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Fusobacterium nucleatum induces cytokine production through T oll‐like‐receptor‐independent mechanism
Author(s) -
Quah S. Y.,
Bergenholtz G.,
Tan K. S.
Publication year - 2014
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/iej.12185
Subject(s) - fusobacterium nucleatum , hek 293 cells , nod , mapk/erk pathway , cytokine , receptor , p38 mitogen activated protein kinases , microbiology and biotechnology , biology , signal transduction , immunology , bacteria , biochemistry , porphyromonas gingivalis , genetics , gene
Abstract Aim To determine whether F usobacterium nucleatum 's ability to invade cells allows the bacteria to activate pro‐inflammatory response through cytosolic pattern recognition receptors, independent of surface T oll‐like receptors ( TLR s). Methodology HEK 293 T cells, which lack endogenous TLR s, and overexpressing dominant negative myeloid differentiation primary response gene 88 ( M y D 88 DN ) protein, were infected with F . nucleatum and the production of interleukin‐8 ( IL ‐8) was determined. The necessity for intracellular invasion of the bacteria for cytokine production was also investigated by blocking bacterial invasion with cytochalasin D . The roles of NF ĸ B and p38 mitogen‐activated protein kinase ( MAPK ) and nucleotide‐binding oligomerization domain‐1 ( NOD ‐1) signalling pathways in F . nucleatum ‐induced IL ‐8 secretion were determined. Results Fusobacterium nucleatum ‐infected HEK 293 T cells produced IL ‐8 independent of the MYD 88 signalling. This response was inhibited by preventing F . nucleatum invasion into HEK 293 T cells. p38 MAPK but not the NF ĸ B signalling pathway was required for F . nucleatum ‐mediated IL ‐8 production. HEK 293 T cells expressed NOD ‐1 but not NOD ‐2. Yet, inhibition of NOD ‐1 signalling did not affect F . nucleatum ‐induced IL ‐8 secretion. Conclusions Fusobacterium nucleatum invasion led to cytokine production, which is mediated by the p38 MAPK signalling but independent of TLR s, NOD ‐1, NOD ‐2 and NF ĸ B signalling.