Artikel
Immune amplification in inflammatory corneal neovascularization
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Autoren
Veröffentlicht: | 22. September 2004 |
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Gliederung
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Objective
Corneal hemangiogenesis (CHA) and corneal lymphangiogenesis (CLA) are associated with inflammatory diseases of the cornea. Aim of this study was to unravel the precise role of inflammatory cells, and especially macrophages, in inducing pathologic corneal neovascularization.
Methods
The effect of systemic depletion of bone marrow derived-cells (by irradiation) and local depletion of macrophages (using clodronate liposomes) on inflammation-induced CHA and CLA was analyzed using the mouse model of suture-induced neovascularization. The extent of CHA and CLA was quantified by morphometry of CD31/LYVE-1 stained corneal flatmounts.
Results
Both systemic as well as local depletion of bone marrow-derived cells and specifically macrophages nearly completely inhibited CHA and CLA. Furthermore, inhibition of macrophage recruitment via VEGF-A/VEGFR1 using a molecular trap for VEGF-A (VEGF TrapR1R2) had the same effect.
Conclusions
VEGF-A mediated recruitment of bone marrow derived macrophages seems to be an essential early step in immune-amplification leading to both pathological corneal hem- and lymphangiogenesis. Targeting of macrophages opens new avenues for inhibiting pathologic hem- and lymphangiogenesis.
Support: DFG (Cu 47/1-1, Cu 47/1-2), IZKF Erlangen, NIH (EY10765)