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Gene Review

CRP  -  C-reactive protein, pentraxin-related

Homo sapiens

Synonyms: C-reactive protein, PTX1
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Disease relevance of CRP

  • The human CRP promoter is expressed in an inducible and cell-specific manner when linked to the bacterial CAT gene and transfected into human hepatoma cell cultures [1].
  • The combined action of these cytokines causes fever, leukocytosis and the production of acute phase proteins such as C-reactive protein (CRP) [2].
  • In protocol B, CRP, SAA, and IL-6 did not change in stable angina patients after angiography but increased in unstable angina patients (all P<0.05) [3].
  • Weight loss was related with increased levels of the sTNF-Rs, sICAM-1, IL-6, LBP, and CRP [4].
  • C-reactive protein (CRP) is a component of the acute phase response to infection, inflammation, and trauma [5].
  • Our results show that hCRP is not proatherogenic but instead slows atherogenesis, possibly through proteasome-mediated protein degradation [6].
  • A high maternal CRP concentration independently predicts HIV disease progression, maternal mortality, and child mortality in a resource-poor setting [7].
  • Nevertheless, external validation of the diagnostic value of procalcitonin and CRP in diabetic foot ulcers is needed before routine use can be recommended [8].
  • These results provide limited support for associations between genetic variation in CRP and colorectal polyp risk [9].
  • Data is shown that illustrates that, as epithelial ovarian cancer (EOC) progresses from stage I to stage IV, mean levels of CRP increase [10].
  • Given the fundamental role of both IFNalpha and CRP in the immune response, our results are of importance for understanding the pathogenesis of SLE and may also contribute to understanding the differences in the CRP response between viral and bacterial infections [11].

Psychiatry related information on CRP

  • Among others, C-reactive protein (CRP), interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, serum amyloid A (SAA), and white blood cells (WBC) were measured, and dietary habits (including fish consumption) were evaluated using a validated food frequency questionnaire [12].
  • Plasma concentrations of interleukin-1beta (IL-1beta), interleukin-6 (IL-6), C reactive protein (CRP) and alpha-1-antichymotrypsin (ACT) in 145 patients with probable Alzheimer's disease (AD) and 51 non-demented controls were measured [13].
  • After adjustment for age, race, smoking status, history of diabetes, history of cardiovascular disease, physical activity, high-density lipoprotein cholesterol, antiinflammatory medications, statins, and total fat mass, alcohol intake showed a J-shaped relationship with mean IL-6 (P for quadratic term <0.001) and CRP (P=0.014) levels [14].
  • Strategies for decreasing elevated CRP include administration of statins, thiazolidinediones, and metformin; moderate alcohol consumption and appropriate weight loss are also helpful in this regard [15].
  • Risk reduction strategies designed to lower plasma CRP may be effective by improving NO bioavailability [16].

High impact information on CRP


Chemical compound and disease context of CRP

  • C-reactive protein (CRP), the major human acute-phase plasma protein, binds to phosphocholine (PCh) residues present in pneumococcal C-polysaccharide (PnC) of Streptococcus pneumoniae and to PCh exposed on damaged and apoptotic cells [21].
  • RESULTS: The index patient's disease was refractory to treatment with prednisone (30 mg/day) and MTX, with spiking fevers, rash, synovitis, a serum ferritin level of 8,400 ng/ml (normal </=200), and a CRP level of 86 mg/liter (normal <8) [22].
  • METHODS: Plasmas (EDTA) as well as clinical data, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were collected in two groups of 10 patients fulfilling the European Spondylarthropathy Study Group criteria for SpA or the 1987 American College of Rheumatology criteria for RA [23].
  • SUBJECTS AND METHODS: We investigated the cross-sectional and longitudinal association of adiponectin with CRP and IL-6 in 41 morbidly obese women with different stages of glucose tolerance before and 17 months after significant weight loss induced by gastric surgery [24].
  • C-reactive protein (CRP) and neopterin were measured in 22 patients with acute coronary syndromes, 50 patients with stable vascular disease and 22 healthy controls [25].

