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Gene Review

CRP  -  C-reactive protein, pentraxin-related

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Disease relevance of CRP


High impact information on CRP


Chemical compound and disease context of CRP


Biological context of CRP

  • Detection of SNPs and linkage and radiation hybrid mapping of the porcine C-reactive protein (CRP ) gene [10].
  • Intraluminal treatment with a clinically relevant concentration of CRP (7 microg/mL; 1 hour) significantly attenuated the NO release and vasodilation to serotonin [11].
  • Herein, we examined whether CRP can modulate endothelium-dependent NO-mediated dilation of coronary arterioles and whether proinflammatory signaling pathways such as stress-activated protein kinases (p38 and c-Jun N-terminal kinase [JNK]) and oxidative stress are involved in the CRP-mediated effect [11].
  • An estimate of the phylogenetic relationship among the pentraxin genes suggests that SAP and CRP arose as the result of a gene duplication event that occurred very early in mammalian evolution, but subsequent to the divergence of the reptilian ancestors of the mammalian and avian lineages [12].
  • Nonsynonymous substitution rates indicate that SAP and CRP are subject to similar, relatively low levels of constraint; at the amino acid sequence level the rate of evolution is approximately two replacements per site per 10(9) years [12].

Anatomical context of CRP

  • We conclude that serum CRP correlates with macrophage accumulation and coronary artery disease in hypercholesterolemic pigs [1].
  • There was little or no positive staining for CRP, SRA, or MCP-1 in the RCA of NF pigs, but there was extensive staining in lipidladen macrophage foam cells in the HF pigs [1].
  • Serum CRP correlated directly with plasma total cholesterol (R = 0.727, P = 0.041) and accumulation of SRA-positive macrophages (R = 0.938, P < 0.001) in RCA of HF pigs [1].
  • Dihydroethidium staining showed that CRP produced SB203850- and TEMPOL-sensitive superoxide production in the arteriolar endothelium [11].
  • These findings suggest that CRP may play a role in attenuating tissue damage secondary to activation of alveolar macrophages by inhibiting superoxide generation and mobilization of intracellular free calcium [13].

Associations of CRP with chemical compounds

  • The effect of CRP required the presence of calcium and was reversed by the addition of phosphocholine in a concentration-dependent manner [14].
  • CRP treatment of coronary arterioles significantly increased NAD(P)H oxidase activity [11].
  • The inhibition of surfactant adsorption by CRP was effectively eliminated by the addition of phosphocholine at a molar ratio of 300:1 (phosphocholine:CRP), but it was not diminished by the addition of identical molar ratios of o-phosphoethanolamine or DL-alpha-glycerophosphate at the same molar ratios [14].
  • The effects of CRP on superoxide production and intracellular calcium mobilization by guinea pig alveolar macrophages challenged with platelet-activating factor (PAF), N-formyl-methionyl-leucyl-phenylalanine (fMLP), and phorbol 12-myristate 13-acetate (PMA) were studied [13].
  • RESULTS: There were significant dose-related increases in CRP and alanine aminotransferase levels with liver electrolysis [15].

Other interactions of CRP

  • Levels of IL-10 and CRP were elevated from 10 and 14 d.p.i. respectively in the PMWS-affected piglets compared to the subclinically infected piglets [2].
  • A bioassay was used to detect IL-6 and ELISAs were used to detect IFN-alpha, IL-10, and CRP [2].
  • Following inoculation, WBC, band cell count, and CRP remained elevated above baseline in all groups throughout the study (P < 0.01) [16].
  • The structure and expression of the pentraxins, serum amyloid P component (SAP), and C-reactive protein (CRP), have been investigated in the guinea pig [12].
  • CD-18 expression and CRP levels were not significantly different between groups and TNF-alpha showed no changes in either group [17].

Analytical, diagnostic and therapeutic context of CRP

  • Serum levels of amylase, lipase, CRP, and TAP taken from the central venous blood were comparable in the two groups, except for higher amylase values 36 h after reperfusion in the CEL group compared to the UW group (P < 0.05) [18].
  • Northern blot analysis of hepatic RNA from animals in which acute inflammation had been induced by intraperitoneal injection of thioglycollate established that neither SAP or CRP is a major acute phase reactant in the guinea pig [12].
  • Blood flow (laser Doppler), partial oxygen tension, histological changes, endothelin-1 (plasma, immunohistochemistry), lipase, amylase, trypsinogen activation peptide, and C-reactive protein (CRP) were measured [18].
  • The CRP concentration was measured by using a CRP enzyme immunoassay [19].
  • We demonstrated an increase of CRP and HPG by livers from control pigs after a three-hour perfusion while pigs from CTC pretreated pigs varied in this response [20].


