Sandbox Reserved 1121: Difference between revisions

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== Function ==

CRP is involved in the first line of innate host defense. Its main function is to clear bacterial pathogens and apoptotic and necrotic cells. In fact, CRP binds to PC located on the surface of pathogenic bacteria that infected the organism. The resulting immune response is the phagocytosis of PC-expressing bacteria <ref name="agrawal"/>. PC is present in teichoic acids, capsular carbohydrates, and lipopolysaccharides of bacteria and other micro-organisms. There are many micro-organisms that synthetize PC, such as ''Streptococcus pneumoniae'', ''Haemophilus influenzae'', ''Pseudomonas aeruginosa'', ''Neisseria meningitides'' and ''Neisseria gonorrhoeae'', ''Proteus morganii and Aspergillus fumigatus'' <ref name="Volanakis"/>.

CRP is involved in the first line of innate host defense. Its main function is to clear bacterial pathogens and apoptotic and necrotic cells. In fact, CRP binds to PC located on the surface of pathogenic bacteria that infected the organism. The resulting immune response is the phagocytosis of PC-expressing bacteria<ref name="agrawal"/>. PC is present in teichoic acids, capsular carbohydrates, and lipopolysaccharides of bacteria and other micro-organisms. There are many micro-organisms that synthetize PC, such as ''Streptococcus pneumoniae'', ''Haemophilus influenzae'', ''Pseudomonas aeruginosa'', ''Neisseria meningitides'' and ''Neisseria gonorrhoeae'', ''Proteus morganii and Aspergillus fumigatus''<ref name="Volanakis"/>.

Because the five PC-binding sites are on the face B of the pentamer, CRP binds with high probability to ligand-covered targets such as bacteria or other biological membranes. On its other face, CRP is able to recognize C1q or Fc receptors which have an inflammatory effect <ref name = "Alex">PMID: 12616974</ref>. Macrophages synthetize membrane C1q and Fc-receptors that will bind to the face A of CRP. C1q and Fc are opsonins, which means that they are molecules that enhance phagocytosis by marking an antigen for an immune response. Therefore, they mark the targeted cell as an antigen. The macrophages have C1q and FC-binding site, they will therefore detect the marked cell and clear it <ref name = "Terheyden">PMID: 16023736</ref>.

Because the five PC-binding sites are on the face B of the pentamer, CRP binds with high probability to ligand-covered targets such as bacteria or other biological membranes. On its other face, CRP is able to recognize C1q or Fc receptors which have an inflammatory effect<ref name = "Alex">PMID: 12616974</ref>. Macrophages synthetize membrane C1q and Fc-receptors that will bind to the face A of CRP. C1q and Fc are opsonins, which means that they are molecules that enhance phagocytosis by marking an antigen for an immune response. Therefore, they mark the targeted cell as an antigen. The macrophages have C1q and FC-binding site, they will therefore detect the marked cell and clear it<ref name = "Terheyden">PMID: 16023736</ref>.

== Biomedical consideration ==

It is known that CRP rate ~~increase~~ rapidly and ~~markedly~~ during inflammatory states. However, minor CRP elevation has been related with future major cardiovascular events. Indeed, studies have shown that a slightly elevated CRP plasma level (between 3 and 10 µg/mL) is associated with a risk of developing cardiovascular disease, metabolic syndrome and colon cancer <ref name="Black"/>.

It is known that CRP rate increases rapidly and remarkably during inflammatory states. However, minor CRP elevation has been related with future major cardiovascular events. Indeed, studies have shown that a slightly elevated CRP plasma level (between 3 and 10 µg/mL) is associated with a risk of developing cardiovascular disease, metabolic syndrome and colon cancer<ref name="Black"/>.

Nevertheless, minor increase of CRP ~~levels~~ is not necessarly associated with inflammation but could be linked to several genetic polymorphisms of ~~the~~ CRP and other gens, ethnicity, various dietary patterns and obesity <ref name="Black"/>.

Nevertheless, minor increase of CRP level is not necessarly associated with inflammation but could be linked to several genetic polymorphisms of CRP and other gens, ethnicity, various dietary patterns and obesity<ref name="Black"/>.

Futhermore, CRP might play a role in the pathogenesis of atherosclerosis, but the exact role of CRP in atherosclerosis is not known. It was found that CRP binds the phosphocholine of oxidized low density lipoproteins, up-regulates the expression of adhesion molecules in endothelial cells, increases low density lipoprotein uptake into macrophages, inhibits endothelial nitric-oxide synthase expression in aortic endothelial cells and increases plasminogen activator inhibitor-1 expression and activity <ref name="Black"/>. Transgenic mice deficient in apolipoprotein E and expressing high levels of CRP display a modest acceleration in aortic atherosclerosis <ref name="Black"/>.

Futhermore, CRP might play a role in the pathogenesis of atherosclerosis, but the exact role of CRP in atherosclerosis is not known yet. It was found that CRP binds the phosphocholine of oxidized low density lipoproteins, up-regulates the expression of adhesion molecules in endothelial cells, increases low density lipoprotein uptake into macrophages, inhibits endothelial nitric-oxide synthase expression in aortic endothelial cells and increases plasminogen activator inhibitor-1 expression and activity<ref name="Black"/>. Transgenic mice deficient in apolipoprotein E and expressing high levels of CRP display a modest acceleration in aortic atherosclerosis<ref name="Black"/>.

