Regulation of gingival keratinocyte monocyte chemoattractant protein‐1‐induced protein (MCPIP)‐1 and mucosa‐associated lymphoid tissue lymphoma translocation protein (MALT)‐1 expressions by periodontal bacteria, lipopolysaccharide, and interleukin‐1β

Abstract

Background:The aim of this study was to evaluate oral bacteria-and interleukin (IL)-1β-induced protein and mRNA expression profiles of monocyte chemoattractant protein-1-induced protein (MCPIP)-1 and mucosa-associated lymphoid tissue lymphoma translocation protein (MALT)-1 in human gingival keratinocyte monolayers and organotypic oral mucosal models. Methods: Human gingival keratinocyte (HMK) monolayers were incubated with Porphyromonas gingivalis, Fusobacterium nucleatum, P. gingivalis lipopolysaccharide (LPS) and IL-1β. The protein levels of MCPIP-1 and MALT-1 were examined by immunoblots and mRNA levels by qPCR. MCPIP-1 and MALT-1 protein expression levels were also analyzed immunohistochemically using an organotypic oral mucosal model. One-way analysis of variance followed by Tukey correction was used in statistical analyses. Results: In keratinocyte monolayers, MCPIP-1 protein expression was suppressed by F. nucleatum and MALT-1 protein expression was suppressed by F. nucleatum, P. gingivalis LPS and IL-1β. P. gingivalis seemed to degrade MCPIP-1 and MALT-1 at all tested time points and degradation was inhibited when P. gingivalis was heat-killed. MCPIP-1 mRNA levels were increased by P. gingivalis, F. nucleatum, and IL-1β, however, no changes were observed in MALT-1 mRNA levels. Conclusion: Gingival keratinocyte MCPIP-1 and MALT-1 mRNA and protein expression responses are regulated by infection and inflammatory mediators. These findings suggest that periodontitis-associated bacteria-inducedThis is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Localization and expression profiles of gingival monocyte chemoattractant protein-1-induced protein-1 (MCPIP-1) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1)

“…In the context of periodontitis, however, little is known about the expression profile of MCPIP-1 and MALT-1 in the gingival tissues in relation to the extension of infection and inflammation. Our group has demonstrated that levels of MCPIP-1 and MALT-1 are regulated by periodontitis-associated bacteria in monolayers of gingival keratinocytes [17]. It was also demonstrated that MCPIP-1 is downregulated by P. gingivalis in gingival keratinocytes.…”

“…It was found that LPSmediated activation of inhibitor of transcription factor NF-kB kinase (IKK) complex phosphorylates MCPIP-1 rapidly and then phosphorylated MCPIP-1 undergoes ubiquitination and rapid degradation [26]. Moreover, it was demonstrated that P. gingivalis gingipain activity leads to a rapid degradation of MCPIP-1 in gingival keratinocytes, [17] which contributes the inflammophilic pathobiont formation [18]. In contrast to the observations, it was shown that lipopolysaccharide treatment increases the expression of MCPIP-1 through the activation of TLR-4 in murine macrophage cell line Raw264.7, in mouse primary bone marrow-derived macrophages, and in human monocyte-derived macrophages [27,28].…”

Association of vitamin K, fibre intake and progression of periodontal attachment loss in American adults

“…For example, IL-23-dependent IL-17 is a powerful proinflammatory mediator that leads to bacterial overgrowth that causes periodontal disease [ 33 ]. Another study found that the modified MCPIP-1 and MALT-1 response and protein expression induced by periodontitis-related bacteria may be part of the pathogenesis of periodontitis [ 34 ]. A recent study found that circRNA forms a circRNA–miRNA‒mRNA network during the osteogenic differentiation of periodontal stem cells, which has the prospect of synchronous periodontal diagnosis and regeneration [ 30 ].…”