To evaluate changes of the NLRP3 inflammasome complex and proinflammatory cytokine interleukin (IL)-1β in ocular tissues and cervical lymph nodes when the ocular surface was exposed to particulate matter.

Five-week-old Sprague Dawley male rats, each weighing 250–300 g, were used in this study. The rats were randomly divided into two groups involving the TiO₂-exposed group (n = 12) and control group (n = 12). Rats in the TiO₂-exposed group were exposed to airborne TiO₂ microparticles in the exposure chamber twice daily for 2 hours for 5 days. The mean particulate matter (PM) 10 concentration in the exposure chamber was 331 ± 83 µg/m³. The score of corneal fluorescein staining for evaluating ocular surface damage and the size of cervical lymph nodes for evaluating the immune response in the lymphatic drainage pathway were measured. The expression of the nucleotide-binding domain leucine-rich repeats, pyrin domain-containing 3 (NLRP3) inflammasome complex (NLRP3, apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (CARD) domain [ASC], and caspase-1) and IL-1β was quantitatively evaluated.

In the TiO₂-exposed group, the mean corneal stain score was significantly increased compared to that of the control group ( p = 0.002), and the size of the cervical lymph nodes in the TiO₂-exposed group was greater than that of the control group ( p = 0.004). The expression of NLRP3 and ASC was significantly increased in the corneo-conjunctival tissue and cervical lymph nodes after TiO₂ exposure (both, p = 0.037). Inactive precursor forms of caspase-1 and IL-1β were decreased, but active forms of caspase-1 and IL-1β were increased after TiO₂ exposure (both, p = 0.037).

When the ocular surface was exposed to ambient particulate matter, the signal pathway of the NLRP3 inflammasome complex was activated, resulting in increased expression of the proinflammatory cytokine, IL-1β. The results suggested that the NLRP3 inflammasome complex was involved in the pathogenesis of ocular surface inflammation caused by exposure to particulate matter.