Disease relevance of CRP

• The purpose of the present study was to test the hypothesis that CRP correlates with macrophage accumulation during the initial stages of coronary vascular disease [1].
• The purpose of this study was to determine serum profiles of cytokines at a protein level and Creactive protein (CRP) during the development of postweaning multisystemic wasting syndrome (PMWS) in experimentally inoculated pigs [2].
• The acute phase response of acid soluble glycoprotein, alpha(1)-acid glycoprotein, ceruloplasmin, haptoglobin and C-reactive protein, in the pig [3].
• Cytokine and C-reactive protein profiles induced by porcine circovirus type 2 experimental infection in 3-week-old piglets [2].
• RESULTS: Cholesterol-rich diet caused LDL-hypercholesterolemia, increased plasma levels of oxidized LDL (ox-LDL) and C-reactive protein (CRP), and induced endothelial dysfunction and coronary atherosclerosis [4].

High impact information on CRP

• C1-esterase inactivator from cancer cells is C-reactive protein [5].
• Apexin is distinct from the pentaxins serum amyloid protein and C-reactive protein and may have evolved to perform functions other than those performed by serum pentaxins, such as intracellular protein sorting to the acrosome [6].
• RESULTS: Prophylactic treatment with ET(A)-RA significantly reduced the severity of graft pancreatitis evidenced by C-reactive protein [7].
• Blood monitoring included lipase, amylase, C-reactive protein, trypsinogen-activation peptide, thiobarbituric acid-reacting substances, and ET-1 [7].
• Dietary cholesterol withdrawal lowered LDL, ox-LDL and CRP [4].

Chemical compound and disease context of CRP

• There was no difference in operating time (mean +/- SD) (36 +/- 9 minutes open vs. 37 +/- 7 minutes laparoscopic), perioperative mortality, degree of leukocytosis, fasting glucose, or C-reactive protein (p > 0.05) [8].
• A single versus a divided dose regimen of danofloxacin was evaluated in treatment of porcine Actinobacillus pleuropneumoniae infection using clinical observations combined with biochemical infection markers: C-reactive protein, zinc and ascorbic acid [9].

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].

References