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Yosuke Asada, Susumu Nakae, Jobu Sugita, Nobuyuki Ebihara, Akira Matsuda; The roles of IL-33 in ragweed-induced experimental allergic conjunctivitis with lacrimal gland excision. Invest. Ophthalmol. Vis. Sci. 2016;57(12):306.
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© ARVO (1962-2015); The Authors (2016-present)
Group 2 innate lymphoid cells (ILC2s) produce large amounts of Th2 cytokines in response to IL-33 and induce eosinophil infiltration. We previously reported the essential roles of IL-33 in ragweed(RW)-induced experimental allergic conjunctivitis (EAC), and identified existence of ILC2s in lacrimal glands (LG) (ARVO2014). To clarify possible roles of LG-derived ILC2 in RW-EAC, we made RW-EAC with LG excision.
LG excision was performed unilaterally on 8-week-old female BALB/C-IL-33 deficient and BALB/C wild-type mice. The mice were sensitized with RW in alum, and then challenged 4 times with RW eye drops. 24 hours after the last challenge, the conjunctivae were collected for histological analyses, cytokine expression analysis by realtime PCR.
Significant attenuation of the numbers of infiltrating eosinophils was observed in the RW-EAC models using IL-33 deficient mice compared to wild type mice, however, there was no significant change of eosinophil infiltration by LG excision. Histological examination revealed augmented epithelial cell defects and inflammatory cell infiltration in the ocular surface of the LG-excised RW-EAC models using IL-33 deficient mice compared to those of wild-type mice.
Contrary to our hypothesis, LG excision did not attenuate the severity of RW-EAC. Moreover, IL-33 deficiency exacerbates ocular surface damage due to RW-EAC with LG excision.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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