• Online Features  This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on Web of Science (12)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Corneal Disorders  • Dry Eye Syndromes  • Drug Therapy  • Drug Therapy, Other  • Alert me on articles by topic  Social Bookmarking   What's this?

Sunali Goyal, MD; Sunil K. Chauhan, PhD; Qiang Zhang, MD; Reza Dana, MD, MSc, MPH

Arch Ophthalmol. 2009;127(7):882-887.

Objective  To determine the effect of a topical antagonist to the chemokine receptor 2 (CCR2) in a murine model of dry eye disease.

Methods  The effects of a topical CCR2 antagonist and a vehicle control treatment were studied in murine dry eyes. A controlled environment chamber induced dry eye by exposing mice to high-flow desiccated air. Corneal fluorescein staining and enumeration of corneal CD11b⁺ and conjunctival CD3⁺ T cells were performed in the different groups. Real-time polymerase chain reaction was performed to quantify expression of different inflammatory cytokine transcripts in the cornea and conjunctiva.

Results  Eyes receiving the formulation containing CCR2 antagonist showed a significant decrease in corneal fluorescein staining and decreased infiltration of corneal CD11b⁺ cells and conjunctival T cells compared with the vehicle-treated and untreated dry eye groups. The CCR2 antagonist also significantly decreased messenger RNA expression levels of interleukins 1 and 1β in the cornea, and tumor necrosis factor and interleukin 1β in the conjunctiva.

Conclusion  Topical application of CCR2 antagonist is associated with significant improvement in dry eye disease and is reflected by a decrease in inflammation at the clinical, molecular, and cellular levels.

Clinical Relevance  Topical application of CCR2 antagonist may hold promise as a therapeutic modality in dry eye disease.

Author Affiliations: Schepens Eye Research Institute (Drs Goyal, Chauhan, Zhang, and Dana), Department of Ophthalmology, Harvard Medical School (Drs Goyal, Chauhan, Zhang, and Dana), and Massachusetts Eye and Ear Infirmary (Dr Dana), Boston, Massachusetts.

CiteULike    Connotea    Delicious    Digg    Facebook    Reddit    Technorati    Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Dry Eye Disease: An Immune-Mediated Ocular Surface Disorder
Stevenson et al.
Arch Ophthalmol 2012;130:90-100.
ABSTRACT | FULL TEXT  

Blockade of Prolymphangiogenic Vascular Endothelial Growth Factor C in Dry Eye Disease
Goyal et al.
Arch Ophthalmol 2012;130:84-89.
ABSTRACT | FULL TEXT  

Ocular Surface APCs Are Necessary for Autoreactive T Cell-Mediated Experimental Autoimmune Lacrimal Keratoconjunctivitis
Schaumburg et al.
J. Immunol. 2011;187:3653-3662.
ABSTRACT | FULL TEXT  

Tear Production and Ocular Surface Changes in Experimental Dry Eye after Elimination of Desiccating Stress
Yoon et al.
IOVS 2011;52:7267-7273.
ABSTRACT | FULL TEXT  

Interferon-{gamma}-secreting NK cells promote induction of dry eye disease
Chen et al.
J. Leukoc. Biol. 2011;89:965-972.
ABSTRACT | FULL TEXT  

CCR2-Antagonist Prophylaxis Reduces Pulmonary Immune Pathology and Markedly Improves Survival during Influenza Infection
Lin et al.
J. Immunol. 2011;186:508-515.
ABSTRACT | FULL TEXT