Serum C1q Research Articles

Abnormal lower expression of GPR183 in peripheral blood T and B cell subsets of systemic lupus erythematosus patients

G protein-coupled receptor 183 (GPR183) has been indicated to mediate the migration and localisation of immune cells in T cell-dependent antibody responses. Systemic lupus erythematosus (SLE) is a canonical autoimmune disease involving B cell-mediated tolerance destruction and excessive pathogenic autoantibody production, in which multiple GPCRs play a role. To date, there has been no systematic study regarding the expression of GPR183 in lymphocyte subsets of SLE patients. In this research, firstly, we observed the expression trends of GRP183 in various T and B cell subsets in human tonsil tissues. These lymphocyte subsets include CD4+, CD8+, naïve T, effector T, Tfh, activated Tfh, Th1, Th2, Th17, Treg, CD19+CD27-, CD19+CD27+, naïve B, germinal centre B, memory B, and plasma cells. Further, compared with healthy controls (HCs), GPR183 expression levels in above peripheral blood lymphocyte subsets of patients with SLE were reduced overall. The differential expression of GPR183 expression between inactive and active SLE patients indicates that GPR183 expression may be concerned with the disease activity of SLE. This was further confirmed through the strong negative correlation with SLEDAI score and positive correlation with serum complement protein C3, C4 and C1q levels. Further receiver operating characteristic (ROC) curve analysis revealed that GPR183 expression in circulating CD27-IgD+ B cells may be beneficial in distinguishing between inactive and active SLE patients. In addition, type I interferon stimulation could down-regulate the expression of GPR183 in peripheral blood T and B cell subsets. Aberrant expression of GPR183 may provide some novel insights into disease activity prediction and underlying pathogenesis of SLE.

C1q and mobility score in predicting sarcopenia in an Australian cohort of cancer surgery patients.

Sarcopenia has been shown to have significant adverse health outcomes in a range of patient populations. Particularly, sarcopenic patients having cancer surgery are a unique group who demonstrate poorer post-operative outcomes. Currently, the gold standard in diagnosing sarcopenia is through the use of computed tomography. However, the widespread use of imaging to diagnose patients with sarcopenia is neither cost-effective nor practical. Identifying a serum biomarker or a simple mobility scoring system as an alternative diagnostic tool may aid in identifying more patients at risk of sarcopenia. C1q, a novel biomarker, has previously been shown to correlate with sarcopenia. Similarly, we sought to explore whether mobility scores may provide a useful surrogate marker for sarcopenia. This was a prospective cohort study of patients who presented for colorectal cancer surgery between the dates of 6/10/2016 and 4/10/2017 at John Hunter Hospital. Computed tomography was utilized to calculate the psoas area at the L3 spinal level. Pre-operative blood samples were obtained for C1q analysis and de Morton Mobility Index (DEMMI) was also performed. A total of 51 patients were included in the study. The median age of the patients were 69 years old. We did not demonstrate a correlation between serum C1q and DEMMI scores with psoas area. Our findings suggest that neither C1q nor DEMMI scores are correlated with psoas area in a colorectal cancer population.

Study of relation between Serum C1Q / TNF-Related Protein 9 (CTRP9) and Diabetic Retinopathy in a Sample of Egyptian Patients With Type 2 Diabetes Mellitus

Study of relation between Serum C1Q / TNF-Related Protein 9 (CTRP9) and Diabetic Retinopathy in a Sample of Egyptian Patients With Type 2 Diabetes Mellitus

