September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
The roles of IL-33 in ragweed-induced experimental allergic conjunctivitis with lacrimal gland excision
Author Affiliations & Notes
  • Yosuke Asada
    Laboratory of Ocular Atopic Diseases, Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan
    Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science,, The University of Tokyo, Tokyo, Japan
  • Susumu Nakae
    Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science,, The University of Tokyo, Tokyo, Japan
  • Jobu Sugita
    Laboratory of Ocular Atopic Diseases, Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan
    Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science,, The University of Tokyo, Tokyo, Japan
  • Nobuyuki Ebihara
    Department of Ophthalmology, Juntendo Urayasu Hospital, Chiba, Japan
  • Akira Matsuda
    Laboratory of Ocular Atopic Diseases, Department of Ophthalmology, Juntendo University School of Medicine, Tokyo, Japan
  • Footnotes
    Commercial Relationships   Yosuke Asada, None; Susumu Nakae, None; Jobu Sugita, None; Nobuyuki Ebihara, None; Akira Matsuda, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 306. doi:
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    • Get Citation

      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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      © 2017 Association for Research in Vision and Ophthalmology.

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Abstract

Purpose : 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.

Methods : 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.

Results : 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.

Conclusions : 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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