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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

J Periodontol. 2022 Jun 17. doi: 10.1002/JPER.22-0093. Online ahead of print.


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 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 (ANOVA) followed by Tukey’s 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. This article is protected by copyright. All rights reserved.

PMID:35712915 | DOI:10.1002/JPER.22-0093

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