Abstract 99. Jahrestagung der DOG, 29. 9. - 2. 10. 01 im ICC, Berlin

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Impressum



Anti-inflammatory effect of amniotic membrane transplantation in experimental HSV keratitis

1,2Heiligenhaus A., 1,2Bauer D., 1Hermans P., 1,2Wasmuth S., 3Meller K., 2Steuhl K. P.

1Ophtha-Lab, Department of Ophthalmology, St. Franziskus Hospital, Muenster; 2Department of Ophthalmology, University of Essen; 3Department of Anatomy, University of Bochum

Purpose: We have previously shown that amniotic membrane transplantation (AMT) improves experimental HSV-1 necrotizing keratitis. This study investigated the anti-inflammatory effect of AMT.
Methods: Ulcerating keratitis was induced in BALB/c mice by infecting the right cornea with HSV-1 (105 PFU, KOS). The eyes of mice of group 1 (n=15) were covered with human AMT as a patch, those of group 2 (n=15) with a tarsorrhaphy. Corneal specimens obtained on day 2 p.i. were studied histologically and with CD11b mAb; secretion of mIP-10 and interleukin-2 (IL- 2) was analyzed by ELISA. TUNEL assays and transmission electron microscopy were performed. The delayed type hypersensitivity (DTH) response was determined.
Results: In contrast to group 2, improvement of ulceration and stromal inflammation was detected in group 1. The corneas in group 1 had fewer PMNs and CD11b+ cells than in group 2. The percentages of non-viable and TUNEL-positive PMNs were increased in group 1, but not in group 2. The IL-2 and mIP-10 concentrations in the corneas of group 1 were less than in group 2. Transmission electron microscopy revealed that the decrease of PMN numbers in group 1 was associated with an early macrophage infiltration. There were no differences between the groups with respect to the DTH response.
Conclusions: AMT improves HSV ulcerating keratitis. This correlates with a reduced secretion of chemokines and interleukines that promote PMN infiltration, and with apoptosis and removal of PMNs that had infiltrated the cornea. This may primarily be by local and not by systemic effects from AMT. Supported by DFG grant He 1877/12-1




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