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