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Invasive Streptococcus mutans induces inflammatory cytokine production in human aortic endothelial cells via regulation of intracellular toll‐like receptor 2 and nucleotide‐binding oligomerization domain 2
Author(s) -
Nagata E.,
Oho T.
Publication year - 2017
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12159
Subject(s) - streptococcus mutans , nod , microbiology and biotechnology , cytokine , biology , interleukin 10 , proinflammatory cytokine , tlr4 , immunology , inflammation , biochemistry , bacteria , gene , genetics
Summary Streptococcus mutans , the primary etiologic agent of dental caries, can gain access to the bloodstream and has been associated with cardiovascular disease. However, the roles of S. mutans in inflammation in cardiovascular disease remain unclear. The aim of this study was to examine cytokine production induced by S. mutans in human aortic endothelial cells ( HAEC s) and to evaluate the participation of toll‐like receptors ( TLR s) and cytoplasmic nucleotide‐binding oligomerization domain ( NOD ) ‐like receptors in HAEC s. Cytokine production by HAEC s was determined using enzyme‐linked immunosorbent assays, and the expression of TLR s and NOD ‐like receptors was evaluated by real‐time polymerase chain reaction, flow cytometry and immunocytochemistry. The involvement of TLR 2 and NOD 2 in cytokine production by invaded HAEC s was examined using RNA interference. The invasion efficiencies of S. mutans strains were evaluated by means of antibiotic protection assays. Five of six strains of S. mutans of various serotypes induced interleukin‐6, interleukin‐8 and monocyte chemoattractant protein‐1 production by HAEC s. All S. mutans strains upregulated TLR 2 and NOD 2 mRNA levels in HAEC s. Streptococcus mutans Xc upregulated the intracellular TLR 2 and NOD 2 protein levels in HAEC s. Silencing of the TLR 2 and NOD 2 genes in HAEC s invaded by S. mutans Xc led to a reduction in interleukin‐6, interleukin‐8 and monocyte chemoattractant protein‐1 production. Cytokine production induced by invasive S. mutans via intracellular TLR 2 and NOD 2 in HAEC s may be associated with inflammation in cardiovascular disease.