Figure 6

Main signaling pathways supposed to be activated in MEC exposed to either E. coli crude LPS (a) or S. aureus culture supernatant (b). Crude LPS (a simplified substitute of outer membrane vesicles, omv) is sensed by both TLR2 and TLR4, which activates the NF-κB pathway by the MyD88-dependent pathway. In addition, the TRAM-TRIF-IRF3 pathway leads to the activation of genes that have an IRF-binding site in their promoter sequence. S. aureus culture supernatant (SaS) is sensed by TLR2 and other unidentified receptors that activate the NF-κB and AP-1 pathways. As a result, E. coli stimulation induces a higher number of genes (IFN-stimulated genes) than does S. aureus stimulation. This is exemplified by the overexpression of a panel of chemokine genes that have the potential to recruit a greater variety of leukocytes (see text). LTA: lipoteichoic acid; MyD88: myeloid differentiation primary-response gene 88; TRIF: TIR-domain-containing adaptor protein inducing IFN-β; TRAM: TRIF related adaptor molecule; IFR3: IFN regulatory factor 3; IRFBS: IRF-binding site; JNK: Janus kinase; AP-1: activator protein 1, composed of the Jun and Fos proteins.