Lipoteichoic acid (LTA) is a major constituent of thecell wall ofgram-positive bacteria. These organisms have an inner (or cytoplasmic) membrane and, external to it, a thick (up to 80nanometer)peptidoglycan layer. The structure of LTA varies between the different species of gram-positive bacteria and may contain long chains ofribitol orglycerol phosphate. LTA is anchored to the cell membrane via adiacylglycerol.[1] It acts as regulator ofautolytic wallenzymes (muramidases). It has antigenic properties being able to stimulate specific immune response.
LTA may bind to target cells non-specifically through membranephospholipids, or specifically toCD14 and toToll-like receptors. Binding toTLR-2 has shown to induceNF-κB expression(a centraltranscription factor), elevating expression of both pro- and anti-apoptotic genes. Its activation also inducesmitogen-activated protein kinases (MAPK) activation along withphosphoinositide 3-kinase activation.
LTA's molecular structure has been found to have the strongest hydrophobic bonds of an entire bacteria[citation needed].
Said et al. showed that LTA causes anIL-10-dependent inhibition ofCD4 T-cell expansion and function by up-regulatingPD-1 levels on monocytes which leads to IL-10 production by monocytes after binding of PD-1 by PD-L.[2]
Lipoteichoic acid (LTA) from Gram-positive bacteria exerts different immune effects depending on the bacterial source from which it is isolated. For example, LTA fromEnterococcus faecalis is a virulence factor positively correlating to inflammatory damage to teeth during acute infection.[3] On the other hand, a study reportedLacticaseibacillus rhamnosus GG LTA (LGG-LTA) oral administration reduces UVB-induced immunosuppression and skin tumor development in mice.[4] In animal studies, specific bacterial LTA has been correlated with induction of arthritis, nephritis, uveitis, encephalomyelitis, meningeal inflammation, and periodontal lesions, and also triggered cascades resulting in septic shock and multiorgan failure.
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