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Myd88 plays a major role in the keratinocyte response to infection with Porphyromonas gingivalis
Author(s) -
Polak David,
Zigron Asaf,
EliBerchoer Luba,
Shapira Lior,
Nussbaum Gabriel
Publication year - 2019
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12641
Subject(s) - porphyromonas gingivalis , fusobacterium nucleatum , keratinocyte , microbiology and biotechnology , beta defensin , intracellular , flow cytometry , cell adhesion , chemistry , biology , adhesion , antimicrobial peptides , cell culture , antimicrobial , bacteria , genetics , organic chemistry
Aim To explore the role of keratinocyte myeloid differentiation primary response 88 (MyD88) expression in the adhesion of Porphyromonas gingivalis to the cells and its subsequent invasion and intracellular survival. Materials and Methods Primary mouse keratinocytes from wild‐type ( WT ) or Myd88 −/− mice were infected with P gingivalis alone or co‐infected with Fusobacterium nucleatum . Bacterial adhesion and invasion were measured using fluorescent microscopy and flow cytometry, and intracellular survival in keratinocytes was quantified by an antibiotic protection assay. Keratinocyte expression of antimicrobial peptides was measured by real‐time PCR . Results In the absence of MyD88, P gingivalis adherence, invasion, and intracellular survival were enhanced compared with WT keratinocytes. The presence of F nucleatum during infection increased the adhesion of P gingivalis to WT keratinocytes but reduced the adhesion to Myd88 −/− keratinocytes. Fusobacterium nucleatum improved mildly the invasion and survival of P gingivalis in both cell types. Baseline expression of beta‐defensin 2, 3, 4 and Reg III ‐γ was elevated in Myd88 −/− keratinocytes compared to WT cells; however, following infection beta‐defensin expression was strongly induced in WT cells but decreased dramatically in the MyD88 deficient cells. Conclusion In the absence of MyD88 expression, P gingivalis adhesion to keratinocytes is improved, and invasion and intracellular survival are increased. Furthermore, keratinocyte infection by P gingivalis induces antimicrobial peptide expression in a MyD88‐dependent manner. Thus, MyD88 plays a key role in the interaction between P gingivalis and keratinocytes.