Biological context of CRP

  • IL-6 is a pleiotropic cytokine acting on several cell lineages, and, at the hepatocyte level, stimulates the synthesis of acute phase proteins, such as the well known C-Reactive Protein (CRP) [26].
  • The data were compared with conventional parameters of inflammation, such as C-reactive protein (CRP), iron and hemoglobin levels, erythrocyte sedimentation rate (ESR), white blood cell (WBC) counts, and platelet counts [27].
  • Adiponectin plasma levels and adipose-tissue gene expression were significantly lower in obese subjects and inversely correlated with obesity-associated variables, including high-sensitive C-reactive protein (hs-CRP) and interleukin-6 (IL-6) [28].
  • These results further identify amino acids involved in the binding sites on CRP for FcgammaRI, FcgammaRIIa, and C1q and indicate that these sites are overlapping [29].
  • CRP binds to microbial antigens and damaged cells, opsonizes particles for phagocytosis and regulates the inflammatory response by the induction of cytokine synthesis [29].

Anatomical context of CRP

  • The pentraxins C-reactive protein (CRP) and serum amyloid P component (SAP) are acute-phase proteins produced by liver epithelial cells [30].
  • The erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) level, and the level of several cytokines in serum and synovial fluid were also determined [31].
  • Incubation of Hep 3B cells with conditioned medium from LPS-stimulated monocytes, in the absence of dexamethasone, led to modest induction of SAA or CRP, but addition of dexamethasone potentiated this response in a dose-dependent manner [32].
  • Because several proatherogenic effects of CRP have been documented in endothelial cells, we examined human aortic endothelial cells (HAEC) for CRP production [33].
  • These results suggest that CRP can alter the cytokine profile of mouse macrophages by acting through FcgammaR leading to a down-regulation of the inflammatory response [5].

Associations of CRP with chemical compounds

  • Cooperativity is maintained when the CRP promoter is linked to a different coding region, that of the bacterial neomycin phosphotransferase II gene [1].
  • Plasma tumor necrosis factor (TNF) and IL-1 beta levels were unaffected, whereas serum C-reactive protein (CRP) concentrations increased slightly and plasma IL-1 receptor antagonist (IL-1RA) levels increased markedly [34].
  • White blood cells (WBCs), C-reactive protein (CRP) levels and/or erythrocyte sedimentation rate, and ferritin levels were measured and, in 1 patient, serum creatinine levels were determined [22].
  • Complement was required for the protective effect of CRP as cobra venom factor treatment eliminated the effect of CRP in both gamma-chain-deficient and wild-type mice, and CRP failed to protect C3- or C4-deficient mice from infection [35].
  • CRP and anti-PC Ab share the ability to bind to PC on the cell wall C-polysaccharide of S. pneumoniae and to activate complement [35].
  • The inhibitory effects of resveratrol and its derivatives on CRP expression were at the level of mRNA production [36].

Physical interactions of CRP

  • Using the surface plasmon resonance technique and a panel of recombinantly expressed FH constructs, we observed that CRP binds to two closely located regions on short consensus repeat (SCR) domains 7 and 8-11 of FH [37].
  • Binding of CRP to oxidized LDL did not interfere with binding of annexin A5, and vice versa [38].
  • Basal CRP expression increased dramatically when binding of both OCT-1 and NF-kappaB was abolished [39].
  • In contrast, all five CRP mutants bound to Fn as well as did wild-type CRP [21].
  • By contrast, the 360 bp promoter of the CRP gene was bound only by STAT3 at consensus sites at -93, -142, -173, and -287 from the start site; however, a single consensus site for C/EBP at -75 was not recognized [40].

Regulatory relationships of CRP

  • In hepatoma Hep3B cells, IL-6 induces CRP expression by activating transcription factors STAT3 and C/EBPbeta [39].
  • While previous studies have indicated that IL-6 induces transcription of CRP, the mode of action of IL-1 has not been clearly defined [41].
  • CRP production was significantly inhibited by the p38 MAPK specific inhibitor RWJ 67657 at 1 micromol/l, which is pharmacologically relevant [42].
  • However, the addition of the RGDS and RGDSPASSLP cell-binding peptides of Fn to cells enhanced attachment to the active peptide from CRP [43].
  • Our findings suggest that in healthy people, basal CRP levels are regulated by IL1B but not by IL6 genetics [44].

Other interactions of CRP

  • IFN-gamma increases were also abrupt, preceding those of fever and CRP by one day [45].
  • TNF alpha and C-reactive protein (CRP) levels were below the detection limit in the same plasma samples [46].
  • Thus, PTX3, unlike the classical pentraxins CRP and SAP, is expressed and released by cells of the monocyte-macrophage lineage exposed to inflammatory signals [30].
  • Ca2+ did not inhibit binding of CRP to Fn at pH 6.5 and lower [47].
  • Transforming growth factor-beta (TGF-beta) modified production of the major human acute phase reactant, C-reactive protein (CRP), induced by the inflammatory cytokines, IL-1 beta or IL-6 [48].

