Reprint

Lipopolysaccharides (LPSs)

Edited by
February 2020
389 pages
  • ISBN978-3-03928-256-2 (Paperback)
  • ISBN978-3-03928-257-9 (PDF)

This book is a reprint of the Special Issue Lipopolysaccharides (LPSs) that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary
The cytoplasm of Gram-negative bacteria is bound by three layers: an inner membrane, a layer of peptidoglycan, and an outer membrane. The outer membrane is an asymmetric lipidic bilayer, with phospholipids on its inner surface and lipopolysaccharides (LPSs) on the outside, with the latter being the major component of the outer leaflet and covering nearly three-quarters of the total outer cell surface. All LPSs possess the same general chemical architecture independently of bacterial activity (pathogenic, symbiotic, commensal), ecological niche (human, animal, soil, plant, water), or growth conditions. Endotoxins are large amphiphilic molecules consisting of a hydrophilic polysaccharide component and a covalently bound hydrophobic and highly conserved lipid component, termed lipid A (the endotoxin subunit). The polysaccharide component can be divided into two subdomains: the internal and conserved core region as well as the more external and highly variable O-specific chain, also referred to as the O-antigen due to its immunogenic properties. LPSs are endotoxins, one of the most potent class of activators of the mammalian immune system; they can be released from cell surfaces of bacteria during multiplication, lysis, and death. LPS can act through its biological center (lipid A component) on various cell types, of which macrophages and monocytes are the most important.
Format
  • Paperback
License
© 2020 by the authors; CC BY licence
Keywords
aspirin; hepcidin; P65 (nuclear factor-κB); IL-6/JAK2/STAT3 pathway; lipopolysaccharide (LPS); nitric oxide (NO); iron regulatory protein 1 (IRP1); Megalobrama amblycephala; lipopolysaccharide induced TNFα factor; lipopolysaccharide stimulation; innate immune; Aeromonas; genomics; inner core oligosaccharide; outer core oligosaccharide; lipopolysaccharide; lipopolysaccharide; Erwinia amylovora; NMR; ESI FT-ICR; structural determination; Bordetellae; Bordetella holmesii; endotoxin; lipid A; structure; mass spectrometry; genomic; Edwardsiella tarda; core oligosaccharide; MALDI-TOF MS; ESI MSn; NMR; genomic; LPS tolerance; hypothalamic inflammation; insulin resistance; pJNK; fibroblast; keratocyte; cornea; lipopolysaccharide; bacteria; chemokine; adhesion molecule; collagen; tear fluid; serum resistance; complement; Salmonella; lipopolysaccharide; sialic acid; reptile-associated salmonellosis; sepsis; time response; inflammation; oxidative stress; endotoxaemia; mouse; rat; lipopolysaccharide; double-stranded RNA; epithelial cell; dendritic cell; allergic respiratory disorder; hygiene hypothesis; rhinovirus; respiratory syncytial virus; toll-like receptor; LPS; lipopolysaccharide; heptosyltransferase; protein dynamics; glycosyltransferase; GT-B; inhibitor design; lipopolysaccharide; Coxiella burnetii; Q fever; phagosome; virenose; Plesiomonas shigelloides; O-antigen; lipopolysaccharide; O-acetylation; d-galactan I; HR-MAS; NMR spectroscopy; endotoxin; lipopolysaccharide; Low Endotoxin Recovery; phase transitions; polysorbate; LPS aggregates; Small Angle X-ray Scattering; MAT; LAL and LER; anti-conjugate serum; core oligosaccharide; lipopolysaccharide; NMR spectroscopy; ESI MS; Proteus penneri