Changes of Serum Complement C1q in Patients with Multiple Myeloma

To analyze the change of serum C1q in the course of multiple myeloma (MM) and its correlation with clinical characteristics. A total of 138 newly diagnosed MM patients in Zhongnan Hospital of Wuhan University from June 2016 to December 2019 were selected as research objects, during the same period 50 age-matched anemia patients, 50 lymphoma patients, 50 leukemia patients, and 50 myelodysplastic syndrome (MDS) patients were selected as control groups. All the patients met WHO disease classification, and were definitely diagnosed by pathology or bone marrow smear/biopsy. The changes of C1q between MM patients and control group, as well as in different therapeutic responses of MM patients before and after treatment were compared, also the difference of clinical characteristics among MM patients with different C1q level, so as to analyze risk factors which led to C1q decline. The average value of C1q in MM patients was (128.18±51.24) mg/L, which was significantly lower than control group (P<0.01). The levels of white blood cell, platelet (PLT), hemoglobin (Hb), serum calcium, albumin, lactate dehydrogenase (LDH) in newly diagnosed high C1q group were significantly higher than those in low C1q group (P<0.05). Logistic analysis showed that the levels of PLT, Hb, albumin, and LDH in newly diagnosed high C1q group were higher than those in low C1q group (r=0.248, r=0.394, r=0.405, r=0.295). After treatment, the levels of C1q in MM patients with complete remission and very good partial remission were significantly higher than before treatment (P<0.05), while those with partial remission and stable disease also increased but not significantly (P>0.05). The C1q level in MM patients is significantly lower than that in patients with other hematologic system diseases, and it increases with the remission of the disease after treatment.

Circulating Levels of Anti-C1q and Anti-Factor H Autoantibodies and Their Targets in Normal Pregnancy and Preeclampsia.

Preeclampsia (PE) generally manifests in the second half of pregnancy with hypertension and proteinuria. The understanding of the origin and mechanism behind PE is incomplete, although there is clearly an immune component to this disorder. The placenta constitutes a complicated immune interface between fetal and maternal cells, where regulation and tolerance are key. Stress factors from placental dysfunction in PE are released to the maternal circulation evoking the maternal response. Several complement factors play a role within this intricate landscape, including C1q in vascular remodeling and Factor H (FH) as the key regulator of alternative pathway complement activation. We hypothesize that decreased levels of C1q or FH, or disturbance of their function by autoantibodies, may be associated with PE. Autoantibodies against C1q and FH and the concentrations of C1q and FH were measured by ELISA in maternal sera from women with preeclamptic and normal pregnancies. Samples originated from cohorts collected in the Netherlands (n=63 PE; n=174 control pregnancies, n=51 nonpregnant), Finland (n=181 PE; n=63 control pregnancies) and Norway (n=59 PE; n=27 control pregnancies). Serum C1q and FH concentrations were higher in control pregnancy than in nonpregnant women. No significant differences were observed for serum C1q between preeclamptic and control pregnancy in any of the three cohorts. Serum levels of FH were lower in preeclamptic pregnancies compared to control pregnancies in two of the cohorts, this effect was driven by the early onset PE cases. Neither anti-C1q autoantibodies nor anti-FH autoantibodies levels differed between women with PE and normal pregnancies. In conclusion, levels of anti-C1q and anti-FH autoantibodies are not increased in PE. C1q and FH are increased in pregnancy, but importantly, a decrease in FH concentration is associated with PE.

Different Complement Activation Pathways Underly Cognitive Impairment and Type 2 Diabetes Mellitus Combined With Cognitive Impairment.

BackgroundThe immune response and the complement system are associated with cognitive impairment and diabetes mellitus, respectively. Activation of the complement system in these diseases occurs mainly through either the classical pathway or the alternative pathway. However, the specific complement proteins involved in the development of the type 2 diabetes mellitus (T2DM) and cognitive impairment are still unclear. Here, we investigated complement proteins in serum from patients with T2DM, cognitive impairment, or both T2DM and cognitive impairment.ObjectiveTo investigate the levels of serum immune complement proteins in patients with T2DM, cognitive impairment, or T2DM combined with cognitive impairment and the associations between these complement proteins and risk factors for T2DM or cognitive impairment.MethodsClinical markers were collected from blood samples of 264 participants. Luminex multiplex assays were used to detect serum complement proteins. All statistical analyses were performed using Prism or R studio.ResultsThere was a difference in serum levels of the complement proteins C1q, C3, C3b, and FH between the three different groups. Hyperglycemia was significantly correlated with elevated C3b or reduced C3, C1q, and FH. In addition, hyperlipidemia was positively correlated with elevated levels of C3, C4, C1q, and FH proteins. There was an association between C1q, C3, C4, and FH and β-pancreas cell function, whereas only FH was associated with insulin resistance. Higher serum C1q was significantly associated with an increased risk of cognitive impairment.ConclusionSerum levels of complement proteins were closely associated with hyperglycemia and hyperlipidemia. We found that classical complement pathway activation mainly occurred in the cognitive impairment only group, whereas the alternative pathway may reflect T2DM and T2DM with cognitive impairment.

