Evaluation of Ocular Surface Inflammation in the Presence of Dry Eye and Allergic Conjunctival Disease

Stern, Michael E.; Siemasko, Karyn F.; Gao, Jianping; Calonge, Margarita; Niederkorn, Jérry Y.; Pflugfelder, Stephen C.

doi:10.1016/s1542-0124(12)70246-x

Cited by 32 publications

(14 citation statements)

References 11 publications

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“…In addition, statins were shown to decrease ocular surface damage in graft-versus-host disease, a T-cell mediated condition in which dry eye is a frequent complication (38). However, although T cells are also implicated in mediating development of DED (39, 40), we did not observe an association with statins in this study. Future studies of systemic medications and risk of DED would be informative.…”

Section: Discussioncontrasting

confidence: 88%

Prevalence of Dry Eye Disease Among US Men

et al. 2009

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To estimate the prevalence and risk factors for dry eye disease (DED) among US men.Methods: Cross-sectional prevalence survey among male participants 50 years and older in the Physicians' Health Studies I (N=18 596) and II (N=6848). We defined DED as the presence of clinically diagnosed dry eye or severe symptoms (both dryness and irritation constantly or often). We calculated the age-standardized prevalence of DED adjusted to the age distribution of US men in 2004 and projected estimates forward to 2030. We compared DED prevalence with a similar cohort of women and examined associations with possible risk factors. Results:The prevalence of DED increased with age, from 3.90% among men aged 50 to 54 years to 7.67% among men 80 years and older (P for trend Ͻ.001). High blood pressure (odds ratio, 1.28; 95% confidence interval, 1.12-1.45) and benign prostatic hyperplasia (odds ratio, 1.26; 95% confidence interval, 1.09-1.44) were associated with a higher risk of DED. Use of antidepressants, antihypertensives, and medications to treat benign prostatic hyperplasia were also associated with increased risk of DED. The age-standardized prevalence of DED was 4.34%, or 1.68 million men 50 years and older, and is expected to affect more than 2.79 million US men by 2030.Conclusions: Dry eye disease is prevalent and increases with age, hypertension, benign prostatic hyperplasia, and antidepressant use.

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Section: Discussioncontrasting

confidence: 88%

Prevalence of Dry Eye Disease Among US Men

et al. 2009

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“…42 Strikingly, there is increasing evidence that DE is an immune-mediated inflammatory disease that is mediated primarily by CD4þ T cells. 43,44 Also, it is generally recognized that ocular surface apoptosis as well as inflammation plays an important role in the pathogenesis of DE. 43 In our study, the percentage of CD4þ CCR5þ T cells showed a significant decrease in the NOD2-KO group compared to the EDE group.…”

Section: Discussionmentioning

confidence: 99%

Expression and Role of Nucleotide-Binding Oligomerization Domain 2 (NOD2) in the Ocular Surface of Murine Dry Eye

Jin

et al. 2019

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. To investigate expression and role of nucleotide-binding oligomerization domain 2 (NOD2) in the ocular surface of experimental dry eye (EDE), which is a nod-like receptor member and is involved in innate immune response. METHODS. C57/BL6 female mice were divided into the groups: untreated (UT), EDE, and NOD2 knockout (KO) mice exposed to desiccating stress for 14 days. Clinical parameters and levels of inflammatory cytokine were measured at 3,5,7, and 14 days. Immunofluorescent staining for NOD2 and Western blot for RIP2 and NF-jB were performed at 14 days. Flow cytometry, PAS staining and TUNEL staining were performed. RESULTS. After EDE induction, NOD2 was expressed in the corneal epithelium of the EDE group. The EDE group showed a significantly increased RIP2 expression compared to the UT and NOD2-KO groups. A significantly lower expression of NF-jB and lower levels of IL-1b, IL-6, IFN-c, and TNF-a were noted in the NOD2-KO group than in the EDE group. The NOD2-KO group had lower CD11bþ and CD4þCCR5þ T cells, TUNEL-positive cells and corneal staining score and higher density of conjunctival goblet cell density, tear volume, and tear film break-up time than the EDE group. The UT group showed significant differences in inflammatory and clinical parameters compared to the EDE and NOD2-KO groups. CONCLUSIONS. The NOD2 receptor pathway induced inflammation and apoptosis by activation of RIP2 and NF-jB on the ocular surface of EDE, thereby reducing tear secretion. Therefore, NOD2 pathway may be involved in the pathogenesis of dry eye.

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“…IFITM1, whose expression can be induced by interferon-gamma, encodes a cell surface protein known to influence cell differentiation 37. Interestingly, production of interferon-gamma at the ocular surface has been implicated in the progress of dry eye disease 38. Previous data in an experimental dry eye model suggested that interferon-gamma may affect conjunctival epithelial homeostasis and promote conjunctival squamous metaplasia 39.…”

Section: Discussionmentioning

confidence: 99%

Glycogene Expression in Conjunctiva of Patients with Dry Eye: Downregulation of Notch Signaling

Mantelli

Schaffer

Dana

et al. 2009

Invest. Ophthalmol. Vis. Sci.

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Purpose Glycoconjugates regulate a variety of biological events in mucosal surfaces, such as differentiation of postmitotic epithelial cells and maintenance of the wet-surfaced phenotype. This study aimed to identify the repertoire of genes (glycogenes) involved in biosynthesis of glycoconjugates in conjunctiva of normal subjects and dry eye patients. Methods RNA from conjunctival impression cytology samples was amplified and hybridized to a custom-designed glycogene microarray. Intensity data were converted to expression values and analyzed by ANOVA. Microarray data for selected Notch glycogenes were confirmed by quantitative real-time PCR. Notch receptors and ligands were immunolocalized on conjunctival biopsies by confocal microscopy. Results By microarray, 424 glycogenes were identified in normal conjunctival epithelium; galectins, glycosyltransferases, mucins, Notch signaling molecules, and proteoglycans were among the most highly expressed. In dry eye, 46 glycogenes were significantly downregulated, and included five members of the Notch signaling pathway (Notch1, -2, -3, Jagged1, Delta1), four Wnt signaling molecules (Wnt4, -5A, Frizzled6, -7), and three heparan sulfate glycotransferases (HS2ST1, HS3ST6, EXTL2). Only interferon-induced transmembrane protein 1 was upregulated. By real-time PCR, expression ratios of Notch1, -3, and Jagged1 in dry eye were 0.43, 0.56 and 0.50, respectively, compared to controls (p<0.05). Notch1, -3, and Jagged1 immunolocalized throughout the conjunctival epithelium, whereas Notch2 and Delta1 were distributed apically. Conclusions This study revealed the differential glycogene expression profiles in normal subjects and dry eye patients. Downregulation of Notch signaling in dry eye may result in abnormal differentiation of the conjunctival epithelium and have implications in the pathogenesis of the disease.

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Evaluation of Ocular Surface Inflammation in the Presence of Dry Eye and Allergic Conjunctival Disease

Cited by 32 publications

References 11 publications

Prevalence of Dry Eye Disease Among US Men

Prevalence of Dry Eye Disease Among US Men

Expression and Role of Nucleotide-Binding Oligomerization Domain 2 (NOD2) in the Ocular Surface of Murine Dry Eye

Glycogene Expression in Conjunctiva of Patients with Dry Eye: Downregulation of Notch Signaling

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