March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Epistatic Interaction Between TLR3 And Ptger3 Genes In Experimental Allergic Conjunctivitis
Author Affiliations & Notes
  • Mayumi Ueta
    Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan
    Research Center for Inflammation and Regenerative Medicine, Faculty of Life and Medical Sciences, Doshisha University, Kyotanabe, Japan
  • Toshiyuki Matsuoka
    Ophthalmology, Tenri Yorozu Hospital, Nara, Japan
  • Shuh Narumiya
    Pharmacology, Faculty of Medicine, Kyoto University, Kyoto, Japan
  • Shizuo Akira
    Host Defense, Research Institute for Microbial Diseases,Osaka University, Osaka, Japan
  • Shigeru Kinoshita
    Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan
  • Footnotes
    Commercial Relationships  Mayumi Ueta, None; Toshiyuki Matsuoka, None; Shuh Narumiya, None; Shizuo Akira, None; Shigeru Kinoshita, None
  • Footnotes
    Support  the Japanese Ministry of Education, Culture, Sports, Science and Technology
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 3999. doi:
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      Mayumi Ueta, Toshiyuki Matsuoka, Shuh Narumiya, Shizuo Akira, Shigeru Kinoshita; Epistatic Interaction Between TLR3 And Ptger3 Genes In Experimental Allergic Conjunctivitis. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3999.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : We previously reported that conjunctival eosinophilic infiltration in murine experimental allergic conjunctivitis (EAC) was significantly less marked in TLR3 KO (knock out) mice, and significantly more marked in ptger3 KO mice than in wild-type mice. Considering the opposite roles of TLR3 and Ptger3 genes in allergic conjunctivitis, we speculate the possibility of unknown functional interaction between TLR3 and EP3, which is the protein of Ptger3 gene. In this study, we examined the functional interaction between TLR3 and EP3 using TLR3KO, Ptger3KO and TLR3/ Ptger3 double KO (DKO) mice in addition to our EAC model.

Methods: : The mice were immunized with an intracutaneous (ic) injection of RW adsorbed on alum (200 μg RW, 2.6 mg alum) into the left hind footpad on day 0. On day 7 they received an intraperitoneal (ip) injection of RW adsorbed on alum, and on day 18 their eyes were challenged with RW in PBS (500 μg in 5 μl per eye) or with PBS alone (5 μl per eye). Their eyes including the conjunctiva were harvested 24 h after the last challenge, fixed in 10% neutral buffered formalin, and embedded in paraffin blocks for histological analysis using Luna stain, which identifies erythrocytes and eosinophil granules. We compared conjunctival eosinophil infiltration in wild-type, TLR3KO, Ptger3KO and TLR3/ Ptger3DKO mice.

Results: : Although sensitization (ic and ip injection of RW) without challenge (RW eyedrop) did not affect the number of eosinophils, after sensitization and challenge their number in the lamina propria mucosae of the conjunctiva was significantly increased in all of them, and the number after sensitization and challenge in Ptger3KO mice was significantly larger, and significantly lower in TLR3KO than in wild-type mice, as we have reported previously. Furthermore, in TLR3/ Ptger3DKO, the number of eosinophils in the lamina propria mucosae of the conjunctiva was decreased to a level similar to that in TLR3KO mice, and was significantly lower than that in not only Ptger3 KO mice but also in wild-type mice.

Conclusions: : Our results suggest that EP3 negatively regulates the eosinophilic infiltration of EAC induced by TLR3, which causes reduced eosinophilic conjunctival inflammation in TLR3/ Ptger3 DKO mice, despite the pronounced eosinophilic conjunctival inflammation in Ptger3 KO mice.

Keywords: conjunctivitis • conjunctiva • inflammation 
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