Allergic inflammatory responses induced by traffic-related PM2.5  in BALB/c mice

Abstract

Previous studies have shown that PM2.5 is associated with airway inflammation and lung injury. However, the association between traffic-related PM2.5 (TR-PM) exposure and OVA-induced allergic inflammation is not fully elucidated. In this study, we assessed allergic inflammatory responses of mice induced by TR-PM. PM2.5 was collected from a roadside with heavy traffic, and its soluble extract was prepared. Mice were treated with OVA, TR-PM alone, and OVA + TR-PM. The inflammatory cells were counted, and inflammation-related cytokines IL-4, IL-17A, and IL-10 in bronchoalveolar lavage fluid (BALF) were determined by the radioimmunity assay. Allergy-induced inflammation and lung injury were investigated by histopathological analyses. The expression of IL-4, IL-17A, and IL-10 mRNA was analyzed by RT-PCR. Our results revealed that TR-PM exposure, combined with OVA allergen sensitization, increased the inflammatory cells in BALF as well as levels of IgE in lung tissue; increased the IL-4 and IL-17A levels in BALF significantly, but decreased IL-10 level. The histopathologic results demonstrated that TR-PM markedly exacerbated the OVA-induced neutrophilic granulocyte, lymphocyte, and macrophage infiltration. Furthermore, the expression of IL-4, IL-17A and IL-10 mRNA was well in agreement with the results of the inflammatory cytokines. In conclusion, during the sensitization to allergic antigens, TR-PM exposure triggers severe allergic inflammation and lung injury. These findings suggest that commuters should use public transportation instead of riding motorcycles or walking during rush hours.