Beyond Systemic Lupus Erythematosus and Anti-Phospholipid Syndrome: The Relevance of Complement From Pathogenesis to Pregnancy Outcome in Other Systemic Rheumatologic Diseases.

Evidence about the relevance of the complement system, a highly conserved constituent of the innate immunity response that orchestrates the elimination of pathogens and the inflammatory processes, has been recently accumulated in many different rheumatologic conditions. In rheumatoid arthritis, complement, mainly the classical pathway, contributes to tissue damage especially in seropositive subjects, with complement activation occurring in the joint. Data about complement pathways in psoriatic arthritis are dated and poorly consistent; among patients with Sjögren syndrome, hypocomplementemia exerts a prognostic role, identifying patients at risk of extra-glandular manifestations. Hints about complement involvement in systemic sclerosis have been recently raised, following the evidence of complement deposition in affected skin and in renal samples from patients with scleroderma renal crisis. In vasculitides, complement plays a dual role: on one hand, stimulation of neutrophils with anti-neutrophil cytoplasmic antibodies (ANCA) results in the activation of the alternative pathway, on the other, C5a induces translocation of ANCA antigens, favouring the detrimental role of antibodies. Complement deposition in the kidneys identifies patients with more aggressive renal disease; patients with active disease display low serum levels of C3 and C4. Even though in dermatomyositis sC5b-9 deposits are invariably present in affected muscles, data on C3 and C4 fluctuation during disease course are scarce. C3 and C1q serum levels have been explored as potential markers of disease activity in Takayasu arteritis, whereas data in Behçet disease are limited to in vitro observations. Pregnancies in women with rheumatologic conditions are still burdened by a higher rate of pregnancy complications, thus the early identification of women at risk would be invaluable. A fine-tuning of complement activation is required from a physiological progression of pregnancy, from pre-implantation stages, through placentation to labour. Complement deregulation has been implicated in several pregnancy complications, such as recurrent abortion, eclampsia and premature birth; low complement levels have been shown to reliably identify women at risk of complications. Given its physiologic role in orchestrating pregnancy progression and its involvement as pathogenic effector in several rheumatologic conditions, complement system is an attractive candidate biomarker to stratify the obstetric risk among women with rheumatologic conditions.

Circulating Complement C1q as a Novel Biomarker is Associated with the Occurrence and Development of COPD.

PurposeIncreasing evidence has shown that the immune response interacts with the chronic inflammatory response and gives rise to the occurrence and development of COPD. Complement component 1q (C1q), as a subcomponent of the C1 complex, could be involved in innate and adaptive immunity. Our study aimed to investigate the relationship between C1q and the clinical characteristics of COPD subjects.Patients and MethodsSerum C1q levels were measured in 203 COPD subjects and 191 non-COPD controls. Correlations between C1q and the characteristics of COPD were analyzed using Spearman’s rho. Receiver operating curve (ROC) analysis was used to evaluate the threshold value in differentiating disease status. All 203 COPD subjects were followed up for 1 year for future acute exacerbations.ResultsThere were significant reductions in serum C1q levels in COPD subjects compared to non-COPD controls. Moreover, serum C1q levels were obviously positively correlated with the FEV1/FVC ratio and predicted FEV1% but had a weakly negative correlation with the %LAA-950 and the percentage of neutrophils in peripheral blood. Using a cutoff value of 137.150 mg/l as the boundary in ROC analysis, the sensitivity and specificity were 65.9% and 76.0%, respectively. The 1-year follow-up results showed that C1q levels less than 137.150 mg/l were negatively related to the time to the next severe exacerbation and the time to death.ConclusionCirculating C1q levels may be a novel biomarker not only related to the pulmonary function of COPD but also having great potential to predict the risk of COPD deterioration in the future. However, further prospective trials are needed to clarify the influences of C1q on the pathogenesis of COPD.

