Abstract
Purpose: :
Many kinds of cytokines are orchestrated in severe vernal keratoconjunctivitis (VKC). TGF-β1 plays as one of the important major cytokines in tissue remodeling. The purpose of the present study is to investigate the role of TGF-β1 in severe VKC and to study the microenvironment which regulates severe VKC.
Methods: :
Tear fluid from 6 patients and 4 control subjects were studied by ELISA techniques using TGF-β1. GPC was removed from 3 patients with severe VKC and conjunctival biopsy was done from one control subjects. We had informed consent from patients. Specimens were studied by immunohistochemistry techniques using monoclonal and polyclonal antibodies directed against the TGF-β1, Integrin Vβ6, Phospho-Smad2, ProcollagenI, Tenascin, Smooth Muscle Actin. We had informed consent from patients. In vitro assay, cultured keratocyte were used. In the presence or absence of 20ng/ml TGF-β1, cultured keratocyte were incubated with 20ng/ml Th2 cytokines, IL-4 and IL-13, for 48 hours. ELISA was used to measure eotaxin, IL-8 and TARC production in cultured keratocyte.
Results: :
Tear fluids in TGF-β1were significantly higher in severe VKC patients compared with normal control subject. In immunohistochemistry study, TGF-β1 was detected in inflammatory cells which infiltrate in conjunctival epithelium and subconjunctival tissue in severe VKC specimen. Integrin Vβ6 was observed in conjunctival epithelial basal layer and capillary endothelium. SMA was seen in capillary endothelium and ProcollagenI was seen capillary endothelium and subconjunctival tissue. In vitro, production of eotaxin and IL-8 was significantly higher with stimulation of Th2 cytokines under the existence of TGF-β1 in cultured keratocyte.
Conclusions: :
These results suggest that TGF-β1 produced from inflammatory cells may contribute to the formation of severe VKC. In addition, our results give evidence for possible involvement of IL-8 and eotaxin which were produced from keratocyte leads to prolong the condition of severe VKC.
Keywords: conjunctivitis • inflammation • pathology: human