| Glycocalyx | |
|---|---|
 TEMmicrograph of aB. subtilis bacterium, with the hair-like glycocalyx visible surrounding the cell membrane (scale bar = 200 nm) | |
| Identifiers | |
| MeSH | D019276 |
| TH | H1.00.01.1.00002 |
| FMA | 66838 |
| Anatomical terms of microanatomy | |
Theglycocalyx (pl.:glycocalyces orglycocalyxes), also known as thepericellular matrix andcell coat, is a layer ofglycoproteins andglycolipids which surround thecell membranes ofbacteria,epithelial cells, and other cells.[1]
Animalepithelial cells have a fuzz-like coating on the external surface of theirplasma membranes. This viscous coating is the glycocalyx that consists of several carbohydratemoieties of membraneglycolipids andglycoproteins, which serve as backbone molecules for support. Generally, thecarbohydrate portion of the glycolipids found on the surface of plasma membranes helps these molecules contribute tocell–cell recognition, communication, and intercellular adhesion.[2]
The glycocalyx is a type of identifier that the body uses to distinguish between its own healthy cells and transplanted tissues, diseased cells, or invading organisms. Included in the glycocalyx are cell-adhesion molecules that enable cells to adhere to each other and guide the movement of cells during embryonic development.[3] The glycocalyx plays a major role in regulation ofendothelialvascular tissue, including the modulation ofred blood cell volume incapillaries.[4]
The term was initially applied to the polysaccharide matrix coating epithelial cells, but its functions have been discovered to go well beyond that.
The glycocalyx is located on theapical surface of vascular endothelial cells which line thelumen. When vessels are stained with cationic dyes such asAlcian blue stain,transmission electron microscopy shows a small, irregularly shaped layer extending approximately 50–100 nm into the lumen of a blood vessel. Another study usedosmium tetroxide staining during freeze substitution, and showed that the endothelial glycocalyx could be up to 11 μm thick.[5] It is present throughout a diverse range of microvascular beds (capillaries) and macrovessels (arteries and veins). The glycocalyx also consists of a wide range of enzymes and proteins that regulateleukocyte andthrombocyte adherence, since its principal role in the vasculature is to maintain plasma and vessel-wall homeostasis. These enzymes and proteins include:
The enzymes and proteins listed above serve to reinforce the glycocalyx barrier against vascular and other diseases. Another main function of the glycocalyx within the vascular endothelium is that it shields the vascular walls from direct exposure to blood flow, while serving as a vascular permeability barrier.[6] Its protective functions are universal throughout the vascular system, but its relative importance varies depending on its exact location in the vasculature. In microvascular tissue, the glycocalyx serves as a vascular permeability barrier by inhibiting coagulation and leukocyte adhesion. Leukocytes must not stick to the vascular wall because they are important components of theimmune system that must be able to travel to a specific region of the body when needed. In arterial vascular tissue, the glycocalyx also inhibits coagulation and leukocyte adhesion, but through mediation ofshear stress-induced nitric oxide release. Another protective function throughout the cardiovascular system is its ability to affect the filtration ofinterstitial fluid from capillaries into the interstitial space.[7]
The glycocalyx, which is located on theapical surface ofendothelial cells, is composed of a negatively charged network ofproteoglycans, glycoproteins, and glycolipids.[8] Along the luminal surface of the vascular glycocalyx exists an empty layer that excludes red blood cells.[9]
Because the glycocalyx is so prominent throughout the cardiovascular system, disruption to this structure has detrimental effects that can cause disease. Certain stimuli that causeatheroma may lead to enhanced sensitivity of vasculature. Initial dysfunction of the glycocalyx can be caused by hyperglycemia or oxidized low-density lipoproteins (LDLs), which then causesatherothrombosis. In microvasculature, dysfunction of the glycocalyx leads to internal fluid imbalance, and potentiallyedema. In arterial vascular tissue, glycocalyx disruption causes inflammation and atherothrombosis.[10]