Elevated Serum Complement C1q Levels After Traumatic Brain Injury and Its Association with Poor Prognosis.

ObjectiveComplement C1q is implicated in neuroinflammation. We intended to discern the relationship between serum C1q levels and severity in addition to prognosis following traumatic brain injury (TBI).MethodsIn this prospective, observational study, serum C1q levels were quantified in 188 TBI patients and 188 healthy controls. Glasgow coma scale (GCS) and Rotterdam computed tomography (CT) classification were used as clinical and radiological indicators of severity. Patients with extended Glasgow outcome scale (GOSE) score of 1–4 at 6 months after trauma were considered to have a poor outcome. Multiple logistic regression model was built to ascertain the independent association of serum C1q levels with 6-month poor outcome. Receiver operating characteristic (ROC) curve was configured for analysis of prognostic capability with respect to serum C1q levels.ResultsTBI patients exhibited substantially higher serum C1q levels than controls (median, 223.9 mg/l versus 75.4 mg/l). Serum C1q levels of patients were tightly correlated with GCS score (r = −0.671), Rotterdam CT classification (r = 0.604) and GOSE score (r = −0.581). An area under the ROC curve was yielded of 0.793 (95% confidence interval = 0.728–0.849), and serum C1q levels above 345.5 mg/l discriminated the risk of 6-month poor outcome with 59.6% sensitivity and 92.6% specificity. Serum C1q levels above 345.5 mg/l retained as an independent predictor for 6-month poor outcome with odds ratio of 4.922 (95% confidence interval = 1.552–15.606; P = 0.017).ConclusionElevated serum C1q levels are closely correlated with traumatic severity and independently predicted the risk of long-term poor prognosis after TBI.

C1q inhibits differentiation of oligodendrocyte progenitor cells via Wnt/β-catenin signaling activation in a cuprizone-induced mouse model of multiple sclerosis

Multiple sclerosis (MS) is a chronic central nervous system demyelinating disease of autoimmune originate. Complement C1q, a complex glycoprotein, mediates a variety of immunoregulatory functions considered important in the prevention of autoimmunity. Although we found that the increased serum C1q level was highly associated with the Fazekas scores and T2 lesion volume of MS patients, the effect and mechanism of C1q on demyelination remains unclear. Cluster analysis and protein array results showed that serum Wnt receptors Frizzled-6 and LRP-6 levels in MS patients were both increased, we proposed that C1q may be involved in demyelination via Wnt signaling. The increased C1q protein levels in the serum and brain tissue were confirmed in a cuprizone (CPZ)-induced demyelination mice model. Moreover, CPZ treatment induced significant increase of LRP-6 and Frizzled-6 protein in mice corpus callosum. LRP-6 extra-cellular domain (LRP-6-ECD) level in the serum and cerebrospinal fluid (CSF) of CPZ mice also significantly increased. Knockdown of the subunit C1s of C1 not only substantially attenuated demyelination, promoted M2 microglia polarization and improved neurological function, but inhibited β-catenin expression and its nuclear translocation in oligodendrocyte progenitor cells (OPCs). In vitro, C1s silence reversed the increased level of LRP-6-ECD in the medium and β-catenin expression in OPCs induced by C1q treatment. Meanwhile, inhibition of C1s also markedly lowered the number of EDU positive OPCs, but enhanced the number of CNPase positive oligodendrocyte and the protein of MBP. The present study indicated that C1q was involved in demyelination in response to CPZ in mice by preventing OPC from differentiating into mature oligodendrocyte via Wnt/β-catenin signaling activation.

Serum Level of Complement C1q is Associated with Contrast-Associated Acute Kidney Injury in Patients Undergoing Emergency Percutaneous Coronary Intervention.

