September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Acute ocular surface injury causes prompt infiltration of circulating monocytes into the retina
Author Affiliations & Notes
  • Fengyang Lei
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States
  • Chengxin Zhou
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States
  • Vassiliki Kapoulea
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States
  • James Chodosh
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States
  • Claes H Dohlman
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States
  • Eleftherios I Paschalis
    Ophthalmology, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, United States
  • Footnotes
    Commercial Relationships   Fengyang Lei, None; Chengxin Zhou, None; Vassiliki Kapoulea, None; James Chodosh, None; Claes Dohlman, None; Eleftherios Paschalis, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 4492. doi:
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    • Get Citation

      Fengyang Lei, Chengxin Zhou, Vassiliki Kapoulea, James Chodosh, Claes H Dohlman, Eleftherios I Paschalis; Acute ocular surface injury causes prompt infiltration of circulating monocytes into the retina. Invest. Ophthalmol. Vis. Sci. 2016;57(12):4492.

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

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Abstract

Purpose : Ocular alkali burns can lead to blindness even if promptly treated. Such patients can exhibit early neuroretinal tissue loss and glaucoma. Using a murine ocular alkali burn model we have shown that injuries lead to early upregulation of pro-inflammatory cytokines and activation of immune cells in the retina, but not pH elevation. We hypothesize that cytokines from the injured anterior segment diffuse posteriorly causing activation of microglia and recruitment of circulating monocytes and subsequent tissue damage. However, the role of microglia and macrophage in alkali burn-induced retinal injury has not previously been elucidated. Here we have adopted a murine bone marrow chimeric model to study the role of monocytes in this retinal damage.

Methods : CX3CR1+/eGFP bone marrow cells were transfused to myelodepleted C57BL/6J mice 1 month prior to corneal alkali burn. Ocular burn was performed by using a 1N NaOH soaked filter paper that was placed on cornea for 20 seconds, and followed by a 15-minute saline irrigation. Mice were euthanized 24 hours and 7 days after the burn and retinas were studied by flowcytometry and confocal microscopy. Ramification index (RI), which measures microglia quiescence, was calculated as the ratio of ramified/ameboid GFP+ cells in the retina.

Results : GFP+ cells infiltrated into retina within 24 hours of burn (5.3%±3.6% of total CD45+ cells versus 0.46%±0.4% in controls; p=0.08). GFP+ cells had the phenotypical ameboid appearance of monocytes. At 7 days of burn, the number of GFP+ cells in the retina significantly increased (40.0%±17.0%; p=0.02) and distributed throughout the retina. GFP+ cells transformed at 7 days post burn from ameboid to ramified, with asymmetric, elongated bodies and processes (RI of GFP+ cells: 0.143 at 24 hours and 4.9 at 7 days). Morphological change was also associated with upregulation of major histocompatibility complex (MHC)-II (5.8-fold increase at 24 hours and 19.4-fold at 7-days), indicating activation of CX3CR1+ cells.

Conclusions : Using a murine model, we demonstrated early and dynamic influx of circulating monocytes into the retina following acute surface injury. Infiltrating CX3CR1+ cells showed remarkable plasticity in adopting a ramified phenotype within a week of entry to the retina, becoming indistinguishable from retinal microglia. However, their roles in the injured retina remains unknown and warrants further investigation.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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