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. 2020 Apr 21;7:130. doi: 10.3389/fmed.2020.00130

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Copyright © 2020 Gandhi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic of LPS-induced signaling in inflammatory cells. LPS in association with LBP (LPS-binding protein) binds to CD14, which then stimulates TLR4 signaling. The adapter proteins MD2 (on the outer side of the cell membrane), and TRIF (TIR-domain-containing adapter-inducing interferon-β), TRAM (TRIF-related adaptor molecule), MyD88 and TIRAP (Toll-Interleukin 1 receptor domain containing adaptor protein) that are associated with the intracellular part of TLR4 are required for LPS-induced and TLR4-stimulated activation of intracellular signaling via NFkB, mitogen activated protein kinases (MAPKs) p38, ERK1/2, and JNK1/2 and well as interferon-regulatory factor (IRF) 1 and 3. Translocation of these activated transcription factors to the nucleus and their subsequent binding to appropriate promoter regions on the DNA instigate transcription of a several cytokines, chemokines and growth mediators specific to a given cell type. The released mediators then act on target cells to promote pathophysiological processes. Adapted from Schwabe et al. (27), Akira et al. (28).