Abstract
Purpose: :
We reported the roles of IL-33, a Th2 type-inflammation initiating cytokine, in human chronic allergic conjunctivitis (IOVS. 50:4646-52). In this study we further analyzed the pathophysiological roles of IL-33, by ragweed-induced experimental allergic (RW) conjunctivitis models and by papain-induced conjunctivitis using IL-33 knockout (KO) mice. (PNAS. 107:18581-18586)
Methods: :
RW-conjunctivitis models were made by alum-RW immunization and three times RW eye drops challenge using IL-33 KO mice (BALB/C background). 24 hours after final challenge, histological analysis was carried out to examine late phase reactions. To examine chronic phase effects of IL-33 for Th2 biased inflammation in the eye, papain-soaked soft contact lens (2mm diameter) were applied to IL-33 KO mice (C57/BL6 background) and the eye lids were sutured. 10 days after contact lens installation, histological analysis was carried out.
Results: :
RW conjunctivitis model showed that significantly reduced eosinophil infiltration in the IL-33 KO mice’s conjunctiva compared to wild-type control mice. (10.4 ± 5.2 versus 24.0 ± 4.1, mean number of eosinophil ± SD per slides) Papain conjunctivitis model also showed reduced eosinophil infiltration in the IL-33 KO mice’s conjunctiva. (59 in KO mice versus 231 in wild-type mice)
Conclusions: :
IL-33 plays essential roles for late phase allergic reaction and chronic conjunctival inflammation through facilitating eosinophil infiltration.
Keywords: conjunctivitis • inflammation