Analytical, diagnostic and therapeutic context of CRP


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  2. The involvement of TNF, IL-1 and IL-6 in the immune response to protozoan parasites. Titus, R.G., Sherry, B., Cerami, A. Immunol. Today (1991) [Pubmed]
  3. Enhanced inflammatory response to coronary angioplasty in patients with severe unstable angina. Liuzzo, G., Buffon, A., Biasucci, L.M., Gallimore, J.R., Caligiuri, G., Vitelli, A., Altamura, S., Ciliberto, G., Rebuzzi, A.G., Crea, F., Pepys, M.B., Maseri, A. Circulation (1998) [Pubmed]
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  6. Human C-reactive protein slows atherosclerosis development in a mouse model with human-like hypercholesterolemia. Kovacs, A., Tornvall, P., Nilsson, R., Tegnér, J., Hamsten, A., Björkegren, J. Proc. Natl. Acad. Sci. U.S.A. (2007) [Pubmed]
  7. C-reactive protein independently predicts HIV-related outcomes among women and children in a resource-poor setting. Drain, P.K., Kupka, R., Msamanga, G.I., Urassa, W., Mugusi, F., Fawzi, W.W. AIDS (2007) [Pubmed]
  8. Serum procalcitonin and C-reactive protein concentrations to distinguish mildly infected from non-infected diabetic foot ulcers: a pilot study. Jeandrot, A., Richard, J.L., Combescure, C., Jourdan, N., Finge, S., Rodier, M., Corbeau, P., Sotto, A., Lavigne, J.P. Diabetologia (2008) [Pubmed]
  9. C-reactive protein genotypes and haplotypes, polymorphisms in NSAID-metabolizing enzymes, and risk of colorectal polyps. Poole, E.M., Bigler, J., Whitton, J., Sibert, J.G., Potter, J.D., Ulrich, C.M. Pharmacogenet. Genomics (2009) [Pubmed]
  10. Absolute quantification of C-reactive protein in human plasma derived from patients with epithelial ovarian cancer utilizing protein cleavage isotope dilution mass spectrometry. Williams, D.K., Muddiman, D.C. J. Proteome Res. (2009) [Pubmed]
  11. Interferon-alpha mediates suppression of C-reactive protein: explanation for muted C-reactive protein response in lupus flares? Enocsson, H., Sjöwall, C., Skogh, T., Eloranta, M.L., Rönnblom, L., Wetterö, J. Arthritis Rheum. (2009) [Pubmed]
  12. Fish consumption among healthy adults is associated with decreased levels of inflammatory markers related to cardiovascular disease: the ATTICA study. Zampelas, A., Panagiotakos, D.B., Pitsavos, C., Das, U.N., Chrysohoou, C., Skoumas, Y., Stefanadis, C. J. Am. Coll. Cardiol. (2005) [Pubmed]
  13. Increased plasma levels of interleukin-1, interleukin-6 and alpha-1-antichymotrypsin in patients with Alzheimer's disease: peripheral inflammation or signals from the brain? Licastro, F., Pedrini, S., Caputo, L., Annoni, G., Davis, L.J., Ferri, C., Casadei, V., Grimaldi, L.M. J. Neuroimmunol. (2000) [Pubmed]
  14. Relationship of alcohol intake with inflammatory markers and plasminogen activator inhibitor-1 in well-functioning older adults: the Health, Aging, and Body Composition study. Volpato, S., Pahor, M., Ferrucci, L., Simonsick, E.M., Guralnik, J.M., Kritchevsky, S.B., Fellin, R., Harris, T.B. Circulation (2004) [Pubmed]
  15. AMPK activation may suppress hepatic production of C-reactive protein by stimulating nitric oxide synthase. McCarty, M.F. Med. Hypotheses (2004) [Pubmed]
  16. A self-fulfilling prophecy: C-reactive protein attenuates nitric oxide production and inhibits angiogenesis. Verma, S., Wang, C.H., Li, S.H., Dumont, A.S., Fedak, P.W., Badiwala, M.V., Dhillon, B., Weisel, R.D., Li, R.K., Mickle, D.A., Stewart, D.J. Circulation (2002) [Pubmed]
  17. Inflammatory biomarkers, hormone replacement therapy, and incident coronary heart disease: prospective analysis from the Women's Health Initiative observational study. Pradhan, A.D., Manson, J.E., Rossouw, J.E., Siscovick, D.S., Mouton, C.P., Rifai, N., Wallace, R.B., Jackson, R.D., Pettinger, M.B., Ridker, P.M. JAMA (2002) [Pubmed]
