PM2.5 suppresses IL-8-mediated epithelial migration of human conjunctival epithelial cells
Chueh-Tan Chen, Zhi-Hu Lin, Tung-Yi Lin, Sang-Nguyen-Cao Phan, Hsin Yeh, Wei-Ting Lin, Yue-Ling Li, Ching-Yao TsaiBackground:
Fine particulate matter (PM2.5) is a major component of ambient air pollution and is a significant environmental health concern. The conjunctiva is continuously exposed to airborne pollutants but the direct effects of PM2.5 on conjunctival epithelial repair remain poorly understood. This study investigated whether PM2.5 disrupts conjunctival epithelial homeostasis and examined the functional role of interleukin-8 (IL-8) in this process.
Methods:
Immortalized human conjunctival epithelial cells (IM-HConEpiC) were exposed to PM2.5. Cell viability, apoptosis, epithelial migration, inflammatory mediators and cytokine profiles were evaluated using biochemical, functional and cytokine array analyses. The functional role of IL-8 was also determined using recombinant IL-8 supplementation and neutralization assays.
Results:
PM2.5 exposure reduced conjunctival epithelial cell viability in a time- and concentration-dependent manner and induced mild apoptotic responses. More importantly, PM2.5 markedly impaired epithelial migration and wound closure. Cytokine profiling revealed that PM2.5 selectively remodeled inflammatory mediators, rather than eliciting a generalized inflammatory response. IL-8 was identified as the most prominently suppressed cytokine. Functional gain- and loss-of-function studies identified IL-8 as a key regulator of conjunctival epithelial repair. Specifically, recombinant IL-8 significantly restored PM2.5-induced impairment of epithelial migration and partially rescued the reduction in cell viability, whereas neutralization of endogenous IL-8 impaired epithelial migration under basal conditions, supporting a critical role for IL-8 in maintaining conjunctival epithelial homeostasis.
Conclusion:
PM2.5 compromises conjunctival epithelial homeostasis, primarily by impairing epithelial repair, rather than inducing extensive cell death. This study identified IL-8 as an important regulator of conjunctival epithelial repair and suggests that suppression of IL-8 contributes to PM2.5-induced conjunctival dysfunction.