Fig. 4

Pathogen associated pattern recognition receptor activated signaling pathways. Graphics of the nuclear factor-kappa B (NF-κB) and mitogen- activated protein kinase (MAPK or MKK) signaling pathways induced by activation of pathogen associated pattern recognition receptor (PAR) toll like receptors (TLR) and nucleotide-binding oligomerization domain receptors (NOD). TLRs and NODs belong to the key initiators of inflammation in host defence. Diffferent TLRs recognize differencial microbial components. TLR4 detects lipopolysaccharide (LPS), TLR1/2 and TLR2/6 recognize triacylated and diacylated lipoproteins from bacterial wall components and TLR5 is activated by flagellin from the flagella of multiple bacteria. TLRs signal via the adaptor protein MyD88, leading to transforming growth factor-β-activated kinase 1 (TAK1) activation that induces NF-kB and p38/c-Jun N-terminal kinase (JNK) pathways. Recognition of NOD ligands recruit caspase activation and recruitment domain (CARD) interaction with receptor-interacting protein kinase RIP2 which leads to activation of RIP2. RIP2 mediates activation IκB kinase. The activation of IκB kinase results in the phosphorylation of inhibitor IκB which releases NF-κB and its nuclear translocation. NF-κB and p38/JNK activated activator protein 1 (AP-1) function as transcription factor for the expression of inflammatory cytokines. The red arrows indicate the upregulated genes in oral epithelial cells induced by P. gingivalis and its total membrane that were detected in this study