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.

本研究旨在探究交通相关颗粒物（PM）对眼表变应性炎症的影响。实验采用卵清蛋白（OVA）联合氢氧化铝经腹腔注射致敏BALB/c小鼠。两周后，分别给予小鼠联合交通相关PM2.5的OVA滴眼剂，或仅含赋形剂的OVA滴眼剂进行激发。随后，先对小鼠单侧结膜下注射磁珠分选的CD11c+树突状细胞（DC），再实施OVA局部激发。本研究评估了以下4项指标：(1) 临床体征；(2) 结膜炎性细胞浸润情况；(3) 血清OVA特异性IgE生成水平；(4) 相较于生理盐水赋形剂组，PM2.5局部给药后的T细胞细胞因子分泌水平。实验结果显示，与赋形剂对照组相比，PM2.5处理可提升血清中OVA特异性IgE以及白细胞介素（IL）-4、IL-17A、IL-13等Th2免疫应答相关细胞因子的生成量。值得关注的是，PM2.5处理还可增加引流淋巴结（LNs）中成熟树突状细胞的数量。同时，PM2.5暴露可显著上调结膜组织中IL-1β、IL-6、IL-17及肿瘤坏死因子（TNF）的表达水平。将来自PM2.5处理的变应性结膜炎（AC）小鼠的CD11c+DCs结膜下注射至未致敏小鼠体内后，后者的T细胞应答及OVA特异性IgE水平同样得到增强。本研究数据表明，交通相关PM2.5可加重变应性结膜炎，具体表现为结膜炎性细胞浸润增多，以及与树突状细胞成熟增强相关的引流淋巴结Th2应答升高。本研究结果为交通相关PM2.5对哮喘、特应性皮炎等变应性疾病的潜在危害提供了新的见解。