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Involvement of NLRP10 in IL-1α induction of oral epithelial cells by periodontal pathogens.

Innate immunity (2017-08-03)
Seok-Joo Lee, Bong-Kyu Choi
RÉSUMÉ

This study investigated the pathogenesis of periodontitis and the role of nucleotide-binding oligomerization domain-like receptor protein 10 (NLRP10). The human oral epithelial cell line HOK-16B was infected with two periodontal pathogens, Tannerella forsythia and Fusobacterium nucleatum, at various MOIs. RT-PCR and immunoblotting demonstrated that infection increased mRNA and protein expression of NLRP10, respectively. The siRNA-mediated NLRP10 knockdown significantly reduced IL-1α expression and secretion. Both bacteria induced phosphorylation of ERK, JNK and p38 MAP kinases in HOK-16B cells. NLRP10 knockdown impaired ERK phosphorylation only. ERK inhibition significantly decreased the expression of T. forsythia- and F. nucleatum-induced IL-1α. Our data suggest that NLRP10 is involved in activating the ERK signalling pathway in HOK-16B cells infected with T. forsythia and F. nucleatum. This pathway likely augments the pro-inflammatory cytokine IL-1α levels, which may play a critical role in periodontitis.

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Sigma-Aldrich
PD 98,059, solid
Sigma-Aldrich
Anti-NLRP10 Antibody, clone 8H2, clone 8H2, from rat