A wide variety of inflammatory conditions can cause elevated C-reactive protein CRP levels, including the following:. The most common cause is a severe infection, but a poorly controlled autoimmune disease or severe tissue damage can also lead to high CRP levels. There is no need to fast or avoid liquids before having a CRP test. However, people having a high-sensitivity CRP hs-CRP test are likely to undergo other blood tests at the same time, and these may require fasting for 9—12 hours beforehand.
Obtaining the sample for the test will only take a few minutes and should be relatively painless aside from a small needle prick. The symptoms of elevated CRP levels depend entirely on the underlying condition that is causing them. Many people who have moderate infections or injuries, or conditions that cause chronic inflammation, may experience similar symptoms.
These include:. However, as a general rule, the following classifications apply to CRP:. A huge range of conditions can raise CRP levels slightly, and, as there is no standard reference range set for CRP, there is usually no way to draw any conclusions by looking at CRP levels alone. Recent studies suggest that probiotics may also have a positive effect in lowering CRP.
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X-ray imaging tests, including the pros and cons of each test, how they compare to CT scans, how much they cost, and…. Health Conditions Discover Plan Connect. C-Reactive Protein Test. Medically reviewed by Judith Marcin, M. What is C-reactive protein? C-reactive protein CRP is a substance produced by the liver in response to inflammation. It is released by a number of cell types in response to events such as oxidative stress, cytokine release, and growth factor release There is increasing evidence that MCP-1 influences T-cell immunity by enhancing the secretion of IL-4 by T cells, as well as having a role in the migration of leukocytes This in turn has a regulatory function on monocytes and macrophages, which are the major source of MCP-1 MCP-1 is known to recruit monocytes to the vessel wall 99 and cause the arrest of rolling monocytes on endothelial monolayers that express E-selectin Evidence suggests that CRP stimulates endothelial cells to express MCP-1 99 in addition to being a direct chemoattractant of monocytes itself CRP can promote monocyte chemotactic activity in response to MCP-1 via upregulation of the monocyte chemotaxis receptor CCR2, with elevated CRP levels promoting the accumulation of monocytes in the atherogenic arterial wall C-reactive protein is a homopentameric acute-phase inflammatory protein that exhibits elevated expression during inflammatory conditions such as rheumatoid arthritis, some cardiovascular diseases, and infection.
Evidence suggests that CRP is an important regulator of inflammatory processes and not just a marker of inflammation or infection. Key areas of inflammation and host responses to infection mediated by CRP include the complement pathway, apoptosis, phagocytosis, NO release, and cytokine production.
However, most research to date has investigated the role of CRP in the vascular tissues, highlighting the need to conduct further work to determine the precise role of CRP in peripheral tissues. C-reactive protein is synthesized primarily in liver hepatocytes but also other cell types such as smooth muscle cells, macrophages, endothelial cells, lymphocytes, and adipocytes. Administration of oral HRT increases background levels of CRP in circulation, whereas evidence suggests that transdermal estrogen supplementation either reduces or has little effect on circulating CRP levels.
A reduction in CRP levels following local administration of estrogen supports findings showing that estrogen reduces the inflammatory response in peripheral tissues such as skin. Further studies are needed to expand on these emerging findings and to fully characterize the differential roles that each CRP isoform play at sites of local inflammation and infection. Both authors contributed equally to the planning, preparation, drafting and writing of the article.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The handling Editor declared a shared affiliation, though no other collaboration, with the authors. This work was funded by Manchester Metropolitan University. National Center for Biotechnology Information , U. Journal List Front Immunol v. Front Immunol. Published online Apr Nicola R.
Sproston and Jason J. Author information Article notes Copyright and License information Disclaimer. Ashworth, ku. Specialty section: This article was submitted to Inflammation, a section of the journal Frontiers in Immunology.
Received Dec 18; Accepted Mar The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. This article has been cited by other articles in PMC. Abstract C-reactive protein CRP is an acute inflammatory protein that increases up to 1,fold at sites of infection or inflammation.
Keywords: C-reactive protein, native C-reactive protein, monomeric C-reactive protein, inflammation, infection. C-Reactive Protein CRP C-reactive protein is a homopentameric acute-phase inflammatory protein, a highly conserved plasma protein that was initially discovered in by Tillet and Francis while investigating the sera of patients suffering from the acute stage of Pneumococcus infection and was named for its reaction with the capsular C -polysaccharide of Pneumococcus 1.
Open in a separate window. Figure 1. CRP and Infection C-reactive protein is a marker for inflammation, and its levels increase during bacterial infection CRP and Complement Complement is one of the major defenses of the human immune system that is involved in the clearance of foreign particles and organisms after recognition by antibody.
