Please use this identifier to cite or link to this item:
Title: Fusobacterium nucleatum induces cytokine production through Toll-like-receptor-independent mechanism
Authors: Quah, S.Y.
Bergenholtz, G.
Tan, K.S. 
Keywords: Bacterial invasion
Fusobacterium nucleatum
Nucleotide-binding oligomerization domain-1
Nucleotide-binding oligomerization domain-2
P38 mitogen-activated protein kinase
Toll-like receptors
Issue Date: 2014
Citation: Quah, S.Y., Bergenholtz, G., Tan, K.S. (2014). Fusobacterium nucleatum induces cytokine production through Toll-like-receptor-independent mechanism. International Endodontic Journal 47 (6) : 550-559. ScholarBank@NUS Repository.
Abstract: Aim: To determine whether Fusobacterium nucleatum's ability to invade cells allows the bacteria to activate pro-inflammatory response through cytosolic pattern recognition receptors, independent of surface Toll-like receptors (TLRs). Methodology: HEK293T cells, which lack endogenous TLRs, and overexpressing dominant negative myeloid differentiation primary response gene 88 (MyD88DN) 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 NFK{green}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 HEK293T cells produced IL-8 independent of the MYD88 signalling. This response was inhibited by preventing F. nucleatum invasion into HEK293T cells. p38 MAPK but not the NFK{green}B signalling pathway was required for F. nucleatum-mediated IL-8 production. HEK293T 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 TLRs, NOD-1, NOD-2 and NFKB signalling. © 2014 by The American College of Veterinary Surgeons.
Source Title: International Endodontic Journal
ISSN: 13652591
DOI: 10.1111/iej.12185
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.


checked on Jan 27, 2023


checked on Jan 27, 2023

Page view(s)

checked on Feb 2, 2023

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.