April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Retinal Inflammation To Sterile Cell Death
Author Affiliations & Notes
  • Heping Xu
    Centre for Vision and Vascular Science, Queen's University Belfast, Belfast, United Kingdom
  • Mei Chen
    Centre for Vision and Vascular Science, Queen's University Belfast, Belfast, United Kingdom
  • Footnotes
    Commercial Relationships  Heping Xu, None; Mei Chen, None
  • Footnotes
    Support  The project was supported by Queen's University Belfast
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2917. doi:
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      Heping Xu, Mei Chen; Retinal Inflammation To Sterile Cell Death. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2917.

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

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Purpose: : Sterile inflammation, an inflammatory response to non-infectious pathogens, underlies the pathogenesis of a number of retinal diseases including autoimmune uveoretinitis, retinal ischemic injuries, diabetic retinopathy, and age-related macular degeneration. Although extensive studies have been carried out in the context of retinal autoimmune diseases, little is known on how retinal immune system responds to de novo non-infectious pathogens. In this study, we investigated retinal immune response to sterile cell death.

Methods: : Adult C57BL/6 mice were injected intravitreally with 0.75 uM paraquat. Retinal changes were monitored clinically with topic endoscopic fundus examination (TEFI). At different days post-injection (p.i.), mice were sacrificed and eyes collected for histological investigations by light-, confocal- and electron microscopy, as well as for molecular investigation by real-time RT-PCR.

Results: : Twenty-four hours after paraquat injection, many propidium iodide positive necrotic cells were detected in the retina. Retinal oedema was observed by TEFI within 1-2 days p.i., and after one week, retinal degeneration became evident. Necrotic cell death was further confirmed by transmission electron microscopy. Microglial activation occurred as early as 12 h p.i., followed by neutrophil infiltration at 2 days p.i. The number of infiltrating neutrophils increased as the disease progressed; however, the majority of the cells were confined in the inner retina. In contrast, activated macrophages/microglia were observed throughout different layers of the retina and many of the cells exhibited multiple intracellular inclusions. Following paraquat injection, the expression of IL-1β, Nlrp3 and caspase-1 increased significantly in the retina. The treatment, however, did not affect the expression of complement C3, C4, and factor B, or the deposition of C3d in the retina.

Conclusions: : Necrotic cell death in the retina induces an acute inflammatory response characterised by neutrophil and macrophage infiltration. Nlrp3 inflammasome may play an important role in necrotic cell death-mediated retinal inflammation.

Keywords: immunomodulation/immunoregulation • retina • apoptosis/cell death 

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