  1. C-reactive protein correlates with macrophage accumulation in coronary arteries of hypercholesterolemic pigs. Turk, J.R., Carroll, J.A., Laughlin, M.H., Thomas, T.R., Casati, J., Bowles, D.K., Sturek, M. J. Appl. Physiol. (2003) [Pubmed]
  2. Cytokine and C-reactive protein profiles induced by porcine circovirus type 2 experimental infection in 3-week-old piglets. Stevenson, L.S., McCullough, K., Vincent, I., Gilpin, D.F., Summerfield, A., Nielsen, J., McNeilly, F., Adair, B.M., Allan, G.M. Viral Immunol. (2006) [Pubmed]
  3. The acute phase response of acid soluble glycoprotein, alpha(1)-acid glycoprotein, ceruloplasmin, haptoglobin and C-reactive protein, in the pig. Eckersall, P.D., Saini, P.K., McComb, C. Vet. Immunol. Immunopathol. (1996) [Pubmed]
  4. Dietary cholesterol withdrawal reduces vascular inflammation and induces coronary plaque stabilization in miniature pigs. Verhamme, P., Quarck, R., Hao, H., Knaapen, M., Dymarkowski, S., Bernar, H., Van Cleemput, J., Janssens, S., Vermylen, J., Gabbiani, G., Kockx, M., Holvoet, P. Cardiovasc. Res. (2002) [Pubmed]
  5. C1-esterase inactivator from cancer cells is C-reactive protein. Darhovsky, D., Ziegenhagen, G., Duchmann, H. Lancet (1980) [Pubmed]
  6. Apexin, an acrosomal pentaxin. Reid, M.S., Blobel, C.P. J. Biol. Chem. (1994) [Pubmed]
  7. Endothelin(A) receptor blockade reduces ischemia/reperfusion injury in pig pancreas transplantation. Witzigmann, H., Ludwig, S., Armann, B., Gäbel, G., Teupser, D., Kratzsch, J., Pietsch, U.C., Tannapfel, A., Geissler, F., Hauss, J., Uhlmann, D. Ann. Surg. (2003) [Pubmed]
  8. Laparoscopic versus open posterior adrenalectomy: comparison of acute-phase response and wound healing in the cushingoid porcine model. Kollmorgen, C.F., Thompson, G.B., Grant, C.S., van Heerden, J.A., Byrne, J., Davies, E.T., Donohue, J.H., Ilstrup, D.M., Young, W.F. World journal of surgery. (1998) [Pubmed]
  9. Evaluation of a single dose versus a divided dose regimen of danofloxacin in treatment of Actinobacillus pleuropneumoniae infection in pigs. Lauritzen, B., Lykkesfeldt, J., Friis, C. Res. Vet. Sci. (2003) [Pubmed]
  10. Detection of SNPs and linkage and radiation hybrid mapping of the porcine C-reactive protein (CRP ) gene. Chomdej, S., Ponsuksili, S., Schellander, K., Wimmers, K. Anim. Genet. (2004) [Pubmed]
  11. C-reactive protein inhibits endothelium-dependent NO-mediated dilation in coronary arterioles by activating p38 kinase and NAD(P)H oxidase. Qamirani, E., Ren, Y., Kuo, L., Hein, T.W. Arterioscler. Thromb. Vasc. Biol. (2005) [Pubmed]
  12. Structure, expression, and evolution of guinea pig serum amyloid P component and C-reactive protein. Rubio, N., Sharp, P.M., Rits, M., Zahedi, K., Whitehead, A.S. J. Biochem. (1993) [Pubmed]
  13. C-reactive protein inhibits intracellular calcium mobilization and superoxide production by guinea pig alveolar macrophages. Földes-Filep, E., Filep, J.G., Sirois, P. J. Leukoc. Biol. (1992) [Pubmed]
  14. Phosphocholine reverses inhibition of pulmonary surfactant adsorption caused by C-reactive protein. McEachren, T.M., Keough, K.M. Am. J. Physiol. (1995) [Pubmed]
  15. Electrolytic liver ablation is not associated with evidence of a systemic inflammatory response syndrome. Teague, B.D., Court, F.G., Morrison, C.P., Kho, M., Wemyss-Holden, S.A., Maddern, G.J. The British journal of surgery. (2004) [Pubmed]
  16. Effects of pneumoperitoneum on hemodynamic and systemic immunologic responses to peritonitis in pigs. Clary, E.M., Bruch, S.M., Lau, C.L., Ali, A., Chekan, E.G., Garcia-Oria, M.J., Eubanks, S. J. Surg. Res. (2002) [Pubmed]
  17. Cardiopulmonary bypass elicits a pro- and anti-inflammatory cytokine response and impaired neutrophil chemotaxis in neonatal pigs. Brix-Christensen, V., Petersen, T.K., Ravn, H.B., Hjortdal, V.E., Andersen, N.T., Tønnesen, E. Acta anaesthesiologica Scandinavica. (2001) [Pubmed]
  18. Comparison of Celsior and UW solution in experimental pancreas preservation. Uhlmann, D., Armann, B., Ludwig, S., Escher, E., Pietsch, U.C., Tannapfel, A., Teupser, D., Hauss, J., Witzigmann, H. J. Surg. Res. (2002) [Pubmed]
  19. Serum acute phase proteins and swine health status. Chen, H.H., Lin, J.H., Fung, H.P., Ho, L.L., Yang, P.C., Lee, W.C., Lee, Y.P., Chu, R.M. Can. J. Vet. Res. (2003) [Pubmed]
  20. Chlortetracycline modulates acute phase response of ex vivo perfused pig livers, and inhibits TNF-alpha secretion by isolated Kupffer cells. Akunda, J.K., Johnson, E., Ahrens, F.A., Kramer, T.T. Comp. Immunol. Microbiol. Infect. Dis. (2001) [Pubmed]
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