OBJECTIVE

Epidemiological studies have shown that elevated concentrations of ambient particulate matter (aerodynamic diameter ≤2.5 μm; PM2.5) correlates with increased incidence of asthma. The aim of this study was to determine whether PM2.5 participates in the exacerbation of asthma.

METHODS

Effects of 1, 10 and 100 μg PM2.5 instilled intratracheally in ovalbumin (OVA)-sensitized or asthmatic mice were compared.

RESULTS

PM2.5 exposure in the OVA-sensitized and especially asthmatic groups increased Mch responsiveness in a dose-dependent manner. In OVA-sensitized groups, exposure to 1 μg of PM2.5 caused no detectable lung inflammation, while 10 and 100 μg of PM2.5 resulted in a slightly increased trend in numbers of neutrophils and macrophages. Compared with the asthmatic control group, both 10 and 100 μg of PM2.5 provoked a significant increase in eosnophils and neutrophils whereas only 100 μg of PM2.5 noticeably enhanced lymphocytes. In asthmatic groups, administration of 100 μg of PM2.5 greatly increased levels of the pro-inflammatory cytokine TNF-α and Th2-related cytokines IL-4 and IL-10 in bronchoalveolar lavage fluid, but it decreased Th1-related INF-γ. In addition, 10 and 100 μg of PM2.5 exacerbated inflammatory infiltration, goblet cell metaplasia and lung ultrastructure lesions in asthmatic mice.

CONCLUSIONS

Our results suggested that acute exposure of PM2.5 could synergize with allergens in the subsequent challenge to aggravate the severity of asthma in sensitized mice, possibly by promoting a Th2-biased immune response.