Peptidoglycan and lipoteichoic acid in gram-positive bacterial sepsis: receptors, signal transduction, biological effects, and synergism.
In sepsis and multiple organ dysfunction syndrome (MODS) caused by gram-negative bacteria, lipopolysaccharide (LPS) initiates the early signaling events leading to the deleterious inflammatory response. However, it has become clear that LPS can not reproduce all of the clinical features of sepsis, which emphasize the roles of other contributing factors. Gram-positive bacteria, which lack LPS, are today responsible for a substantial part of the incidents of sepsis with MODS. The major wall components of gram-positive bacteria, peptidoglycan and lipoteichoic acid, are thought to contribute to the development of sepsis and MODS. In this review, the literature underlying our current understanding of how peptidoglycan and lipoteichoic acid activate inflammatory responses will be presented, with a focus on recent advances in this field.
Wang
Jacob E
JE
The William Harvey Research Institute, Charterhouse Square, London EC1M 6BC, United Kingdom. jacob.wang@klinmed.uio.no
Dahle
Maria K
MK
McDonald
Michelle
M
Foster
Simon J
SJ
Aasen
Ansgar O
AO
Thiemermann
Christoph
C
D000818:Animals; D002473:Cell Wall / Q000737:chemistry / Q000187:drug effects; D016207:Cytokines / Q000187:drug effects* / Q000378:metabolism; D004357:Drug Synergism; D004731:Endotoxins / Q000276:immunology / Q000494:pharmacology; D006801:Humans; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology*; D008954:Models, Biological; D010457:Peptidoglycan / Q000276:immunology / Q000494:pharmacology*; D011956:Receptors, Cell Surface / Q000502:physiology; D018805:Sepsis / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology; D015398:Signal Transduction / Q000502:physiology; D013682:Teichoic Acids / Q000276:immunology / Q000494:pharmacology*
D016207:Cytokines; D004731:Endotoxins; D008070:Lipopolysaccharides; D010457:Peptidoglycan; D011956:Receptors, Cell Surface; D013682:Teichoic Acids; C009900:lipoteichoic acid