  18. CVD risk factors and ethnicity--a homogeneous relationship? Forouhi, N.G., Sattar, N. Atherosclerosis. Supplements. (2006) [Pubmed]
  19. C-reactive protein: a physiological activator of interleukin 6 receptor shedding. Jones, S.A., Novick, D., Horiuchi, S., Yamamoto, N., Szalai, A.J., Fuller, G.M. J. Exp. Med. (1999) [Pubmed]
  20. The major receptor for C-reactive protein on leukocytes is fcgamma receptor II. Bharadwaj, D., Stein, M.P., Volzer, M., Mold, C., Du Clos, T.W. J. Exp. Med. (1999) [Pubmed]
  21. A C-reactive protein mutant that does not bind to phosphocholine and pneumococcal C-polysaccharide. Agrawal, A., Simpson, M.J., Black, S., Carey, M.P., Samols, D. J. Immunol. (2002) [Pubmed]
  22. Rapid responses to anakinra in patients with refractory adult-onset Still's disease. Fitzgerald, A.A., Leclercq, S.A., Yan, A., Homik, J.E., Dinarello, C.A. Arthritis Rheum. (2005) [Pubmed]
  23. Increased Ed-B fibronectin plasma levels in spondyloarthropathies: comparison with rheumatoid arthritis patients and a healthy population. Claudepierre, P., Allanore, Y., Belec, L., Larget-Piet, B., Zardi, L., Chevalier, X. Rheumatology (Oxford, England) (1999) [Pubmed]
  24. Effects of marked weight loss on plasma levels of adiponectin, markers of chronic subclinical inflammation and insulin resistance in morbidly obese women. Kopp, H.P., Krzyzanowska, K., Möhlig, M., Spranger, J., Pfeiffer, A.F., Schernthaner, G. International journal of obesity (2005) (2005) [Pubmed]
  25. Circulating monocytes in patients with acute coronary syndromes lack sufficient interleukin-10 production after lipopolysaccharide stimulation. van Haelst, P.L., Tervaert, J.W., Bijzet, J., Baljé-Volkers, C., May, J.F., Langeveld, B., Gans, R.O. Clin. Exp. Immunol. (2004) [Pubmed]
  26. C-reactive protein and beta-2 microglobulin produce a simple and powerful myeloma staging system. Bataille, R., Boccadoro, M., Klein, B., Durie, B., Pileri, A. Blood (1992) [Pubmed]
  27. Serum cytokines in juvenile rheumatoid arthritis. Correlation with conventional inflammation parameters and clinical subtypes. Mangge, H., Kenzian, H., Gallistl, S., Neuwirth, G., Liebmann, P., Kaulfersch, W., Beaufort, F., Muntean, W., Schauenstein, K. Arthritis Rheum. (1995) [Pubmed]
  28. Association between adiponectin and mediators of inflammation in obese women. Engeli, S., Feldpausch, M., Gorzelniak, K., Hartwig, F., Heintze, U., Janke, J., Möhlig, M., Pfeiffer, A.F., Luft, F.C., Sharma, A.M. Diabetes (2003) [Pubmed]
  29. Analysis of binding sites in human C-reactive protein for Fc{gamma}RI, Fc{gamma}RIIA, and C1q by site-directed mutagenesis. Bang, R., Marnell, L., Mold, C., Stein, M.P., Clos, K.T., Chivington-Buck, C., Clos, T.W. J. Biol. Chem. (2005) [Pubmed]
  30. Inducible expression of PTX3, a new member of the pentraxin family, in human mononuclear phagocytes. Alles, V.V., Bottazzi, B., Peri, G., Golay, J., Introna, M., Mantovani, A. Blood (1994) [Pubmed]
  31. Accumulation of soluble Fas in inflamed joints of patients with rheumatoid arthritis. Hasunuma, T., Kayagaki, N., Asahara, H., Motokawa, S., Kobata, T., Yagita, H., Aono, H., Sumida, T., Okumura, K., Nishioka, K. Arthritis Rheum. (1997) [Pubmed]
  32. Effect of combinations of cytokines and hormones on synthesis of serum amyloid A and C-reactive protein in Hep 3B cells. Ganapathi, M.K., Rzewnicki, D., Samols, D., Jiang, S.L., Kushner, I. J. Immunol. (1991) [Pubmed]
