Purpose

We aimed to clarify the role of particulate allergen exposure to the conjunctiva in the development of allergic conjunctivitis.

Methods

We administered ragweed pollen suspension, pollen extract, pollen shell, particulate air pollutants, and their combinations to the mouse conjunctiva five days a week without prior sensitization. Clinical signs were scored. Histological changes, cellular infiltrations, mRNA expressions, lymph node cell recall responses, and serum immunoglobulin levels were assessed. Immune cell-depleting antibodies and ST2 knockout mice were used to investigate the cellular and molecular requirements.

Results

Pollen suspension, but not the extract or shell alone, induced robust eosinophilic conjunctivitis, accompanied by a proliferative response of epithelial cells. A combination of pollen extract and shell completely restored eosinophil accumulation. In addition, eosinophilic conjunctivitis was induced by a mixture of particulate air pollutants and pollen extract. Mechanistically, eosinophil accumulation was ameliorated by deficiency of the IL-33 receptor ST2 and abolished by depleting CD4⁺ T cells. Pollen shells, but not the extract, induced IL-33 release from conjunctival epithelial cells in vivo.

Conclusions

Our results indicate the non-redundant roles for the allergens’ particulate properties and soluble factors in the development of allergic conjunctivitis.

中文翻译：

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花粉壳和可溶性因子在小鼠过敏性结膜炎的发展中发挥非冗余作用

目的

我们旨在阐明颗粒状过敏原暴露于结膜在过敏性结膜炎发展中的作用。

方法

我们每周五天将豚草花粉悬浮液、花粉提取物、花粉壳、颗粒空气污染物及其组合施用于小鼠结膜，而无需事先致敏。对临床体征进行评分。评估了组织学变化、细胞浸润、mRNA 表达、淋巴结细胞回忆反应和血清免疫球蛋白水平。使用免疫细胞耗竭抗体和 ST2 敲除小鼠来研究细胞和分子需求。

结果

花粉悬浮液，而不是单独的提取物或壳，诱导强烈的嗜酸性结膜炎，伴随着上皮细胞的增殖反应。花粉提取物和壳的组合完全恢复了嗜酸性粒细胞的积累。此外，嗜酸性结膜炎是由颗粒空气污染物和花粉提取物的混合物引起的。从机制上讲，嗜酸性粒细胞的积累因 IL-33 受体 ST2 的缺乏而改善，并通过消耗 CD4 ⁺ T 细胞而消除。花粉壳诱导 IL-33 从 体内 结膜上皮细胞释放，但不是提取物。

结论

我们的结果表明过敏原的颗粒特性和可溶性因子在过敏性结膜炎的发展中具有非冗余作用。