Lipopolysaccharide Binding Protein
The concentration of Lipopolysaccharide Binding Protein plays a major role in the development of gram-negative sepsis. Essentially, low concentration of Lipopolysaccharide Binding Protein enhances the activation of mononuclear cells, which are induced by LPS. On the other hand, high levels of Lipopolysaccharide Binding Proteins suppress the cellular stimulation of LPS. While this is the case, experiments show that LBP usually mediates LPS release from MNC even in cases where serum is absent. Thus, it is possible to deduce that that the presence of Lipopolysaccharide Binding Protein is not limited to serum in soluble but could also be incorporated in form of a trans-membrane protein, mainly on the cytoplasmic membrane.
In human beings, Lipopolysaccharide Binding Protein belongs to lipid-binding proteins. Some of these proteins include permeability-increasing protein (BPI), cholesterol ester transfer protein and phospholipid ester transfer protein. In terms of composition, it contains 456 residues of amino acid, which is preceded by a hydrophobic signal pattern that has 25 residues. Hepatocytes and intestinal epithelial cells, are responsible for the synthesis of lipopolysaccharide binding protein, and are usually present in normal serum, at a level of 5 to 10 μg/ml. However, this concentration could rise to 200 μg/ml, twenty-four hours after the introduction of an acute-state reaction.
What causes the rise in Lipopolysaccharide Binding Protein? This occurs because of transcriptional activation of the protein gen, which is linked by (IL-1) and IL-6. It is important to note that LBP plays a wide range of functions. For instance, it binds a range of LPS chemotypes against rough and smooth strains of gram-negative bacteria, compounded with lipid A. Thus, LPS molecules play a crucial role in mediating during pathogenesis of septic shock and gram-negative sepsis. Additionally, lipid A is commonly considered endotoxic code of LPS since it is responsible for most of its biological activities.
For monocytes and macrophages to produce inflammatory cytokines, they need activation by LPSs together with other vital mediators. This is possible through the intracellular signal intensification. Besides acting as mediators, these elements further act on more target cells, which results into the production of cardiovascular shock, septic shock and multisystem organ failure. It is saddening to mention that this is one of the leading causes of deaths in intensive care units around the world. Moreover, receptors are widely known to mediate in different cellular responses.
Lipopolysaccharide Binding Protein further increases the activity of LPS to stimulate mononuclear phagocytes to release cytokine. Noteworthy, when LBP is neutralized with anti-LBP antibodies, this inhibits LPS to attach on monocytes. Importantly, there is research evidence, showing how LPS neutralization contrasts LPS induced activation. For instance, when the concentration is too high, LBP does not permit the release of LPS-linked cytokine. This further stops hepatic failure, resulting in low death rate of mice with LPS difficulty. Furthermore, experts often compare LBP to BPI. In both cases, the protein binds LPS. In human beings, a sequence comparison for the two shows that there is 44% resemblance of amino acids. The presence of BPI has also been detected on cell surfaces for blood monocytes.
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Retrieved from:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC100074/
http://www.uniprot.org/uniprot/P18428