Lipopolysaccharide
You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.
Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [1] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Lipopolysaccharide (LPS) is a large molecule consisting of a lipid and a polysaccharide (carbohydrate) joined by a covalent bond.
Functions
LPS is a major component of the outer membrane of Gram-negative bacteria, contributing greatly to the structural integrity of the bacteria, and protecting the membrane from certain kinds of chemical attack. LPS is an endotoxin, and induces a strong response from normal animal immune systems. The only Gram-positive bacteria that possesses LPS is Listeria monocytogenes, the common infective agent in unpasteurized milk.
LPS acts as the prototypical endotoxin, because it binds the CD14/TLR4/MD2 receptor complex, which promotes the secretion of pro-inflammatory cytokines in many cell types, but especially in macrophages. An "LPS challenge" in immunology is the exposing of the subject to an LPS which may act as a toxin.
LPS also increases the negative charge of the cell membrane and helps stabilize the overall membrane structure.
Composition
It comprises three parts:
- polysaccharide (O) side chains
- core polysaccharide (core oligosaccharide in genus Neisseria)
- lipid A
Lipid A
Lipid A contains unusual fatty acids (e.g. hydroxy-myristic acid) and is embedded into the outer membrane while the rest of the LPS projects from the surface. This is the key in the toxicity.
Core oligosaccharide
Core oligosaccharide contains unusual sugars (e.g. KDO, keto-deoxyoctulonate and heptose).
The core oligosaccharide is attached to lipid A, which is also in part responsible for the toxicity of gram-negative bacteria.
O-antigen
The polysaccharide side chain is referred to as the O-antigen of the bacteria. O side chain (O-antigen) is also a polysaccharide chain that extends from the core polysaccharide. The composition of the O side chain varies between different gram-negative bacterial strains. The presence or absence of O chains determine whether the LPS is considered rough or smooth. Full length O-chains would render the LPS smooth while the absence or reduction of O-chains would make the LPS rough. [1]Bacteria with rough LPS usually have more penetrable cell membranes to hydrophobic antibiotics since a rough LPS is more hydrophobic. [1]
O side chains are easily recognized by the antibodies of the host, however, the nature of the chain can easily be modified by Gram-negative bacteria to avoid detection. The structure of the core and the O-antigen is often determined by methylation analysis or NMR-spectroscopy.
LPS modifications
The making of LPS can be modified in order to present a specific sugar structure. Those can be recognised by either other LPS (which enables to inhibit LPS toxins) or glycosyltransferases which use those sugar structure to add more specific sugars.
Variability and effect upon specificity
O-antigens (the outer carbohydrates) are the most variable portion of the LPS molecule, imparting the antigenic specificity. In contrast, lipid A is the most conserved part. However, —lipid A composition also may vary (e.g., in number and nature of acyl chains even within or between genera). Some of these variations may impart antagonistic properties to these LPS. For example Rhodobacter sphaeroides diphosphoryl lipid A (RsDPLA) is a potent antagonist of LPS in human cells, but is an agonist in hamster and equine cells.
It has been speculated that conical Lipid A (eg from E coli) are more agonistic, less conical lipid A like those of Porphyromonas gingivalis may activate a different signal (TLR2 instead of TLR4), and completely cylindrical lipid A like that of Rhodobacter sphaeroides is antagonistic to TLRs.[1][1]
Functions
LPS function has been under experimental research for several years due to its role in activating many transcription factors. LPS also produces many types of mediators involved in septic shock.
Diversity
Lipololysaccharide gene clusters are highly variable between different strains, subspecies, species of bacterial pathogens of plants and animals.[1][1]
References
See also
External links
it:Lipopolisaccaride he:ליפופוליסכרידsv:Lipopolysackarider uk:Ліпополісахариди
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
