Batch dependent - please inquire should you have specific requirements
Buffer
0.1M Tris, pH 7.5 with 0.2M NaCl and 4 mM CaCl₂
Preservative
None
Storage
Short Term: 2-8°C. Long Term: -22°C. Avoid repeated freezing and thawing.
Antigen Description
C-reactive protein (CRP) is aprotein found in the blood, the levels of which rise in response toinflammation (i.e. C-reactive protein is an acute-phase protein). Itsphysiological role is to bind to phosphocholine expressed on the surface ofdead or dying cells (and some types of bacteria) in order to activate thecomplement system via the C1Q complex. CRP is synthesized by the liver inresponse to factors released by fat cells (adipocytes). It is a member of thepentraxin family of proteins. It is not related to C-peptide or protein C. C-reactiveprotein was the first pattern recognition receptor (PRR) to be identified.
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Background
C-reactive protein (CRP) is a member of an ancient family of proteins that is highly conserved and, based on its five subunit structure, is known as pentraxins. CRP in all species exhibits high sequence homology and calcium-dependent ligand binding. The biological role of CRP has been elusive, but most researchers believe that CRP is part of the innate immune system, acting as a pattern recognition molecule that binds to damaged and inflamed cells in the body, thereby amplifying inflammation. The pathogenic role of CRP in mediating a range of important human diseases and therapeutic approaches targeting CRP are now of particular interest.
Routine analysis of serum CRP concentration as a measure of inflammatory and disease activity remains one of the most widely used tests in the clinic. CRP testing has important clinical value because CRP is rapidly upregulated in a variety of important clinical conditions, such as infections, cardiovascular diseases, inflammatory diseases, trauma, and malignancies. In addition to being a marker of disease activity, CRP has prognostic value for myocardial infarction and is a reliable predictor of the onset of cardiovascular disease, so high-sensitivity CRP has been incorporated into cardiovascular risk assessments.
CRP has a pentameric structure consisting of five identical noncovalently linked 23 kDa protomers, each consisting of 206 amino acids. The ability of CRP to elicit an inflammatory response is structurally related to the fact that each protomer contains both a binding and an effector surface, and that the binding surface contains a phosphocholine site that facilitates calcium-dependent interactions with PCs exposed to apoptotic and inflamed cell membranes and bacterial cell walls. Phe-66 and Glu-81 in the hydrophobic pocket are two key residues that mediate the binding of PC to CRP. The exposed surface of the Phe-66 residue in the hydrophobic pocket interacts hydrophobically with the methyl group of PC, and the Glu-81 residue interacts with the positively charged nitrogen. The effector surface activates the innate immune system by binding to the complement C1q globular head and FCγ receptor, and optimal interaction between CRP and C1q requires some degree of conformational change of the CRP pentamer, which raises the notion that CRP undergoes a conformational change at the site of tissue injury to exert its proinflammatory effects.
Figure 1. CRP structure (Source: McFadyen JD, et al. 2020)
Alternative Names
CRP antigen
References
1. McFadyen JD, et al. C-Reactive Protein and Its Structural Isoforms: An Evolutionary Conserved Marker and Central Player in Inflammatory Diseases and Beyond. Subcell Biochem. 2020;94:499-520.
2. Rizo-Téllez SA, et al. C-reactive protein: a target for therapy to reduce inflammation. Front Immunol. 2023 Jul 26;14:1237729.
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References
CRP Versus SAA for Identification of Inflammatory Hepatic Adenomas
Subtyping hepatic adenomas is important for patient management due to differing complication risks. Immunohistochemical staining with C-reactive protein (CRP) and serum amyloid-A (SAA) is widely accepted as a surrogate for molecular classification to identify inflammatory hepatocellular adenomas. Limited data, however, has been published on how these 2 stains compare for sensitivity. We conducted a large, multicenter, retrospective study to examine the sensitivity and staining characteristics of CRP and SAA in inflammatory hepatic adenomas, with focal nodular hyperplasia (FNHs) as a control group. Inflammatory adenomas were identified in 133 patients (average age 37 years, 109 were female). In all, 69.9% of cases were resection specimens and 90.2% of all cases showed positive staining for both CRP and SAA; 10 (7.5%) were positive for CRP only and 3 (2.3%) were positive for SAA only. CRP was more sensitive than SAA (97.74% vs. 92.48%, P -value = 0.0961) and showed more extensive and intense staining, with a significantly higher modified H-score ( P <0.001). Focal nodular hyperplasia can also show positive CRP and SAA staining but with a lower modified H-score ( P <0.0001). Based on beta-catenin and glutamine synthetase staining, 26 of inflammatory adenomas also had beta-catenin activation (19.5%). All 3 cases with positive SAA and negative CRP staining were beta-catenin activated. In contrast, the proportion of cases that were CRP positive and SAA negative was similar regardless of beta-catenin activation. The data affirms the strategy of using both CRP and SAA immunostains for hepatic adenoma subtyping and raises the awareness of the highly variable nature of SAA staining characteristics.
CRP Monitoring in Early Hospitalization: Implications for Predicting Outcomes in Patients with COVID-19
Pathogens
Authors: Avihai B, Sundel EP, Lee E, Greenberg PJ, Cook BP, Altomare NJ, Ko TM, Chaia AI, Parikh PD, Blaser MJ.
Elevated C-reactive protein (CRP) levels have been associated with poorer COVID-19 outcomes. While baseline CRP levels are higher in women, obese individuals, and older adults, the relationship between CRP, sex, body mass index (BMI), age, and COVID-19 outcomes remains unknown. To investigate, we performed a retrospective analysis on 824 adult patients with COVID-19 admitted during the first pandemic wave, of whom 183 (22.2%) died. The maximum CRP value over the first five hospitalization days better predicted hospitalization outcome than the CRP level at admission, as a maximum CRP > 10 mg/dL independently quadrupled the risk of death (p < 0.001). Males (p < 0.001) and patients with a higher BMI (p = 0.001) had higher maximum CRP values, yet CRP levels did not impact their hospitalization outcome. While CRP levels did not statistically mediate any relation between sex, age, or BMI with clinical outcomes, age impacted the association between BMI and the risk of death. For patients 60 or over, a BMI < 25 kg/m2 increased the risk of death (p = 0.017), whereas the reverse was true for patients <60 (p = 0.030). Further impact of age on the association between BMI, CRP, and the risk of death could not be assessed due to a lack of statistical power but should be further investigated.
COA
Publication 
Figure 1. CRP structure
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