CRP and Nitric Oxide NO C-reactive protein has the ability to attenuate NO production with a marked reduction in in vitro angiogenesis, cell migration, and capillary-like tube formation by CRP at concentrations known to cause cardiovascular risk IL-6 and CRP Interleukin-6 is a pro-inflammatory cytokine secreted by various cells including inflammatory cells, keratinocytes, fibroblasts, and endothelial cells.
Interleukin-8 IL-8 and CRP Interleukin-8 is a cytokine produced by numerous cell types including inflammatory cells, keratinocytes, fibroblasts, and endothelial cells. MCP-1 and CRP Monocyte chemoattractant protein-1 is a cytokine that plays a role in the regulation of migration and infiltration of monocytes and macrophages Conclusion C-reactive protein is a homopentameric acute-phase inflammatory protein that exhibits elevated expression during inflammatory conditions such as rheumatoid arthritis, some cardiovascular diseases, and infection.
Author Contributions Both authors contributed equally to the planning, preparation, drafting and writing of the article. Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Footnotes Funding. References 1. Tillet WS, Francis T. Serological reactions in pneumonia with a non-protein somatic fraction of Pneumococcus. J Exp Med 52 4 — Volanakis JE. Human C-reactive protein: expression structure and function. Mol Immunol 38 — C-reactive protein. J Biol Chem 47 — C-reactive protein and the acute phase response.
Adv Intern Med 27 — Monomeric C-reactive protein and Notch-3 co-operatively increase angiogenesis through PI3K signalling pathway. Cytokine 69 — C-reactive protein: an activator of innate immunity and a modulator of adaptive immunity. Immunol Res 30 3 — Gabay C, Kushner I.
Acute-phase proteins and other systemic responses to inflammation. N Engl J Med 6 — The physiological structure of human C-reactive protein and its complex with phosphocholine. Structure 7 2 — Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation —9. Production of modified C-reactive protein in Uderived macrophages. Exp Biol Med 10 — Testosterone and IL-6 requirements for human C-reactive protein gene expression in transgenic mice.
J Immunol 11 —9. Interleukin-6 is necessary, but not sufficient, for induction of the human C-reactive protein gene in vivo. Biochem J 3 — C-reactive protein gene polymorphisms, C-reactive protein blood levels and cardiovascular disease risk. J Am Coll Cardiol 50 12 — Native pentameric C-reactive protein displays more potent pro-atherogenic activities in human aortic endothelial cells than modified C-reactive protein.
Atherosclerosis — C-reactive protein: how conformational changes influence inflammatory properties. Cell Cycle 8 23 — C-reactive protein: a critical update. J Clin Investig 12 — Atherosclerosis 3 —9. Oral postmenopausal hormone therapy, C-reactive protein and cardiovascular outcomes.
Menopause 18 1 —9. Sex hormone modulation of proinflammatory cytokine and CRP expression in macrophages from older men and postmenopausal women. J Endocrinol 2 — Hormone replacement therapy and increased plasma concentration of C-reactive protein.
Circulation 7 —6. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 12 — Effect of transdermal estradiol and oral conjugated estrogen on C-reactive protein in retinoid-placebo trial in healthy women.
Circulation 10 —8. Differential effects of oral versus transdermal estrogen replacement therapy on C-reactive protein in postmenopausal women.
J Am Coll Cardiol 41 8 — Low-dose oral or non-oral hormone therapy: effects on C-reactive protein and atrial natriuretic peptide in menopause. Climacteric 18 1 — Hormone replacement therapy and sensitive C-reactive protein concentrations in women with type-2 diabetes. Lancet —8. Topical estrogen accelerates cutaneous wound healing in aged humans associated with an altered inflammatory response. Am J Pathol 4 — Boncler M, Watala C. Regulation of cell function by isoforms of C-reactive protein: a comparative analysis.
Acta Biochim Pol 56 1 — Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells. Circulation 16 —2. The evolving role of C-reactive protein in atherothrombosis.
It can take a few days to get your results. Your doctor will explain to you what the results of your test mean. Results for a standard CRP test are usually given as follows:.
Note: Abnormal range values may vary depending on the laboratory doing the test. A high CRP test result is a sign of acute inflammation. It may be due to serious infection, injury or chronic disease. Your doctor will recommend other tests to determine the cause. Results for an hs-CRP test are usually given as follows:. A person's CRP levels vary over time. A coronary artery disease risk assessment should be based on the average of two hs-CRP tests, ideally taken two weeks apart.
Values above 2. Remember that your hs-CRP level is only one risk factor for coronary artery disease. If you have a high hs-CRP level, it doesn't definitely mean you have an overall higher risk of developing heart disease. Other tests need to be done to further evaluate your risk. Talk to your doctor about all your risk factors and ways you can try to prevent coronary artery disease and a heart attack.
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