ResultsShort-term CSS administration intensified allergic responses including increased infiltration of eosinophils and inflammatory cells and upregulation of interleukin-5 expression in the nasal RM of OVA-immunized mice, although only CSS induced neither allergic responses nor impairment of the RM and OE. Notably, repetitive OVA-immunization partially impaired the OE in the upper-lateral area, but CSS administration did not reinforce this impairment in OVA-induced allergic mice.ConclusionShort-term CSS exposure strengthened allergic responses in the nasal RM and did not change the structure of the OE. These results suggest that patients with allergic rhinitis could experience exacerbation of allergic symptoms after CS exposure.

Highlights

  • Allergy is a predisposing factor for multiple respiratory conditions including allergic rhinitis and asthma (Gelber et al, 1993; Monico et al, 2019)

  • We examined the effect of 10 doses of CS solution (CSS) intranasal administration on the nasal respiratory mucosa (RM) and olfactory epithelium (OE)

  • As the olfactory receptor neurons (ORNs) in the OE differ according to their zonal expression patterns, in the present study, we investigated the number of ORNs in the OE of three different areas; nasal septum (NS), named “upper-lateral area“ (UL), and “uppermost-lateral area” (UML) (Figure 6A-a)

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Summary

Introduction

Allergy is a predisposing factor for multiple respiratory conditions including allergic rhinitis and asthma (Gelber et al, 1993; Monico et al, 2019). Cigarette smoke (CS) is a risk factor of developing allergic diseases, mediated by excessive immune responses to various allergens, and impacts the immune system (Mehta et al, 2008). Smoking has been recognized as a cause of acute eosinophilic pneumonia (AEP), which can occur within a few weeks or months of initiating smoking or even as a result of passive smoking exposure (De Giacomi et al, 2017). This may imply that smoking can amplify allergic responses, as eosinophilia is strongly associated with allergy. The effects of smoking on allergic rhinitis have been mainly discussed and verified on the serum level and in in vitro studies, and the influence of cigarette-smoke exposure on allergic rhinitis is not entirely understood; in vivo studies are indispensable to elucidate the effects of smoking on allergic responses in the nasal mucosa

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