  33. Macrophage conditioned medium induces the expression of C-reactive protein in human aortic endothelial cells: potential for paracrine/autocrine effects. Venugopal, S.K., Devaraj, S., Jialal, I. Am. J. Pathol. (2005) [Pubmed]
  34. Phase I evaluation of thrice-daily intravenous bolus interleukin-4 in patients with refractory malignancy. Atkins, M.B., Vachino, G., Tilg, H.J., Karp, D.D., Robert, N.J., Kappler, K., Mier, J.W. J. Clin. Oncol. (1992) [Pubmed]
  35. Protection from Streptococcus pneumoniae infection by C-reactive protein and natural antibody requires complement but not Fc gamma receptors. Mold, C., Rodic-Polic, B., Du Clos, T.W. J. Immunol. (2002) [Pubmed]
  36. Effect of wine phenolics on cytokine-induced C-reactive protein expression. Kaur, G., Rao, L.V., Agrawal, A., Pendurthi, U.R. J. Thromb. Haemost. (2007) [Pubmed]
  37. Regulation of complement activation by C-reactive protein: targeting the complement inhibitory activity of factor H by an interaction with short consensus repeat domains 7 and 8-11. Jarva, H., Jokiranta, T.S., Hellwage, J., Zipfel, P.F., Meri, S. J. Immunol. (1999) [Pubmed]
  38. C-reactive protein and annexin A5 bind to distinct sites of negatively charged phospholipids present in oxidized low-density lipoprotein. van Tits, L., de Graaf, J., Toenhake, H., van Heerde, W., Stalenhoef, A. Arterioscler. Thromb. Vasc. Biol. (2005) [Pubmed]
  39. Regulation of basal and induced expression of C-reactive protein through an overlapping element for OCT-1 and NF-kappaB on the proximal promoter. Voleti, B., Agrawal, A. J. Immunol. (2005) [Pubmed]
  40. Role of STAT3 and C/EBP in cytokine-dependent expression of the mouse serum amyloid P-component (SAP) and C-reactive protein (CRP) genes. Ochrietor, J.D., Harrison, K.A., Zahedi, K., Mortensen, R.F. Cytokine (2000) [Pubmed]
  41. The effect of interleukin-1 on C-reactive protein expression in Hep3B cells is exerted at the transcriptional level. Zhang, D., Jiang, S.L., Rzewnicki, D., Samols, D., Kushner, I. Biochem. J. (1995) [Pubmed]
  42. Differential influence of p38 mitogen activated protein kinase (MAPK) inhibition on acute phase protein synthesis in human hepatoma cell lines. Westra, J., Bijzet, J., Doornbos-van der Meer, B., van Rijswijk, M.H., Limburg, P.C. Ann. Rheum. Dis. (2006) [Pubmed]
  43. A cell attachment peptide from human C-reactive protein. Fernandez, M.C., Mullenix, M.C., Christner, R.B., Mortensen, R.F. J. Cell. Biochem. (1992) [Pubmed]
  44. Interleukin 1B gene polymorphism is associated with baseline C-reactive protein levels in healthy individuals. Eklund, C., Jahan, F., Pessi, T., Lehtimäki, T., Hurme, M. Eur. Cytokine Netw. (2003) [Pubmed]
  45. Serum cytokine profiles in experimental human malaria. Relationship to protection and disease course after challenge. Harpaz, R., Edelman, R., Wasserman, S.S., Levine, M.M., Davis, J.R., Sztein, M.B. J. Clin. Invest. (1992) [Pubmed]
  46. Interferon-alpha induces circulating tumor necrosis factor receptor p55 in humans. Tilg, H., Vogel, W., Dinarello, C.A. Blood (1995) [Pubmed]
  47. Interaction of calcium-bound C-reactive protein with fibronectin is controlled by pH: in vivo implications. Suresh, M.V., Singh, S.K., Agrawal, A. J. Biol. Chem. (2004) [Pubmed]
  48. Regulation of cytokine-induced human C-reactive protein production by transforming growth factor-beta. Taylor, A.W., Ku, N.O., Mortensen, R.F. J. Immunol. (1990) [Pubmed]
  49. Interleukin 10 reduces the incidence of pancreatitis after therapeutic endoscopic retrograde cholangiopancreatography. Devière, J., Le Moine, O., Van Laethem, J.L., Eisendrath, P., Ghilain, A., Severs, N., Cohard, M. Gastroenterology (2001) [Pubmed]
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