Abstract
Diesel exhaust particles (DEPs), traffic-related air pollutants, are considered environmental factors adversely affecting allergic diseases. However, the immunological basis for the adjuvant effects of DEP in allergic rhinitis (AR) remains unclear. Therefore, this study aimed to investigate the effect of DEP exposure on AR using a mouse model. BALB/c mice sensitized to house dust mite (HDM) were intranasally challenged with HDM in the presence and absence of DEP. Allergic symptom scores, serum total and HDM-specific immunoglobulins (Igs), eosinophil infiltration in the nasal mucosa, cytological profiles in bronchoalveolar lavage fluid (BALF), and cytokine levels in the nasal mucosa and spleen cell culture were analyzed. Mice co-exposed to HDM and DEP showed increased allergic symptom scores compared with mice exposed to HDM alone. Reduced total IgE and HDM-specific IgE and IgG1 levels, decreased eosinophil infiltration in the nasal mucosa, and increased proportion of neutrophils in BALF were found in mice co-exposed to HDM and DEP. Interleukin (IL)-17A level was found to be increased in the nasal mucosa of the co-exposure group compared with that in the HDM-exposed group. The levels of IL-4, IL-13, interferon-γ, IL-25, IL-33, and TSLP expression showed no difference between the groups with and without DEP treatment. Increased expression of IL-17A in the nasal mucosa may contribute to DEP-mediated exacerbation of AR in HDM-sensitized murine AR model.
Highlights
The worldwide incidence of allergic diseases such as asthma, atopic dermatitis, and allergic rhinitis (AR) has gradually increased in recent years[1]
This study evaluated the effect of co-exposure to Diesel exhaust particles (DEPs), a major airborne fine particulate pollutant, on the HDMsensitized AR mouse model
Histological analysis showed that eosinophil infiltration was decreased in the nasal tissue and the neutrophil infiltration was increased in the bronchoalveolar lavage fluid (BALF), upon co-exposure to DEP
Summary
The worldwide incidence of allergic diseases such as asthma, atopic dermatitis, and allergic rhinitis (AR) has gradually increased in recent years[1]. Among various types of air pollution, traffic-related air pollutants such as diesel exhaust particles (DEPs) are strongly linked to the development and exacerbation of allergic d iseases[4]. Epidemiological and observational studies have revealed that exposure to DEPs increases the risk for allergic d iseases[7,8,9], and even increases the morbidity and daily mortality[10,11]. Experimental studies in animal models have reported that an adjuvant effect of DEP is positively related with the exacerbation of respiratory d iseases[12,13]. The present study investigated the exacerbation of AR symptoms and the increase in expression of inflammatory cytokines caused by exposure to DEP in AR mice
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