Traffic-related particulate matter aggravates ocular allergic inflammation by mediating dendritic cell maturation.

The aim of this study was to determine the effects of traffic-related particulate matter (PM) on allergic inflammation of ocular surfaces. BALB/c mice were sensitized with ovalbumin (OVA) and aluminum hydroxide via intraperitoneal injection. Two weeks later, mice were challenged with eye drops containing OVA concomitant with either traffic-related PM2.5 or vehicle eye drops. Topical OVA challenges were administered following unilateral subconjunctival injection of magnetic-bead-sorted CD11c+ dendritic cells (DC). The following were assessed: (1) clinical signs, (2) infiltration of inflammatory cells into conjunctiva, (3) serum levels of OVA-specific IgE production, and (4) T-cell cytokine secretion with topical application of PM2.5, compared to saline vehicle. PM2.5 was found to increase production of OVA-specific IgE in serum and Th2 immune response-related cytokines including interleukin (IL)-4, IL-17A, and IL-13 compared to vehicle control. It is of interest that PM2.5 treatment also elevated the population of mature DCs in draining lymph nodes (LNs). Exposure with PM2.5 was associated with a significant rise in conjunctival expression of IL-1β, IL-6, IL-17, and TNF. After subconjunctival injection of CD11c+DCs from PM2.5-treated allergic conjunctivitis (AC) mice into naïve mice, T cell responses and OVA-specific IgE were also enhanced. Data suggest that traffic-related PM2.5 exacerbated allergic conjunctivitis as evidenced by increased infiltration of inflammatory cells into the conjunctiva and Th2 responses in the draining LNs associated with enhanced maturation of DCs. Our findings provide new insight into the hazardous potential of traffic-related PM2.5 on allergic diseases, such as asthma or atopic dermatitis.