C-Reactive Protein, High Sensitivity, Human, BioAssay™ ELISA Kit (CRP)
|Kits and Assays||Storage: 4°CShipping: Blue Ice|
The United States Biological C-Reactive Protein, High Sensitivity, Human, BioAssay™ ELISA Kit is intended for the quantitative determination of C-Reactive Protein (CRP) in human serum. Enhanced sensitivity measurements of CRP can be useful for the detection and evaluation of infection, tissue injury, inflammatory disorders and associated diseases.
C-Reactive Protein (CRP) was identified by Tilet and Francis (1930) in the plasma of patients with pneumonia, and was named for its ability to bind and precipitate the C-polysaccharide of pneumococcus. It is an alpha globulin with a molecular mass of ~110-140kD, and is composed of five identical subunits, which are noncovalently assembled as a cyclic pentamer. CRP is synthesized in the liver and is normally present as a trace constituent of serum or plasma at levels less than 0.3mg/dl. Its physiological roles are numerous and varied, but with several functions similar to those of immunoglobulins, CRP appears to function in host defense.
CRP is one of the acute-phase proteins, the serum or plasma levels of which rise during general, nonspecific response to a wide variety of diseases. This include infections by gram-positive and gram-negative organisms, acute phase of rheumatoid arthritis, abdominal abscesses, and inflammation of the bile duct. CRP may also be found in patients with Guillain-Barre syndrome and multiple sclerosis, certain viral infections, tuberculosis, acute infectious hepatitis, many other necrotic and inflammatory diseases, burned patients and after surgical trauma.
Although the detection of elevated levels of CRP in the serum is not specific for any particular disease, it is a useful indicator of inflammatory processes. CRP levels rise in serum or plasma within 24 to 48 hours following acute tissue damage, reach a peak during the acute stage (approximately 1000x constitutive level) and decrease with the resolution of inflammation or trauma. The concentration increase of CRP in human serum or plasma may last for several days before decreasing to normal levels.
The detection of CRP is a more reliable and sensitive indicator of the inflammatory process than the erythrocyte sedimentation rate13, which may also be influenced by physiological changes not associated with an inflammatory process. Current testing methods including latex agglutination, nephelometry, and radial immunodiffusion (RID) have the general disadvantages of low sensitivity, whereas ELISAs provide the highest sensitivity and specificity.
As elevated CRP values are always associated with pathological changes, the CRP assay provides useful information for the research of inflammatory processes and associated disease. Additionally, measurement of CRP by high-sensitivity CRP assays may add to the predictive value of other cardiac markers (myoglobin, creatine-kinase-MB, troponin I and T), which are used to assess the risk of cardiovascular and peripheral vascular disease.
C7907-02P1: Microtiter Plate, 1x96 wells
C7907-02P2: Standard, 0ug/ml, 1x1ml
C7907-02P3: Standard 0.005ug/ml, 1x1ml
C7907-02P4: Standard 0.01ug/ml, 1x1ml
C7907-02P5: Standard 0.025ug/ml, 1x1ml
C7907-02P6: Standard 0.05ug/ml, 1x1ml
C7907-02P7: Standard 0.1ug/ml, 1x1ml
C7907-02P8: Sample Diluent, 1x50ml
C7907-02P9: Pab (HRP) Reagent, 1x12ml
C7907-02P10: TMB Solution, 1x11ml
C7907-02P11: Stop Solution, 1N HCl, 1x11ml
Storage and Stability:
Store all components at 4°C. Stable for 6 months. For maximum recovery of product, centrifuge the original vial prior to removing the cap.
Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications without the expressed written authorization of United States Biological.
1. Schultz, D.R., and Arnold P.I.: “Properties of four acute phase proteins: C-reactive protein, serum amyloid A protein, glycoprotein, and fibrinogen.” Seminars in Arthritis and Rheumatism 20: 129-147, 1990. 2. Kindmark, C.O.: The Concentration of C-reactive protein in Sera from Healthy Individuals. Scand J Clin Lab Invest, 29: 407- 411, 1972. 3. Dowling, P., and Cook, S.: Immune events in demyelinating disease. In Wolfgang, F., Ellison, G.W., Stevens J.G., and Andrew, J.M. (eds.): Multiple sclerosis. Academic Press Inc., New York, 269-277, 1972. 4. Yudkin, J.S., et. al.: C-Reactive Protein in Healthy Subjects: Association with Obesity, Insulin Resistance, and endothelial dysfunction. A potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 19: 972-8, 1999. 5. Kushner, I., et al., Bailliere’s Clinical Rheumatology 8: 513-530, 1994. 6. Macy, E.M., et al., Clin Chem, 43;1:52-58, 1997. 7. Hedlund, P.: Clinical and experimental studies on C-reactive protein (acute phase protein). Thesis Acta Med Scand, 128 (Suppl, 361):1-71, 1961. 8. Hedlund, P.: The appearance of acute phase protein in various diseases. Acta Med Scand, 128, (Suppl,196): 579-601, 1947. 9. Morley, J.J., et al., Annals of N.Y. Acad Sci, 389: 406-417, 1982. 10. Shine, B., et al., J Lab Clinica Chimica Acta 117:13-23, 1981. 11. Kushner, I.: “C-reactive protein in rheumatology,” Arthritis Rheum 34:1065-1068, 1991. 12. Dixon, J.S., et al.: C-reactive protein in the serial assessment of disease activity in rheumatoid arthritis. Scand J Rheum, 13: 39-44, 1984. 13. Hind, C.R.H., and Pepys, M.B.: The role of serum C-reactive (CRP) measurement in clinical practice. Int Med. 5: 112-151, 1984. 14. Van Leeuwen, M., et al., Bailliere’s Clinical Rheumatology 8: 531-552, 1994. 15. Powell, L., et al., Am J Med Technol, 87: 138-142, 1979. 16. Roberts, W. L., et. al.: Evaluation of Four Automated High-Sensitivity C-Reactive Protein Methods: Implications for Clinical and Epidemiological Applications. Clin Chem 46:4, 461-468, 2000. 17. Ridker, P.M., et. al.: Plasma Concentration of C-reactive protein and the risk of developing peripheral vascular disease. Circulation, 97:425-428, 1998. 18. Ridker, P.M., et. al.: Propestive study of C-reactive protein and the risks of future Cardiovascular events among apparently healthy women. Circulation, 98:731-733, 1998. 19. Ridker, P.M., et al., Circulation, 97:2007- 2011, 1998. 20. Ridker, P.M., et. al.: Inflammation, Pravastatin, and the risk of coronary events after myocardial infarction in samples with average cholesterol levels. Circulation, 98: 839-844, 1998. 21. Tracy, R.P., et. al.: Arter. Thromb. Vasc. Biol. 17:1121-1127, 1997. 22. Macy, E. M., et al., Clin. Chem. 43(1):52-58, 1997. 23. Ridker, P.M., et. al.: Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N. Engl. J. Med., 336: 973-979, 1997. 24. Votila, M., et. el.: Immunol Methods, 42: 11, 1981. 25. USA Center for Disease Control/National Institute of Health Manual, “Biosafety in Microbiological and Biomedical Laboratories”, (1984). 26. “Clinical Guide to Laboratory Tests”. Edited by N.W. Tietz, 3rd Edition. W.B. Saunders Company, Philadelphia, PA. 19106 (1995).