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

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‐induced modifications in MCPIP‐1 and MALT‐1 responses can be a part of periodontal disease pathogenesis.