The core mechanism of dry eye disease is inflammation

Research output: Contribution to journalReview article

66 Citations (Scopus)

Abstract

Purpose: The purpose of this article is to review the evidence for the hypothesis that the core mechanism of dry eye disease (DED) is inflammation, including evidence from recent basic, clinical, and translational research involving human patients, animal models, and cell cultures. Methods: Using the key words "dry eye + inflammation, " the authors conducted a comprehensive search of the PubMed and Web of Science databases for scientific articles published in English between January 1, 1900 and August 30, 2013 on the role of inflammation in DED in cell cultures, animal models, and humans. The resulting articles were then categorized and reviewed. Results: The literature search revealed a total of 458 publications, almost all published after 1992. The percentages of original studies and review articles are 77.29% (354) and 22.71% (104), respectively. Among the original studies, the number of reports on human DED is 200 (43.7%), on animal models is 115 (25.1%), and cell cultures is 39 (8.5%). A yearly distributing plot revealed that 76% were published from 2003 to 2011, 53% from 2008 to 2012, and 11% during the first 9 months of 2013. This distribution signifies a rapidly growing awareness of the importance of inflammation in DED pathogenesis. Conclusions: Inflammation plays a key role in the pathogenesis of DED as evidenced by research using tissue culture, animal models, and subjects with DED. Developing biomarkers for inflammation of the ocular surface will provide improved understanding of the mechanisms leading to DED, classification of the severity of DED, and objective metrics for outcome measures of treatment. The chronicity of the disease suggests that dysregulation of immune mechanisms leads to a cycle of continued inflammation, accompanied by alterations in both innate and adaptive immune responses. Given the underlying mechanism for DED, developing effective and safe antiinflammatory treatments is likely to be beneficial for patients with DED.

Original languageEnglish (US)
Pages (from-to)248-256
Number of pages9
JournalEye and Contact Lens
Volume40
Issue number4
DOIs
StatePublished - Jan 1 2014

Fingerprint

Eye Diseases
Inflammation
Animal Models
Cell Culture Techniques
Translational Medical Research
Adaptive Immunity
PubMed
Innate Immunity
Publications
Anti-Inflammatory Agents
Biomarkers
Outcome Assessment (Health Care)
Databases

All Science Journal Classification (ASJC) codes

  • Ophthalmology

Cite this

The core mechanism of dry eye disease is inflammation. / Wei, Yi; Asbell, Penny.

In: Eye and Contact Lens, Vol. 40, No. 4, 01.01.2014, p. 248-256.

Research output: Contribution to journalReview article

@article{7136f1ce16ef4401afc9ffd6781037ff,
title = "The core mechanism of dry eye disease is inflammation",
abstract = "Purpose: The purpose of this article is to review the evidence for the hypothesis that the core mechanism of dry eye disease (DED) is inflammation, including evidence from recent basic, clinical, and translational research involving human patients, animal models, and cell cultures. Methods: Using the key words {"}dry eye + inflammation, {"} the authors conducted a comprehensive search of the PubMed and Web of Science databases for scientific articles published in English between January 1, 1900 and August 30, 2013 on the role of inflammation in DED in cell cultures, animal models, and humans. The resulting articles were then categorized and reviewed. Results: The literature search revealed a total of 458 publications, almost all published after 1992. The percentages of original studies and review articles are 77.29{\%} (354) and 22.71{\%} (104), respectively. Among the original studies, the number of reports on human DED is 200 (43.7{\%}), on animal models is 115 (25.1{\%}), and cell cultures is 39 (8.5{\%}). A yearly distributing plot revealed that 76{\%} were published from 2003 to 2011, 53{\%} from 2008 to 2012, and 11{\%} during the first 9 months of 2013. This distribution signifies a rapidly growing awareness of the importance of inflammation in DED pathogenesis. Conclusions: Inflammation plays a key role in the pathogenesis of DED as evidenced by research using tissue culture, animal models, and subjects with DED. Developing biomarkers for inflammation of the ocular surface will provide improved understanding of the mechanisms leading to DED, classification of the severity of DED, and objective metrics for outcome measures of treatment. The chronicity of the disease suggests that dysregulation of immune mechanisms leads to a cycle of continued inflammation, accompanied by alterations in both innate and adaptive immune responses. Given the underlying mechanism for DED, developing effective and safe antiinflammatory treatments is likely to be beneficial for patients with DED.",
author = "Yi Wei and Penny Asbell",
year = "2014",
month = "1",
day = "1",
doi = "10.1097/ICL.0000000000000042",
language = "English (US)",
volume = "40",
pages = "248--256",
journal = "Eye and Contact Lens",
issn = "1542-2321",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

