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K. Kimura, S. Teranishi, T. Nishida; IL-1β-Induced Disruption of Barrier Function Through the NF-B Activation in Corneal Epithelial Cells. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5528.
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The corneal epithelium contributes to corneal homeostasis as a barrier and barrier function is impaired by inflammation. Adherens (AJs) and tight (TJs) junctions of the corneal epithelium have an important role in cell-cell adhesion and barrier function. We examined the effects of the proinflammatory cytokine interleukin (IL)-1β on the structure of AJs and TJs as well as on barrier function in simian virus 40-transformed human corneal epithelial (HCE) cells.
Barrier function was estimated by evaluating measurement of transepithelial electrical resistance (TER). The subcellular distributions of the AJ proteins E-cadherin and β-catenin, the TJ proteins ZO-1 and occludin, and the p65 subunit of nuclear factor (NF)-ΚB were determined by immunofluorescence staining. The expression of junctional proteins as well as the phosphorylation and degradation of the NF-ΚB-inhibitory protein IΚB- were examined by immunoblot analysis.
IL-1β impaired the localization of ZO-1 and occludin at the interfaces of neighboring HCE cells without affecting the localization of E-cadherin or β-catenin. It also reduced the TER of HCE cells in a concentration- and time-dependent manner. The overall abundance of TJ proteins ZO-1 and occludin and AJ proteins E-cadherin and β-catenin was not affected by IL-1β. IL-1β induced the phosphorylation and down-regulation of IΚB- as well as the translocation of p65 to the nucleus. The NF-ΚB inhibitor curcumin blocked the effects of IL-1β on both TER and the subcellular localization of ZO-1 and occludin.
IL-1β disturbed the distribution of ZO-1 and occludin at TJs of HCE cells and thereby disrupted the barrier function of these cells in a manner dependent on NF-ΚB activity. These effects of IL-1β may contribute to the loss of corneal epithelial barrier function associated with ocular inflammation.
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