BackgroundAs an inflammatory factor, complement C1q is related to the prevalence and progression of atherosclerosis; however, in patients undergoing emergency percutaneous coronary intervention (PCI), it is unclear whether C1q is related to the prevalence of contrast-associated acute kidney injury (CA-AKI).MethodsFrom November 2018 to March 2021, 1182 patients who underwent emergency PCI were continuously recruited. Patients were divided into CA-AKI group (n = 234) and non-CA-AKI group (n = 948). CA-AKI was defined as an increase in serum creatinine from the baseline level (≥25% or ≥0.5 mg/dL) 48–72 hours after contrast exposure. All subjects were tested for serum C1q levels when they were admitted to the hospital.ResultsAmong the 1182 patients undergoing emergency PCI, 234 patients (19.80%) developed CA-AKI. The level of preoperative serum complement C1q in the CA-AKI group was significantly higher than that in the non-CA-AKI group. Logistic regression and restricted cubic spline analyses showed that the incidence of CA-AKI was positively associated with the serum C1q level pre-PCI. Univariate and multivariate logistic regression analyses showed that C1q was an independent predictor of whether CA-AKI occurred after emergency PCI. The area under the curve (AUC) of the C1q was 0.703 [95% confidence interval (CI) 0.667–0.739] in patients receiving emergency PCI. CA-AKI model included the following three predictors: C1q, eGFR, and IABP use. The AUC of forecast probability was 0.718 [95% CI 0.682–0.754].ConclusionIn patients receiving emergency PCI procedure, a high C1q level before PCI is associated with the increased risk of CA-AKI.

Association Between Serum C1q Tumor Necrosis Factor-Related Protein 9 and the Clinical Characteristics and Prognosis of Ischemic Stroke.

Introduction C1q tumor necrosis factor (TNF)-related protein 9 (CTRP9) is a novel member of the C1q/TNF superfamily. According to our previous review, CTRP9 plays a vital role in the process of cardiovascular diseases, including regulating energy metabolism, modulating vasomotion, protecting endothelial cells, inhibiting platelet activation, inhibiting pathological vascular remodeling, stabilizing atherosclerotic plaques, and protecting the heart. We proposed that CTRP9 could play multiple positive and beneficial roles in vascular lesions in ischemic stroke (IS). Here, we aimed to study the relationship between serum CTRP9 and the etiology, severity, and prognosis of IS patients. MethodsA total of 302 patients with IS and 173 non-stroke controls were selected from the same hospital, and all patients with IS were followed up 12 months after stroke onset. Stroke etiology was classified according to the Trial of ORG 10172 in Acute Stroke Treatment classification. Symptomatic severity was determined using the National Institutes of Health Stroke Scale score. The lesion volume of acute cerebral ischemia was measured using magnetic resonance imaging (MRI). The unfavorable functional outcome was a combination of death or major disability 12 months after stroke onset. Receiver operating characteristic (ROC) curves and integrated discrimination improvement (IDI) and net reclassification improvement (NRI) statistics were applied in the statistical analysis.ResultsWe found that serum CTRP9 levels and the ratios of CTRP9/total cholesterol (TC), CTRP9/triglyceride (TG), CTRP9/low-density lipoprotein cholesterol (LDL-C), and CTRP9/high-density lipoprotein cholesterol (HDL-C) were associated with the presence of IS. Moreover, the serum CTRP9 concentration was positively associated with the severity of IS. Incorporation of CTRP9/LDL-C levels into a fully adjusted model for IS-cardioembolic (CE) improved discrimination and calibration, and significantly improved reclassification. In addition, CTRP9 was a predictor of unfavorable functional outcomes.ConclusionsAll the findings indicated that serum CTRP9 could be a promising blood-derived biomarker for the early evaluation and prognosis assessment of IS.Trial RegistrationChinese Clinical Trial Registry, ChiCTR1800020330.Supplementary InformationThe online version contains supplementary material available at 10.1007/s40120-021-00296-7.

A Preliminary Study of the Complement Component 1q Levels in Predicting the Efficacy of Combined Immunotherapy in Patients with Lung Cancer.