TY - JOUR

T1 - The core mechanism of dry eye disease is inflammation

AU - Wei, Yi

AU - Asbell, Penny

PY - 2014/1/1

Y1 - 2014/1/1

N2 - Purpose: The purpose of this article is to review the evidence for the hypothesis that the core mechanism of dry eye disease (DED) is inflammation, including evidence from recent basic, clinical, and translational research involving human patients, animal models, and cell cultures. Methods: Using the key words "dry eye + inflammation, " the authors conducted a comprehensive search of the PubMed and Web of Science databases for scientific articles published in English between January 1, 1900 and August 30, 2013 on the role of inflammation in DED in cell cultures, animal models, and humans. The resulting articles were then categorized and reviewed. Results: The literature search revealed a total of 458 publications, almost all published after 1992. The percentages of original studies and review articles are 77.29% (354) and 22.71% (104), respectively. Among the original studies, the number of reports on human DED is 200 (43.7%), on animal models is 115 (25.1%), and cell cultures is 39 (8.5%). A yearly distributing plot revealed that 76% were published from 2003 to 2011, 53% from 2008 to 2012, and 11% during the first 9 months of 2013. This distribution signifies a rapidly growing awareness of the importance of inflammation in DED pathogenesis. Conclusions: Inflammation plays a key role in the pathogenesis of DED as evidenced by research using tissue culture, animal models, and subjects with DED. Developing biomarkers for inflammation of the ocular surface will provide improved understanding of the mechanisms leading to DED, classification of the severity of DED, and objective metrics for outcome measures of treatment. The chronicity of the disease suggests that dysregulation of immune mechanisms leads to a cycle of continued inflammation, accompanied by alterations in both innate and adaptive immune responses. Given the underlying mechanism for DED, developing effective and safe antiinflammatory treatments is likely to be beneficial for patients with DED.

AB - Purpose: The purpose of this article is to review the evidence for the hypothesis that the core mechanism of dry eye disease (DED) is inflammation, including evidence from recent basic, clinical, and translational research involving human patients, animal models, and cell cultures. Methods: Using the key words "dry eye + inflammation, " the authors conducted a comprehensive search of the PubMed and Web of Science databases for scientific articles published in English between January 1, 1900 and August 30, 2013 on the role of inflammation in DED in cell cultures, animal models, and humans. The resulting articles were then categorized and reviewed. Results: The literature search revealed a total of 458 publications, almost all published after 1992. The percentages of original studies and review articles are 77.29% (354) and 22.71% (104), respectively. Among the original studies, the number of reports on human DED is 200 (43.7%), on animal models is 115 (25.1%), and cell cultures is 39 (8.5%). A yearly distributing plot revealed that 76% were published from 2003 to 2011, 53% from 2008 to 2012, and 11% during the first 9 months of 2013. This distribution signifies a rapidly growing awareness of the importance of inflammation in DED pathogenesis. Conclusions: Inflammation plays a key role in the pathogenesis of DED as evidenced by research using tissue culture, animal models, and subjects with DED. Developing biomarkers for inflammation of the ocular surface will provide improved understanding of the mechanisms leading to DED, classification of the severity of DED, and objective metrics for outcome measures of treatment. The chronicity of the disease suggests that dysregulation of immune mechanisms leads to a cycle of continued inflammation, accompanied by alterations in both innate and adaptive immune responses. Given the underlying mechanism for DED, developing effective and safe antiinflammatory treatments is likely to be beneficial for patients with DED.

UR - http://www.scopus.com/inward/record.url?scp=84905444773&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84905444773&partnerID=8YFLogxK

U2 - 10.1097/ICL.0000000000000042

DO - 10.1097/ICL.0000000000000042

M3 - Review article

C2 - 25390549

AN - SCOPUS:84905444773

VL - 40

SP - 248

EP - 256

JO - Eye and Contact Lens

JF - Eye and Contact Lens

SN - 1542-2321

IS - 4

ER -