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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAfs1rQmvVH_UxW3HENzAzXs2TPM_NWjmTK6gRmv0MHQE#_4 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAfs1rQmvVH_UxW3HENzAzXs2TPM_NWjmTK6gRmv0MHQE#_3 http://www.w3.org/ns/prov#value Figure 7 Model of PMN NADPH oxidase–derived oxidant signaling in mediating the TLR4-TLR2 cross talk in endothelial cells. LPS stimulation induces NADPH oxidase activation and production of reactive oxygen species (ROS) in PMNs as well as the initiation of MyD88-dependent NF-κB signaling in endothelial cells and the consequent expression of TLR2 and ICAM-1. Adhesion of PMNs to endothelial cells is mediated by binding of constitutive ICAM-1 to CD18 integrin and provides the appropriate coupling required for PMNs to transmit oxidant signals to endothelial cells. The oxidants augment NF-κB signaling and TLR2 expression (+), which results in the augmented response of the cell to PGN, thereby amplifying ICAM-1 expression (circled +) and promoting stable adhesion of PMNs to endothelial cells and increased PMN migration. 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