The pathogenesis of depression is not fully understood yet, but studies have suggested higher circulating C reactive protein (CRP) level might relate to depression occurrence. However, due to high variability of patients' individual condition, the results to date are inconsistent. Considering CRP single-nucleotide polymorphisms (SNPs) could also regulate plasma CRP levels, in the present study, we hypothesized that inherited CRP allelic variations may co-vary with depressive symptomatology.

Serum C-reactive protein (CRP) has been identified in prospective epidemiological research as an independent risk marker for cardiovascular disease. In this paper, short-term biological variation of CRP is documented and a strategy to test the reliability of a single CRP sample is proposed.

Elevated baseline C-reactive protein (CRP) levels are associated with increased risk for developing cardiovascular disease. Several CRP gene variants have been associated with altered baseline CRP levels in ambulatory populations. However, the influence of CRP gene variants on CRP levels during inflammatory states, such as surgery, is largely unexplored. We describe the association between candidate CRP gene variants and postoperative plasma CRP levels in patients undergoing primary, elective coronary artery bypass graft (CABG) surgery with cardiopulmonary bypass (CPB).

C-reactive protein (CRP) has been shown to be a potential candidate target in the immunotherapy of severe influenza A infection. However, it is unclear on the pathogenesis associated with CRP in influenza infections. Here, we used influenza A H1N1 CA04 to infect human CRP transgenic mice (KI), CRP knockout mice (KO), and wild-type mice (WT), respectively, and compared the viral pathogenicity and associated immune response in those mice. The results showed that CA04 infection resulted in 100%, 80%, and 60% death in KO, KI, and WT mice, respectively. Compared to WT mice, CA04 infection resulted in higher TCID50 in lungs on day 3 after infection but lowered HI antibody titers in sera of survivors on day 21 after infection in KI mice. ELISA assay showed that IFN-γ concentration was significantly increased in sera of WT, KI, or KO mice on day 7 after infection, and IL-17 was remarkably increased in sera of WT mice but decreased in sera of KI mice while no significant change in sera of KO mice on day 3 or 7 after infection. Quantitative RT-PCR showed that the relative expression levels of immune checkpoint CTLA-4, LAIR-1, GITR, BTLA, TIM-3, or PD-1 mRNA in the lung presented decreased levels on day 3 or 7 after infection in KI or KO mice. The correlation analysis showed that mRNA expression levels of the 6 molecules positively correlated with viral TICD50 in WT mice but negatively correlated with viral TCID50 in KI or KO mice. However, only LAIR-1 presented a significant correlation in each lung tissue of WT, KI, or KO mice with CA07 infection statistically. IHC results showed that LAIR-1 positive cells could be found in WT, KO, or KI mice lung tissues with CA04 infection, and the positive cells were mainly distributed in an inflammatory dense area. Our results suggested that deficiency of CRP or human CRP transgenic treatment aggravates influenza A virus infection in mice. CRP is a double sword in immune regulation of influenza infection in which IL-17 and immune checkpoint may be involved.

Background: Emerging evidence suggests that inflammatory response biomarkers are predictive factors that can improve the accuracy of colorectal cancer (CRC) prognoses. We aimed to evaluate the prognostic significance of C-reactive protein (CRP), the Glasgow Prognostic Score (GPS), and the CRP-to-albumin ratio (CAR) in CRC. Methods: Overall, 307 stage I-III CRC patients and 72 colorectal liver metastases (CRLM) patients were enrolled between October 2013 and September 2019. We investigated the correlation between the pretreatment CRP, GPS, and CAR and the clinicopathological characteristics. The Cox proportional hazards model was used for univariate or multivariate analysis to assess potential prognostic factors. A receiver operating characteristic (ROC) curve was constructed to evaluate the predictive value of each prognostic score. We established CRC survival nomograms based on the prognostic scores of inflammation. Results: The optimal cutoff levels for the CAR for overall survival (OS) in all CRC patients, stage I-III CRC patients, and CRLM patients were 0.16, 0.14, and 0.25, respectively. Kaplan-Meier analysis and log-rank tests demonstrated that patients with high CRP, CAR, and GPS had poorer OS in CRC, both in the cohorts of stage I-III patients and CRLM patients. In the different cohorts of CRC patients, the area under the ROC curve (AUC) of these three markers were all high. Multivariate analysis indicated that the location of the primary tumor, pathological differentiation, and pretreatment carcinoembryonic antigen (CEA), CRP, GPS, and CAR were independent prognostic factors for OS in stage I-III patients and that CRP, GPS, and CAR were independent prognostic factors for OS in CRLM patients. The predictors in the prediction nomograms included the pretreatment CRP, GPS, and CAR. Conclusions: CRP, GPS, and CAR have independent prognostic values in patients with CRC. Furthermore, the survival nomograms based on CRP, GPS, and CAR can provide more valuable clinical significance.

High-sensitivity C-reactive protein (hs-CRP) is a commonly used inflammatory marker. The association between hs-CRP and cancer is less consistent than that between hs-CRP and cardiovascular diseases. This study explored the association between hs-CRP and cancer, using a large database of Korean health examination records.

