'The purpose of the current study was to examine the binding of pulmonary surfactant protein A (SP-A) to TLR4 and MD-2, which are critical signaling receptors for lipopolysaccharides (LPSs). The direct binding of SP-A to the recombinant soluble form of extracellular TLR4 domain (sTLR4) and MD-2 was detected using solid-phase ... More
Activation of innate immunity in the CNS triggers neurodegeneration through a Toll-like receptor 4-dependent pathway.
Innate immunity is an evolutionarily ancient system that provides organisms with immediately available defense mechanisms through recognition of pathogen-associated molecular patterns. We show that in the CNS, specific activation of innate immunity through a Toll-like receptor 4 (TLR4)-dependent pathway leads to neurodegeneration. We identify microglia as the major lipopolysaccharide (LPS)-responsive ... More
Lipopolysaccharide (LPS) labeled with Alexa 488 hydrazide as a novel probe for LPS binding studies.
AuthorsTriantafilou K, Triantafilou M, Fernandez N
JournalCytometry
PubMed ID11084617
BACKGROUND: Lipopolysaccharide (LPS) comprises the outer cell wall of all gram-negative bacteria. It consists of an oligosaccharide core and lipid A. All LPS-induced biological responses are lipid A-dependent. Once released, LPS triggers a host systemic inflammatory response that leads to septic shock. Binding studies have helped to reveal some of ... More
The toll-like receptor TLR4 is necessary for lipopolysaccharide-induced oligodendrocyte injury in the CNS.
The immediate or innate immune response is the first line of defense against diverse microbial pathogens and requires the expression of recently discovered toll-like receptors (TLRs). TLR4 serves as a specific receptor for lipopolysaccharide (LPS) and is localized on the surface of a subset of mammalian cells. Although innate immunity ... More
Lipopolysaccharide Is Cleared from the Circulation by Hepatocytes via the Low Density Lipoprotein Receptor.
Authors
JournalPLoS One
PubMed ID27171436
Direct binding of polymeric GBP1 to LPS disrupts bacterial cell envelope functions.