Ophthalmology Department, Zhongnan Hospital of Wuhan University, Wuhan, China.
School of Resource and Environmental Sciences, Wuhan University, Wuhan, China.
Exp Eye Res. 2024 Aug;245:109956. doi: 10.1016/j.exer.2024.109956. Epub 2024 Jun 6.
Exposure to particulate matters in air pollution of 2.5 μm or less (PM) was associated with loss of meibomian glands. The aim of this study was to verify that PM could directly impact meibomian gland epithelial cells and damage their function. To investigate the impact of PM on meibomian gland, immortalized human meibomian gland epithelial cells were treated with various concentrations of PMin vitro. Meibomian gland cell microstructure, cell viability, expression of proliferating cell nuclear antigen and IL-1β, and intracellular accumulation of acidic vesicles were measured by transmission electron microscopy, cell counting, Western blot and LysoTracker staining, respectively. To further study the effect of PMin vivo, male C57BL/6J mice were treated with 5 mg/ml PM or vehicle for 3 months. Corneal fluorescein staining and ocular examinations were done before and after the treatment. Eyelids tissues were processed for morphological studies, immunostaining and Oil Red O staining. Our data suggest that exposure to PM caused significant meibomian gland dropout, clogged gland orifice and increased corneal fluorescein staining that were consistent with the clinical presentations of meibomian gland dysfunction. Prominent changes in the morphology and ultrastructure of meibomian glands was observed with PM treatment. PM promoted ductal keratinization, inhibited cell proliferation, induced cell apoptosis and increased Interleukin-1β production in meibomian gland epithelial cells. This study may explain the association between PM exposure and meibomian gland dropout observed in clinic. PM resuspension instillation could be used to induce a meibomian gland dysfunction animal model.
空气污染中 2.5μm 或更小粒径的颗粒物(PM)暴露与睑板腺丧失有关。本研究旨在验证 PM 是否可以直接影响睑板腺上皮细胞并损害其功能。为了研究 PM 对睑板腺的影响,我们在体外用人永生化的睑板腺上皮细胞处理不同浓度的 PM。通过透射电子显微镜、细胞计数、Western blot 和 LysoTracker 染色分别测量睑板腺细胞的超微结构、细胞活力、增殖细胞核抗原和 IL-1β的表达以及酸性囊泡的细胞内积累。为了进一步研究 PM 的体内作用,雄性 C57BL/6J 小鼠用 5mg/ml PM 或载体处理 3 个月。治疗前后进行角膜荧光素染色和眼部检查。处理眼睑组织进行形态学研究、免疫染色和油红 O 染色。我们的数据表明,暴露于 PM 会导致明显的睑板腺丧失、腺体口堵塞和角膜荧光素染色增加,这与睑板腺功能障碍的临床表现一致。PM 处理后观察到睑板腺形态和超微结构的明显变化。PM 促进了导管角化、抑制了细胞增殖、诱导了细胞凋亡,并增加了睑板腺上皮细胞中白细胞介素-1β的产生。这项研究可能解释了临床观察到的 PM 暴露与睑板腺丧失之间的关联。PM 再悬浮滴注可用于诱导睑板腺功能障碍动物模型。