Diesel exhaust particles increase nasal symptoms and IL-17A in house dust mite-induced allergic mice

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.

Effect of Airborne Particulate Matter on the Immunologic Characteristics of Chronic Rhinosinusitis with Nasal Polyps

“…It has long been noted that PM can produce an inflammatory response in airways. PM has been shown to induce the expression of several pro-inflammatory cytokines, including TNF-α, IFN-γ, IL-1, IL-6, IL-8, and IL17A by neutrophils, macrophages, and epithelial cells in the airway [14][15][16]. One recent study also revealed that IL-32 induced by Asian sand dust is known to play an important role in the late stages of chronic inflammatory airway diseases [17].…”

Immunologic, genetic, and ecological interplay of factors involved in allergic diseases

“…The effect of pollution on allergy pathogenesis manifests in different ways—through the accumulation of reactive oxygen species leading to oxidative stress, enhancement of Th2 responses, upregulation of IgE production, eosinophilia, and impaired mucosal barrier function. Firstly, Jung et al highlighted in their study the impact of environmental pollutants such as diesel exhaust particles, showing that exposure led to increased levels of the proinflammatory cytokine, IL-17, and worsened disease outcomes ( 77 ). Particulate matter and other air pollutants, which are known to carry microbes and viruses from the environment, found in haze are associated with house dust mite allergic sensitization.…”

Biological impact of sequential exposures to allergens and ultrafine particle‐rich combustion aerosol on human bronchial epithelial BEAS‐2B cells at the air liquid interface

“…We recently showed that the cellular inflammatory response to whole birch pollen was induced faster in human bronchial epithelial cells pre‐treated to diesel exhaust (Candeias et al, 2022). Jung et al (2021) similarly observed that coexposure to house dust mite extract (HDME) and diesel exhaust particles (DEP) caused an increase in symptoms of allergic rhinitis with neutrophils infiltration in the lungs and increased interleukin (IL‐)17A levels in the nasal mucosa of HDME‐induced allergic BALB/c mice. Additionally, Weng et al (2018) observed a similar adjuvant effect of DEP in primary bronchial epithelial cells from patients with severe asthma, with an activation of aryl hydrocarbon receptor (AhR) leading to the upregulation of IL‐33, IL‐25, and thymic stromal lymphopoietin (TSLP).…”