Experiments have been performed to test precisely how the glycocalyx can be altered or damaged. One particular study used an isolated perfused heart model designed to facilitate detection of the state of the vascular barrier portion, and sought to cause insult-induced shedding of the glycocalyx to ascertain the cause-and-effect relationship between glycocalyx shedding and vascular permeability.Hypoxic perfusion of the glycocalyx was thought to be sufficient to initiate a degradation mechanism of the endothelial barrier. The study found that flow of oxygen throughout the blood vessels did not have to be completely absent (ischemic hypoxia), but that minimal[clarification needed] levels of oxygen were sufficient to cause the degradation. Shedding of the glycocalyx can be triggered by inflammatory stimuli, such astumor necrosis factor-alpha. Whatever the stimulus is, however, shedding of the glycocalyx leads to a drastic[clarification needed] increase in vascular permeability. Vascular walls being permeable is disadvantageous, since that would enable passage of some macromolecules or other harmful antigens.[11]
Other sources of damage to the endothelial glycocalyx have been observed in several pathological conditions such as inflammation,[12] hyperglycemia,[13] ischemia-reperfusion,[14] viral infections[15] and sepsis.[16]
Some key components of the glycocalyx such assyndecans,heparan sulphate,chondroitin sulphate andhyaluronan can be shed of the endothelial layer by enzymes.Hyaluronidase, hepararanse/heparinase, matrix and membrane-typematrix metalloproteases, thrombin, plasmin and elastase are some examples of enzymes that can induce shedding of the glycocalyx and these sheddases can therefor contribute to degradation of the glycocalyx layer in several pathological conditions.[17] Research shows that plasma hyaluronidase activity is decreased in experimental as well as in clinical septic shock and is therefore not considered to be a sheddase in sepsis.[18] Concomitant, the endogenous plasma inhibition of hyaluronidase is increased and could serve as a protection against glycocalyx shedding.
Fluid shear stress is also a potential problem if the glycocalyx is degraded for any reason. This type of frictional stress is caused by the movement of viscous fluid (i.e. blood) along the lumen boundary. Another similar experiment was carried out to determine what kinds of stimuli cause fluid shear stress. The initial measurement was taken with intravital microscopy, which showed a slow-moving plasma layer, the glycocalyx, of 1 μm thick. Light dye damaged the glycocalyx minimally, but that small change increased capillaryhematocrit. Thus, fluorescence light microscopy should not be used to study the glycocalyx because that particular method uses a dye. The glycocalyx can also be reduced in thickness when treated with oxidized LDL.[19] These stimuli, along with many other factors, can cause damage to the delicate glycocalyx. These studies are evidence that the glycocalyx plays a crucial role in cardiovascular system health.
A glycocalyx, literally meaning "sugar coat" (glykys = sweet,kalyx = husk), is a network ofpolysaccharides that project from cellular surfaces ofbacteria, which classifies it as a universal surface component of a bacterial cell, found just outside the bacterial cell wall. A distinct, gelatinous glycocalyx is called acapsule, whereas an irregular, diffuse layer is called aslime layer. This coat is extremely hydrated and stains withruthenium red.
Bacteria growing in natural ecosystems, such as in soil, bovine intestines, or the human urinary tract, are surrounded by some sort of glycocalyx-enclosedmicrocolony.[20] It serves to protect the bacterium from harmfulphagocytes by creating capsules or allowing the bacterium to attach itself to inert surfaces, such as teeth or rocks, viabiofilms (e.g.Streptococcus pneumoniae attaches itself to either lung cells,prokaryotes, or other bacteria which can fuse their glycocalices to envelop the colony).
A glycocalyx can also be found on the apical portion ofmicrovilli within thedigestive tract, especially within the small intestine. It creates a meshwork 0.3 μm thick and consists of acidicmucopolysaccharides and glycoproteins that project from theapicalplasma membrane of epithelial absorptive cells. It provides additional surface foradsorption and includesenzymes secreted by the absorptive cells that are essential for the final steps of digestion of proteins and sugars.
