Cornea - ARVO

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ARVO 2013 Annual Meeting Abstracts by Scientific Section/Group - CorneaAssociate Principal Researcher Department of Ophthalmology CheilEye Research Institute Cheil Eye HospitalCommercial Relationships: Yeoun-Hee Kim, None; Young JeungPark, None; Sun-Hee Kang, None; Jae-Chang Jung, None; KyooWon Lee, NoneProgram Number: 2079 Poster Board Number: D0218Presentation Time: 11:00 AM - 12:45 PMTopical Cyclosporine A for the Management of ChronicFollicular ConjunctivitisNatasha V. Nayak 1 , Anton M. Kolomeyer 1 , Jason S. Kim 2 , Eliott S.Kim 2 , Christina Fang 1 , David S. Chu 1, 2 . 1 Institute of Ophthalmologyand Visual Science, University of Medicine and Dentistry of NJ,Newark, NJ; 2 Metropolitan Eye Research & Surgery Institute,Palisades Park, NJ.Purpose: To describe the use of Cyclosporine A (CsA) in patientswith chronic follicular conjunctivitis (CFC).Methods: This study was a retrospective chart review at a tertiarycare center. Patients treated with topical CsA (1% emulsion) foridiopathic CFC between August 2001 and November 2012 wereincluded. Biopsies were performed. Main outcome measures includedtime to reduced inflammation, final grade of inflammation (0-4;grading performed by one physician [DSC]), ability to taper steroids,final visual acuity (VA), and reported side effects. Unless otherwisenoted, mean ± standard deviation (SD) were reported.Results: Twenty-two eyes of 13 patients (nine [69%] females; 12[92%] Caucasians; age of 49.5 ± 14.7 years) met study criteria. Two(15%) patients had an associated autoimmune disease (Sarcoidosisand Hashimoto’s thryroiditis/Sjogren’s syndrome). Mean follow-uptime was 233 days (range, 33-887 days). CsA was initiated 50.6 days± 46.9 days after diagnosis. Six (46%) patients ended CsA use after182.2 ± 95.0 days, in all cases after inflammation was controlled. Theremaining seven (54%) patients have ongoing management with CsA(currently for 278.9 ± 206.1 days). Final grade of inflammation (0.2 ±0.4) was improved compared to initial grade of inflammation (2.1 ±1.0) [two-tailed t-test, p-value < 0.0001]. Inflammation wascontrolled on average 40.1 ± 23.1 days (range, 5-84 days) afterinitiation of CsA. Eleven (85%) patients tapered and eventuallydiscontinued topical steroids 31.5 ± 27.9 days after initiation of CsAtreatment. One patient required re-initiation of topical steroids threemonths after initial discontinuation secondary to a flare up. Meaninitial log MAR VA for right and left eyes was 0.090 and 0.067,respectively, whereas mean final VA was 0.089 and 0.028. Three(23%) patients reported mild ocular irritation and/or burning;however, none discontinued the eye drops.Conclusions: Management of CFC with topical CsA resulted ininflammation control and allowed for steroid taper in the majority ofpatients without severe complications. Most patients require longtermCsA treatment.Commercial Relationships: Natasha V. Nayak, None; Anton M.Kolomeyer, None; Jason S. Kim, None; Eliott S. Kim, None;Christina Fang, None; David S. Chu, Abbott (F), Novartis (F),Santen (F), Eyegate (F), Lux Biosciences (F), Bausch & Lomb (R)Program Number: 2080 Poster Board Number: D0219Presentation Time: 11:00 AM - 12:45 PMSuppression of TLR3-Inducible Gene Expression by EP3 inConjunctival EpitheliumMayumi Ueta 1, 2 , Shuh Narumiya 3 , Shigeru Kinoshita 1 .1 Ophthalmology, Kyoto Prefectural Univ of Medicine, kyoto, Japan;2 Research Center for Inflammation and Regenerative Medicine,Faculty of Life and Medical Sciences, Doshisha University,kyotanabe, Japan; 3 Department of Pharmacology and Faculty ofMedicine, Kyoto University, kyoto, Japan.Purpose: We previously reported that prostaglandin E receptor 3(EP3) negatively regulates the eosinophilic infiltration of murineexperimental allergic conjunctivitis induced by toll-like receptor 3(TLR3), which causes reduced