NDLI: Effect of desiccating environmental stress versus systemic muscarinic AChR blockade on dry eye immunopathogenesis.

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Effect of desiccating environmental stress versus systemic muscarinic AChR blockade on dry eye immunopathogenesis.

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Effect of desiccating environmental stress versus systemic muscarinic AChR blockade on dry eye immunopathogenesis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Stern, Michael E. Lee, Hyun Soo Dana, Reza Chen, Yihe Schaumburg, Chris S. Kodati, Shilpa Sadrai, Zahra Stevenson, William Chauhan, Sunil K. Saban, Daniel R.
Description	Country affiliation: United States Author Affiliation: Chen Y ( Schepens Eye Research Institute, Massachusetts Eye and Ear Infirmary, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts 02114, USA.)
Abstract	PURPOSE: A majority of experimental data on dry eye disease (DED) immunopathogenesis have been derived from a murine model of DED that combines desiccating environmental stress with systemic muscarinic acetylcholine receptor (mAChR) inhibition. However, to our knowledge the effects of pharmacologic mAChR blockade on the pathogenesis of experimental DED have not been evaluated systemically. The purpose of our study was to investigate the differential effects of desiccating environmental stress and mAChR inhibition on the pathogenesis of DED. METHODS: DED was induced in female C57BL/6 mice by exposure to a desiccating environment in the controlled-environment chamber or to systemic scopolamine, or by performing extraorbital lacrimal gland excision. Clinical disease was assessed using corneal fluorescein staining (CFS) and the cotton thread test (CTT). Corneal CD11b(+) and conjunctival CD3(+) T-cell infiltration were evaluated by flow cytometry. T-cells from draining cervical lymph nodes (CLN) and distant inguinal lymph nodes (ILN) were analyzed for Th1, Th2, Th17, and Treg responses by flow cytometry and ELISA. RESULTS: Desiccating environmental stress and systemic mAChR blockade induced similar clinical signs of DED. However, desiccating environmental stress imparted higher conjunctival CD3(+) T-cell infiltration, and greater Th17-cell activity and Treg dysfunction than mAChR blockade, while mAChR blockade decreased tear secretion to a greater extent than desiccating environmental stress. Systemic mAChR blockade attenuated Th17 activity and enhanced Th2 and Treg responses without affecting Th1 activity. CONCLUSIONS: In vivo inhibition of mAChRs variably affects CD4(+) T-cell subsets, and desiccating environmental stress and systemic mAChR blockade induce DED through different primary pathogenic mechanisms.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.12-11121
Journal	Investigative Opthalmology & Visual Science
Issue Number	4
Volume Number	54
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2013-04-03
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Dry Eye Syndromes Immunology Muscarinic Antagonists Pharmacology Scopolamine Hydrobromide Stress, Physiological T-lymphocyte Subsets Animals Cytokines Metabolism Disease Models, Animal Enzyme-linked Immunosorbent Assay Flow Cytometry Lacrimal Apparatus Surgery Lymph Nodes Mice Mice, Inbred C57bl Receptors, Muscarinic Physiology T-lymphocytes, Regulatory Th1 Cells Th17 Cells Th2 Cells Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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