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. 2019 Mar:115:64-75.
doi: 10.1016/j.cyto.2018.12.009. Epub 2019 Jan 11.

Tea polyphenols protect gingival keratinocytes against TNF-α-induced tight junction barrier dysfunction and attenuate the inflammatory response of monocytes/macrophages

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Tea polyphenols protect gingival keratinocytes against TNF-α-induced tight junction barrier dysfunction and attenuate the inflammatory response of monocytes/macrophages

Amel Ben Lagha et al. Cytokine. 2019 Mar.

Abstract

Tea, an aromatic beverage prepared with the leaves of the Camellia sinensis plant, is well known to contain bioactive polyphenols. Green tea contains mainly catechins such as epigallocatechin-3-gallate (EGCG), while black tea is characterized by the presence of theaflavins. TNF-α, which is a pro-inflammatory cytokine that activates the endogenous inflammatory cascade, plays a key role in periodontitis. In the present study, we investigated the ability of tea compounds to attenuate TNF-α-mediated activation of the host inflammatory response in monocytes/macrophages as well as the protective effect of green and black tea polyphenols on gingival keratinocyte barrier dysfunction induced by TNF-α. Tea compounds inhibited both the activation of NF-κB and caspase-1 as well as IL-1β secretion by monocytes/macrophages. TNF-α time-dependently damaged keratinocyte tight junction barrier integrity, as determined by changes in transepithelial electrical resistance and FITC-dextran transport. Green tea extract, EGCG, theaflavins, and to a lesser extent, black tea extract protected keratinocytes against the TNF-α-mediated breakdown of barrier integrity. The treatment of keratinocytes with tea polyphenols markedly mitigated the morphological changes of tight junction proteins such as zonula occludens-1 and occludin compared to cells exposed only to TNF-α, as determined by immunofluorescence. Tea polyphenols also time-dependently decreased the paracellular flux of TNF-α-treated keratinocytes. In conclusion, the ability of tea polyphenols to exert an anti-inflammatory effect and to attenuate the gingival epithelial barrier dysfunction induced by TNF-α supports their potential for the prevention and treatment of periodontal disease.

Keywords: Epithelial barrier; Keratinocytes; Macrophages; Periodontal disease; TNF-α.

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