- Lipoteichoic acid
Lipoteichoic acid (LTA) is a surface-associated
adhesion amphiphilefrom Gram-positivebacteria and regulator of autolytic wall enzymes( muramidases). It is released from the bacterial cells mainly after bacteriolysisinduced by lysozyme, cationic peptidesfrom leucocytes, or beta-lactamantibiotics.
LTA may bind to target cells non-specifically through membrane
phospholipids, or specifically to CD14and to Toll-like receptors. Binding to TLR-2has shown to induce NF-kBexpression(a central transcription factor), elevating expression of both pro- and anti- apoptoticgenes. Its activation also induces mitogen-activated protein kinases(MAPK) activation along with Phosphoinositide 3-kinaseactivation.
LTA bound to targets can interact with circulating
antibodiesand activate the complement cascadeto induce a passive immune kill phenomenon. It also triggers the release from neutrophils and macrophages of reactive oxygen and nitrogen species, acid hydrolases, highly cationic proteinases, bactericidal cationic peptides, growth factors, and cytotoxic cytokines, which may act in synergy to amplify cell damage. Therefore, LTA shares many pathogenic similarities with endotoxins (lipopolysaccharide).
tudies on Lipoteichoic acid
In animal studies, LTA has induced
arthritis, nephritis, uveitis, encephalomyelitis, meningeal inflammation, and periodontal lesions, and also triggered cascades resulting in septic shockand multiorgan failure. Binding of LTA to targets can be inhibited by phospholipids and antibodies directed at LTA, CD14, or Toll-like receptors. In vitro, LTA release can be inhibited by non- bacteriolyticantibiotics and by polysulphatessuch as heparin.
LTA can be considered a
virulence factorthat has an important role in infections and in postinfectious sequelaecaused by Gram-positive bacteria. The development of effective antibacteriolitic drugs and multidrug strategies to attenuate LTA-induced secretion of proinflammatory agonists is of great importance to combat septic shock and multiorgan failure caused by Gram-positive bacteria.
*Department of Oral Biology, Hebrew University-Hadassah Faculty of Dental Medicine, Ein-Kerem Campus, Jerusalem, Israel.
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