== References ==

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@@ Line 34: / Line 34: @@
 == Function ==
-CRP is involved in the first line of innate host defense. Its main function is to clear bacterial pathogens and apoptotic and necrotic cells. In fact, CRP binds to PC located on the surface of pathogenic bacteria that infected the organism. The resulting immune response is the phagocytosis of PC-expressing bacteria <ref name="agrawal"/>. PC is present  in teichoic acids, capsular carbohydrates, and lipopolysaccharides of bacteria and other micro-organisms. There are many micro-organisms that synthetize PC, such as ''Streptococcus pneumoniae'', ''Haemophilus influenzae'', ''Pseudomonas aeruginosa'', ''Neisseria meningitides'' and ''Neisseria gonorrhoeae'', ''Proteus morganii and Aspergillus fumigatus''  <ref name="Volanakis"/>.
+CRP is involved in the first line of innate host defense. Its main function is to clear bacterial pathogens and apoptotic and necrotic cells. In fact, CRP binds to PC located on the surface of pathogenic bacteria that infected the organism. The resulting immune response is the phagocytosis of PC-expressing bacteria<ref name="agrawal"/>. PC is present  in teichoic acids, capsular carbohydrates, and lipopolysaccharides of bacteria and other micro-organisms. There are many micro-organisms that synthetize PC, such as ''Streptococcus pneumoniae'', ''Haemophilus influenzae'', ''Pseudomonas aeruginosa'', ''Neisseria meningitides'' and ''Neisseria gonorrhoeae'', ''Proteus morganii and Aspergillus fumigatus''<ref name="Volanakis"/>.
-Because the five PC-binding sites are on the face B of the pentamer, CRP binds with high probability to ligand-covered targets such as bacteria or other biological membranes. On its other face, CRP is able to recognize C1q or Fc receptors which have an inflammatory effect <ref name = "Alex">PMID: 12616974</ref>. Macrophages synthetize membrane C1q and Fc-receptors that will bind to the face A of CRP. C1q and Fc are opsonins, which means that they are molecules that enhance phagocytosis by marking an antigen for an immune response. Therefore, they mark the targeted cell as an antigen. The macrophages have C1q and FC-binding site, they will therefore detect the marked cell and clear it <ref name = "Terheyden">PMID: 16023736</ref>.
+Because the five PC-binding sites are on the face B of the pentamer, CRP binds with high probability to ligand-covered targets such as bacteria or other biological membranes. On its other face, CRP is able to recognize C1q or Fc receptors which have an inflammatory effect<ref name = "Alex">PMID: 12616974</ref>. Macrophages synthetize membrane C1q and Fc-receptors that will bind to the face A of CRP. C1q and Fc are opsonins, which means that they are molecules that enhance phagocytosis by marking an antigen for an immune response. Therefore, they mark the targeted cell as an antigen. The macrophages have C1q and FC-binding site, they will therefore detect the marked cell and clear it<ref name = "Terheyden">PMID: 16023736</ref>.
 == Biomedical consideration ==
-It is known that CRP rate increase rapidly and markedly during inflammatory states. However, minor CRP elevation has been related with future major cardiovascular events. Indeed, studies have shown that a slightly elevated CRP plasma level (between 3 and 10 µg/mL) is associated with a risk of developing cardiovascular disease, metabolic syndrome and colon cancer <ref name="Black"/>.
+It is known that CRP rate increases rapidly and remarkably during inflammatory states. However, minor CRP elevation has been related with future major cardiovascular events. Indeed, studies have shown that a slightly elevated CRP plasma level (between 3 and 10 µg/mL) is associated with a risk of developing cardiovascular disease, metabolic syndrome and colon cancer<ref name="Black"/>.
-Nevertheless, minor increase of CRP levels is not necessarly associated with inflammation but could be linked to several genetic polymorphisms of the CRP and other gens, ethnicity, various dietary patterns and obesity <ref name="Black"/>.
+Nevertheless, minor increase of CRP level is not necessarly associated with inflammation but could be linked to several genetic polymorphisms of CRP and other gens, ethnicity, various dietary patterns and obesity<ref name="Black"/>.
-Futhermore, CRP might play a role in the pathogenesis of atherosclerosis, but the exact role of CRP in atherosclerosis is not known. It was found that CRP binds the phosphocholine of oxidized low density lipoproteins, up-regulates the expression of adhesion molecules in endothelial cells, increases low density lipoprotein uptake into macrophages, inhibits endothelial nitric-oxide synthase expression in aortic endothelial cells and increases plasminogen activator inhibitor-1 expression and activity <ref name="Black"/>. Transgenic mice deficient in apolipoprotein E and expressing high levels of CRP display a modest acceleration in aortic atherosclerosis <ref name="Black"/>.
+Futhermore, CRP might play a role in the pathogenesis of atherosclerosis, but the exact role of CRP in atherosclerosis is not known yet. It was found that CRP binds the phosphocholine of oxidized low density lipoproteins, up-regulates the expression of adhesion molecules in endothelial cells, increases low density lipoprotein uptake into macrophages, inhibits endothelial nitric-oxide synthase expression in aortic endothelial cells and increases plasminogen activator inhibitor-1 expression and activity<ref name="Black"/>. Transgenic mice deficient in apolipoprotein E and expressing high levels of CRP display a modest acceleration in aortic atherosclerosis<ref name="Black"/>.
 == References ==
 <references/>