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-1 beta

Firatli Y., Firatli E., Loimaranta V., Elmanfi S., Gürsoy U. K.

JOURNAL OF PERIODONTOLOGY, cilt.94, sa.1, ss.130-140, 2023 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 94 Sayı: 1
  • Basım Tarihi: 2023
  • Doi Numarası: 10.1002/jper.22-0093
  • Dergi Adı: JOURNAL OF PERIODONTOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, CAB Abstracts, CINAHL, EMBASE, MEDLINE, Veterinary Science Database, DIALNET
  • Sayfa Sayıları: ss.130-140
  • Anahtar Kelimeler: infections, inflammation, periodontal diseases, FUSOBACTERIUM-NUCLEATUM, HOST RESPONSE, MCPIP1, MALT1, DEGRADATION, MECHANISMS, MIGRATION, CLEAVAGE, CELLS, MODEL
  • İstanbul Üniversitesi Adresli: Evet

Özet

Background The aim of this study was to evaluate oral bacteria- and interleukin (IL)-1 beta-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-1 beta. 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-1 beta. 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-1 beta, 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.