September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
The Role of VEGF-A in Exogenous Endophthalmitis: A Potential Role for Targeted Immunomodulation
Author Affiliations & Notes
  • Mark Seamone
    Ophthalmology , Dalhousie University , Halifax, Nova Scotia, Canada
  • Ian Haidl
    Microbiology and Immunology , Dalhousie University , Halifax, Nova Scotia, Canada
  • Darrell Lewis
    Ophthalmology , Dalhousie University , Halifax, Nova Scotia, Canada
  • R. Rishi Gupta
    Ophthalmology , Dalhousie University , Halifax, Nova Scotia, Canada
  • Daniel O'Brien
    Ophthalmology , Dalhousie University , Halifax, Nova Scotia, Canada
  • John DIckinson
    Ophthalmology , Dalhousie University , Halifax, Nova Scotia, Canada
  • Jean Marshall
    Microbiology and Immunology , Dalhousie University , Halifax, Nova Scotia, Canada
  • Alan F Cruess
    Ophthalmology , Dalhousie University , Halifax, Nova Scotia, Canada
  • Footnotes
    Commercial Relationships   Mark Seamone, None; Ian Haidl, None; Darrell Lewis, None; R. Rishi Gupta, None; Daniel O'Brien, None; John DIckinson, None; Jean Marshall, None; Alan Cruess, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 5869. doi:
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      Mark Seamone, Ian Haidl, Darrell Lewis, R. Rishi Gupta, Daniel O'Brien, John DIckinson, Jean Marshall, Alan F Cruess; The Role of VEGF-A in Exogenous Endophthalmitis: A Potential Role for Targeted Immunomodulation. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5869.

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

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Abstract

Purpose : Exogenous endophthalmitis is an ophthalmologic emergency defined by inflammation of the intraocular cavities, typically by an infectious agent. This entity occurs following intraocular surgery, and may result in debilitating visual impairment. Vascular Endothelial Growth Factor-A (VEGF-A) has been linked to pathologic angiogenesis in ocular diseases. VEGF-A also contributes to inflammation by promoting the chemotaxis of monocytes and granulocytes, and by increasing vascular permeability. To date, few studies have characterized the inflammatory response to intraocular infection in humans. Moreover, the role of VEGF-A in promoting ocular inflammation in the setting of exogenous endophthalmitis remains unexplored.

Methods : Undiluted vitreous samples (0.5-1.0 ml) were obtained from individuals with a diagnosis of exogenous endophthalmitis (n=17). Samples were obtained by pars plana vitrectomy or vitreous tap. Vitreous samples were analyzed via Luminex Assay for the cytokines VEGF-A TNF-α, IL-6, IL-8, IL-10, IL-12p70, IL-33, IFN-γ, INF-α, IFN-β, CCL3, IL-2, IL-5, IL-15, CXCL10, CCL2, IL-1Ra, CCL5, IL-17, GM-CSF, and CCL11. Levels of VEGF-A were further analyzed via ELISA. Vitreous samples obtained at the time of macular hole surgery served as controls (n=8). Statistical analysis was conducted using Mann-Whitney U testing where appropriate.

Results : Results: Intraocular infection was a potent inducer of pro-inflammatory cytokines and chemokines. Levels of VEGF-A were significantly elevated in vitreous samples from individuals with exogenous endophthalmitis when compared to macular hole (p=0.001). In a subgroup analysis, VEGF-A was significantly upregulated in vitreous samples obtained from individuals with exogenous endophthalmitis following cataract surgery (p=0.002). Similar results were observed in vitreous samples obtained from exogenous endophthalmitis following vitrectomy (p=0.012). No significant difference in VEGF-A concentration was observed between post-cataract and post-vitrectomy populations (p>0.05). Levels of VEGF-A were also similar in culture-positive and culture-negative populations (p>0.05).

Conclusions : Conclusions: Taken together, this data demonstrates that VEGF-A is potently upregulated in exogenous endophthalmitis. This manuscript is of great clinical significance as it provides a foundation for the future study of targeted VEGF-A blockade in the management of endophthalmitis.

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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