C-reactive protein (CRP) from the American horseshoe crab, Limulus polyphemus, exhibits complex membrane activities. Here, we describe the behavior of protein and lipid as CRP interacts with model liposomes and bacterial membranes. Limulus C-reactive protein (L-CRP) forms extended fibrilar structures that encapsulate liposomes in the presence of Ca(2+). We have observed structures consistent in size and shape with these fibers bound to the surface of Gram-negative bacteria. The membranes of Limulus CRP-treated bacteria exhibit significantly different mechano-elastic properties than those of untreated bacteria. In vitro, bilayer lipids undergo a rigidification and reorganization of small domains. We suggest that these interactions reflect the protein's role as a primary defense molecule, functioning in the entrapment and killing of potential pathogens.

Background. Inflammation in the Brugada syndrome (BrS) and its clinical implication have been little studied. Aims. To assess the level of inflammation in BrS patients. Methods. All studied BrS patients underwent blood samples drawn for C-reactive protein (CRP) levels at admission, prior to any invasive intervention. Patients with a previous ICD placement were controlled to exclude those with a recent (<14 days) shock. We divided subjects into symptomatic (syncope or aborted sudden death) and asymptomatic groups. In a multivariable analysis, we adjusted for significant variables (age, CRP ≥ 2 mg/L). Results. Fifty-four subjects were studied (mean age 45 ± 13 years, 49 (91%) male). Twenty (37%) were symptomatic. Baseline characteristics were similar in both groups. Mean CRP level was 1,4 ± 0,9 mg/L in asymptomatic and 2,4 ± 1,4 mg/L in symptomatic groups (P = .003). In the multivariate model, CRP concentrations ≥ 2 mg/L remained an independent marker for being symptomatic (P = .018; 95% CI: 1.3 to 19.3). Conclusion. Inflammation seems to be more active in symptomatic BrS. C-reactive protein concentrations ≥ 2 mg/L might be associated with the previous symptoms in BrS. The value of inflammation as a risk factor of arrhythmic events in BrS needs to be studied.

Our study aimed to explore the association between serum C-reactive protein (CRP) and post-stroke depressive symptoms. We prospectively recruited 572 patients with ischemic stroke or transient ischemic attack in whom serum CRP level was measured within 48 h after stroke onset. Depressive symptoms were assessed at day 8 and 3 months after stroke in 405 and 306 patients, respectively. Patients with greater depressive symptoms at day 8 and patients with greater depressive symptoms 3 months after stroke had higher CRP level (median: 7.9 vs 4.3 mg/L, P < 0.01 and 6.7 vs 3.4 mg/L, P = 0.01, respectively). In the univariate analysis, CRP > 9.2 mg/L was associated with depressive symptoms at day 8 (OR: 2.06, 95%CI: 1.30-3.28, P < 0.01) and CRP > 4.3 mg/L was associated with depressive symptoms 3 months after stroke (OR: 1.79, 95%CI: 1.06-3.02, P = 0.03). In the multivariate analysis, higher CRP level was related to depressive symptoms at day 8 (OR: 2.23, 95%CI: 1.28-3.90, P < 0.01), but not depressive symptoms 3 months after stroke (OR: 1.13, 95%CI: 0.59-2.17, P = 0.71). In conclusion, higher levels of CRP are associated with greater depressive symptoms at day 8 after stroke, but their effects on depressive symptoms 3 months after stroke are less significant.

C-reactive protein (CRP) is a candidate biomarker for major depressive disorder (MDD), but it is unclear how peripheral CRP levels relate to the heterogeneous clinical phenotypes of the disorder.AimTo explore CRP in MDD and its phenotypic associations.

In this study, we examined whether C-reactive protein (CRP) play causal roles in Alzheimer's disease (AD) using Mendelian randomization (MR) analysis. Summary-level data for AD (71,880 cases and 383,378 controls) was obtained from the large meta-analyses of genome-wide association studies. As instrumental variables, we used 56 single nucleotide polymorphisms (n = 4 for conservative CRP instruments; n = 52 for liberal CRP instruments), previously identified to be associated with CRP levels (n = 194,418 and 204,402 European individuals, respectively). MR estimates were calculated using the inverse-variance weighted approach and complemented with the weighted median, MR-PRESSO, and MR-Egger methods. Genetically predicted elevated CRP levels were significantly associated with an increased risk of AD (conservative CRP instruments: odds ratio, 1.02; 95% CI, 1.01-1.04; p = 0.008). Results for liberal CRP instruments showed a consistent trend. Sensitivity analyses generated similar results and no pleiotropic bias was observed. This study indicates that genetically predicted elevated CRP levels may be a causal risk factor for AD.

The ultrasensitive C-reactive protein (us-CRP) is used for the diagnosis of cardiovascular disease, but it is not well described as a marker for the diagnosis of metabolic syndrome (MS).

