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Abstract
Lipopolysaccharide (LPS [endotoxin]) is the principal component of the outer membrane
of Gram-negative bacteria. Recent studies have elucidated how LPS is recognized by
monocytes and macrophages of the innate immune system. Human monocytes are exquisitely
sensitive to LPS and respond by expressing many inflammatory cytokines. LPS binds
to LPS-binding protein (LBP) in plasma and is delivered to the cell surface receptor
CD14. Next, LPS is transferred to the transmembrane signaling receptor toll-like receptor
4 (TLR4) and its accessory protein MD2. LPS stimulation of human monocytes activates
several intracellular signaling pathways that include the IkappaB kinase (IKK)-NF-kappaB
pathway and three mitogen-activated protein kinase (MAPK) pathways: extracellular
signal-regulated kinases (ERK) 1 and 2, c-Jun N-terminal kinase (JNK) and p38. These
signaling pathways in turn activate a variety of transcription factors that include
NF-kappaB (p50/p65) and AP-1 (c-Fos/c-Jun), which coordinate the induction of many
genes encoding inflammatory mediators.