June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Altered micro-RNA expression contributes to the inflammatory environment observed in patients with primary Sjögren's syndrome.
Author Affiliations & Notes
  • Joan Ní Gabhann
    Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland
    Department of Ophthalmology, Royal College of Surgeons in Ireland, Dublin, Ireland
  • Qistina Pilson
    Department of Ophthalmology, Royal College of Surgeons in Ireland, Dublin, Ireland
    Department of Ophthalmology, Royal Victoria Eye and Ear Hospital, Dublin 2, Ireland
  • Caroline A Jefferies
    Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland
  • Conor C Murphy
    Department of Ophthalmology, Royal College of Surgeons in Ireland, Dublin, Ireland
    Department of Ophthalmology, Royal Victoria Eye and Ear Hospital, Dublin 2, Ireland
  • Footnotes
    Commercial Relationships Joan Ní Gabhann, None; Qistina Pilson, None; Caroline Jefferies, None; Conor Murphy, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 881. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Joan Ní Gabhann, Qistina Pilson, Caroline A Jefferies, Conor C Murphy; Altered micro-RNA expression contributes to the inflammatory environment observed in patients with primary Sjögren's syndrome.. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):881.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Purpose: Sjögren's syndrome (SS) is a systemic autoimmune disorder characterized by inflammation that affects mucous membranes particularly those of the exocrine glands, causing dry eyes and dry mouth. The exocrine glands become infiltrated with lymphocytes resulting in severe damage to both the salivary glands and the lacrimal glands. Previous investigations have suggested that dysregulated systemic inflammation contributes to the development and pathogenesis of SS. This study aimed to investigate potential mechanisms responsible for over production of pathogenic cytokines in SS patients.

Methods: Peripheral blood mononuclear cells and serum were prepared from whole blood taken from both healthy controls and pSS patients. Gene induction and micro-RNA expression were analysed by real-time PCR. Cytokine levels were determined by ELISA. Differences in miR expression, cytokine levels and gene induction between patients and controls were examined using the non-parametric Mann-Whitney test. Spearman’s rank correlation was used to assess the interrelationship between miR expression, gene induction and peripheral cytokine levels.

Results: We observed significantly enhanced expression of the pro-inflammatory micro-RNA, miR-155 (p≤0.05) and significantly reduced levels of the IL-10 promoting miR, miRNA-21 (p≤0.05) compared to healthy controls. In keeping with this altered pattern of miR expression we observed significantly increased serum levels of pro-inflammatory cytokines (IL-6, IL-8 and TNF-a) as well as the Th17 promoting cytokine, IL-23p19 (p ≤0.05). Altered expression of previously identified targets of miR-155 (SHIP-1, SOCS1 - potent anti-inflammatory regulators) and miR-21 (IL12p35 and PDCD4, positive regulators of inflammation) was also observed. Significantly a moderate negative correlation (r =-0.657, p≤0.05) was observed between reduced miR-21 expression and increased peripheral IL-23p19 levels in pSS patients, suggesting a link between altered miR expression and disease pathogenesis.

Conclusions: Our data suggest that abnormal expression or regulation of miRs and consequently miR regulated genes in innate immunity may contribute to the initiation and progression of SS via overproduction of pathogenic cytokines.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×