The acute phase reactant C-reactive protein (CRP) binds with high affinity to fibronectin (FN), but this binding occurs only at pH 6.5 or lower, and the binding is inhibited by calcium ions at physiological pH. Since CRP in the circulating blood exists in a calcium-binding form, the interaction between CRP and FN in vivo has been uncertain. CRP can undergo a conformational rearrangement in the absence of calcium or in the local microenvironment (e.g., acidic pH) of inflamed tissue to dissociate into monomeric CRP (mCRP). Therefore, we tested whether these discrepancies can be explained by the different isoforms and locations of CRP. Surface plasmon resonance and ELISA assays showed that mCRP binds with high affinity to FN, and the binding of mCRP to FN was unaffected by calcium or pH. Peptide competition assay, deletion mutant binding assay and protein docking analyse verified that the binding site of mCRP to FN is residues a.a.35-47. Furthermore, mCRP can significantly enhance the adhesion of monocytes to FN as well as upregulate the adhesion molecules expression on endothelial cell. Colocalization of mCRP with FN was observed in mice with DSS-induced colitis, whereas there was very little signal orcolocalization of CRP. These results provide in vitro and in vivo evidence that mCRP formed by local dissociation from circulating CRP is the major isoform that interacts with FN and regulates FN-mediated monocyte adhesion, which is involved in the pro-inflammatory process.

Conventional C-reactive protein assays have been used to detect or guide the treatment of acute sepsis. The objective of this study was to determine the association between elevated baseline high-sensitivity C-reactive protein (hsCRP) and the risk of future sepsis events.

Cardiovascular disease is the leading cause of death in the world. Human C-reactive protein (CRP) has been used in the risk assessment of coronary events. Human saliva mirrors the body's health and well-being and is non-invasive, easy to collect and ideal for third world countries as well as for large patient screening. The aim was to establish a saliva CRP reference range and to demonstrate the clinical utility of salivary CRP levels in assessing the coronary events in a primary health care setting.

No abstract available

C-reactive protein (CRP) levels are elevated in patients with abdominal aortic aneurysms (AAA). However, it has not been investigated whether CRP contributes to AAA pathogenesis.

Osteoarthritis (OA) is a chronic joint disease characterized by articular cartilage degeneration and secondary bone hyperplasia. C-reactive protein (CRP) is an acute-phase protein that is widely used as a marker of inflammation. Elevated plasma levels of CRP are commonly observed in patients with OA during the acute phase. Current evidence indicates that CRP dissociating into a monomeric form (mCRP) is the main functional conformation at inflammatory loci. However, it remains unclear whether mCRP is associated with OA and whether mCRP can be used as a biomarker for its pathogenesis. In the present study, the concentration of CRP, mCRP and anti-mCRP autoantibody were detected by performing ELISA. The levels of plasma CRP, mCRP and anti-mCRP autoantibody between healthy subjects and patients with OA were compared. The results revealed that plasma mCRP was strongly associated with OA, while mCRP autoantibodies exhibited little correlation with this condition. Additionally, it was identified that the plasma mCRP levels in Kellgren-Lawrence (KL) grade 4 patients were significantly higher than in those with KL grade 3. Thus, it was revealed in the present study that plasma level of mCRP is associated with OA, which may directly reflect the disease degree of patients. Therefore, mCRP may be a potential indicator that can be used to monitor the disease activity and evaluate the efficiency of OA therapy.

A surface acoustic wave (SAW) sensor was investigated for its application in C-reactive protein (CRP) detection. Piezoelectric lithium niobate (LiNbO3) substrates were used to study their frequency response characteristics in a SAW sensor with a CRP sensing area. After the fabrication of the SAW sensor, the immobilization process was performed for CRP/anti-CRP interaction. The CRP/anti-CRP interaction can be detected as mass variations in the sensing area. These mass variations may produce changes in the amplitude of sensor response. It was clearly observed that a CRP concentration of 0.1 μg/mL can be detected in the proposed SAW sensor. A good fitting linear relationship between the detected insertion loss (amplitude) and the concentrations of CRP from 0.1 μg/mL to 1 mg/mL was obtained. The detected shifts in the amplitude of insertion loss in SAW sensors for different CRP concentrations may be useful in the diagnosis of risk of cardiovascular diseases.

Earlier, we showed that the offspring from exceptionally long-lived families have a more favorable glucose metabolism when compared with controls. As chronic low-grade inflammation has been regarded as a strong risk factor for insulin resistance, we evaluated if and to what extent the favorable glucose metabolism in offspring from long-lived families could be explained by differences in subclinical inflammation, as estimated from circulating levels of C-reactive protein. We found no difference between the two groups in C-reactive protein levels or in the distribution of C-reactive protein haplotypes. However, among controls higher levels of C-reactive protein were related to higher glucose levels, whereas among offspring levels of C-reactive protein were unrelated to glucose levels. It is a limitation of the current study that its cross-sectional nature does not allow for assessment of cause-effect relationships. One possible interpretation of these data is that the offspring from long-lived families might be able to regulate glucose levels more tightly under conditions of low-grade inflammation. To test this hypothesis, our future research will be focused on assessing the robustness of insulin sensitivity in response to various challenges in offspring from long-lived families and controls.