eosinophilic conjunctivalinflammation in TLR3/EP3 double knockout (DKO) mice, despitethe pronounced eosinophilic conjunctival inflammation in EP3 KOmice. It was also reported that EP3 was dominantly expressed inepithelial cells such as conjunctival epithelial cells, airway epithelialcells, and keratinocytes. In this study, to examine the effects of EP3against TLR3-inducible gene expression in conjunctival epithelium,we performed gene expression analysis of polyinosinic:polycytidylicacid (polyI:C)-stimulated murine conjunctival epithelium in wildtype(WT)-, EP3-, and EP3/TLR3 DKO mice.Methods: First, we examined the comprehensive effects of geneexpression in polyI:C-stimulated murine conjunctival epithelium ofWT mice using GeneChip® oligonucleotide microarrays. Then, tofind the transcript regulated by EP3, we compared the geneexpression of the transcripts, which were significantly and more than3-fold upregulated, in polyI:C-stimulated conjunctival epitheliumbetween WT and EP3 KO mice by quantitative reverse transcriptionpolymerase chain reaction (RT-PCR).Results: GeneChip® analysis showed that 131 transcripts wereupregulated more than 3-fold and that 31 transcripts were upregulatedmore than 10-fold upon polyI:C stimulation of murine for 6 hours.Quantitative RT-PCR findings confirmed that 21 of 31 transcriptswere significantly and more than 3 fold upregulated upon polyI:Cstimulation in murine conjunctival epithelium. All of those 21transcripts were found to be expressed in the polyI:C-stimulatedconjunctival epithelium of EP3 KO mice significantly stronger thanin that of WT mice. Moreover, mRNA expression of those 21transcripts were confirmed to be significantly reduced in the polyI:Cstimulatedconjunctival epithelium of EP3/TLR3 DKO mice than inthat of EP3 KO mice.Conclusions: EP3 suppressed the TLR3-inducible genes in polyI:Cstimulatedconjunctival epithelium, which causes reduced geneexpression in the conjunctival epithelium of TLR3/EP3 DKO mice,despite the pronounced gene expression in the conjunctivalepithelium of EP3 KO mice.Commercial Relationships: Mayumi Ueta, None; Shuh Narumiya,ONO Pharmaceuticals (F); Shigeru Kinoshita, Senju PharmaceuticalCo (P), Santen Pharmaceutical Co (P), Otsuka Pharmaceutical Co(C), Alcon (R), AMO (R), HOYA (R)Support: Japanese Ministry of Education, Culture, Sports, Scienceand TechnologyProgram Number: 2081 Poster Board Number: D0220Presentation Time: 11:00 AM - 12:45 PM©2013, Copyright by the Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Go to iovs.org to access the version of record. For permissionto reproduce any abstract, contact the ARVO Office at arvo@arvo.org.
ARVO 2013 Annual Meeting Abstracts by Scientific Section/Group - CorneaModel of allergic keratoconjunctivitis - Stat6 signaling in chronicinflammationMichael Conwell 1 , Sonia DaSilva-Arnold 2 , Na Luo 1 , Wei Li 3 , JefferyTravers 2 , Yang Sun 1, 2 . 1 Ophthalmology, Glick Eye Institute,Indianapolis, IN; 2 Dermatology, Indiana University, Indianapolis, IN;3 Xiamen Eye Institute, Xiamen University, Xiamen, China.Purpose: The purpose of this study is to characterize the cornealinflammatory lesions found in the Stat6VT mouse as a model foratopic dermatitis. We hypothesize that the constitutive activation ofStat6 results in corneal neovascularization and pannus formation.Methods: SKH1-HrHr wild-type mice and mice which express anintegrally active Stat6 (Stat6VT), V547A/T548A, (N=20, 24respectively) where examined for the development ofkeratoconjunctivitis. Corneas were removed and examined by H&Eand PAS staining. Immunoblot analysis was performed withInterleukin-4, Interferon gamma, and CD3. Steroid treatment withclobetasol was performed on affected lesions.Results: Compared to wild-type, Stat6VT transgenic mice exhibitedincreased frequency of corneal neovascularization (N=24, P
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