Abstract
Purpose: :
A wound healing response giving rise to posterior capsule opacification (PCO) is known to follow cataract surgery. Histamine has been associated with intraocular inflammation and thus levels are likely to increase following cataract surgery. In the present study we investigate a putative mechanism by which the lens can control histamine release from ocular stores and thus influence PCO progression.
Methods: :
The human lens cell line FHL124 was used throughout this study. Expression and release of histamine releasing factor was detected in cell lysates and corresponding culture medium by western blot analysis. Activation of MAPK signalling components and interleukin levels were assessed by a suspended bead protein array (BIOPLEX). Cell growth was assessed by a MTS assay.
Results: :
Histamine releasing factor (HRF) was detected in FHL124 cells. HRF release was stimulated by application of histamine (100 µM) and through oxidative stress induced by application of H2O2 (30 µM) Application of histamine (100 µM) significantly increased release of IL-6 and IL-8 in to the culture medium. IL-6 and IL-8 are capable of promoting cell growth. IL-8 appeared to promote HRF release, but IL-6 had no effect. IL-8 (0.1 ng/ml) significantly increased levels of phosphorylated ERK, while IL-6 (0.1 ng/ml) significantly increased levels of phosphorylated ERK and phosphorylated p38 in FHL 124 cells.
Conclusions: :
Lens cells express histamine releasing factor, which is likely to enter the ocular environment in response to cataract surgery. This in turn could free histamine release from ocular stores. Histamine can release interleukins which actively induce MAPK signalling and can also promote cell growth. HRF in the lens could therefore play an important role in the development of PCO.
Keywords: inflammation • wound healing • signal transduction