ObjectiveTo evaluate the value of serum complement component 1q (C1q) levels in predicting the efficacy of combined immunotherapy in patients with lung cancer.MethodsA total of 42 patients with lung cancer who received combined immunotherapy in the cancer center of Renmin Hospital of Wuhan University were included in this study. The clinical data of serum C1q and lactate dehydrogenase (LDH) levels before and three weeks after immunotherapy were collected.ResultsResponse evaluation showed that the number of patients with complete response (CR), partial response (PR), stable disease (SD), and progressive disease (PD) was 0 (0%), 26 (61.9%), 14 (33.3%), and 2 (4.8%), respectively. The CR/PR group (patients with CR or PR) showed higher pC1q (C1q level before immunotherapy) and iC1q (C1q level 3 weeks after immunotherapy) than the SD/PD group (patients with SD or PD). The LDH reduction (96.2%) and C1q increment (84.6%) in the CR/PR group 3 weeks after immunotherapy were higher than those of the SD/PD group, and the differences were statistically significant. Logistic regression analysis indicated that pC1q, iC1q, and LDH level trends 3 weeks after the treatment were significantly correlated to the efficacy of combined immunotherapy with odds ratios of 8.185, 5.500, and 0.031, respectively.ConclusionHigh C1q levels before immunotherapy and increased C1q levels and decreased LDH levels 3 weeks afterward suggest good therapeutic effects of combined immunotherapy in patients with lung cancer. Serum C1q levels have certain clinical significance in predicting the efficacy of combined immunotherapy.

Serum C1q Levels Have Prognostic Value for Sepsis and are Related to the Severity of Sepsis and Organ Damage.

ObjectiveTo explore the clinical application value of serum complement component C1q levels in sepsis.MethodsThe clinical data and laboratory examination data of 320 research subjects (including 132 cases as sepsis group, 93 cases as nonsepsis group and 95 cases as control group) who were diagnosed and treated in Renmin Hospital of Wuhan University from July 2020 to March 2021 were collected. We compared the levels of each index among the three groups and further analyzed the C1q levels of different severity subgroups and different outcome subgroups of sepsis. Afterwards, we explored the correlation between C1q levels and SOFA score, organ damage indexes and coagulation indexes. Finally, the receiver operating characteristic curve (ROC) was used to analyze the prognostic value of C1q in patients with sepsis.ResultsC1q levels were significantly reduced in the serum of patients with sepsis; the level of C1q in the death group was lower than that in the survival group (127.1 mg/L vs 153.2 mg/L, P < 0.05), and the mortality in the C1q decreased group was higher when compared with C1q normal group; in addition, serum C1q levels were correlated with SOFA score, organ damage indexes and coagulation indexes; C1q had a high area under the curve (AUC) for the prognosis of sepsis, and the combination of other indexes can further improve the prognostic value.ConclusionSerum C1q levels have potential clinical value for the condition and prognosis of sepsis.

Novel Monoclonal Antibodies Against Mouse C1q: Characterisation and Development of a Quantitative ELISA for Mouse C1q

Recent studies have identified roles for complement in synaptic pruning, both physiological during development and pathological in Alzheimer’s disease (AD). These reports suggest that C1q initiates complement activation on synapses and C3 fragments then tag them for removal by microglia. There is an urgent need to characterise these processes in rodent AD models; this requires the development of reagents and methods for detection and quantification of rodent C1q in fluids and pathological tissues. These will enable better evaluation of the role of C1q in disease and its value as disease biomarker. We describe the generation in C1q-deficient mice of novel monoclonal antibodies against mouse and rat C1q that enabled development of a sensitive, specific, and quantitative ELISA for mouse and rat C1q capable of measuring C1q in biological fluids and tissue extracts. Serum C1q levels were measured in wild-type (WT), C1q knockout (KO), C3 KO, C7 KO, Crry KO, and 3xTg and APPNL-G-F AD model mice through ageing. C1q levels significantly decreased in WT, APPNL-G-F, and C7 KO mice with ageing. C1q levels were reduced in APPNL-G-F compared to WT at all ages and in 3xTg at 12 months; C3 KO and C7 KO, but not Crry KO mice, also demonstrated significantly lower C1q levels compared to matched WT. In brain homogenates, C1q levels increased with age in both WT and APPNL-G-F mice. This robust and adaptable assay for quantification of mouse and rat C1q provides a vital tool for investigating the expression of C1q in rodent models of AD and other complement-driven pathologies.

C1q intrathecal synthesis can be performed using IgM reibergram

INTRODUCTION C1q is a component of the classical complement system pathway and it has a functional link between the innate and adaptive immune system. Usually C1q is a blood-derived protein and it can be synthesized in the central nervous system. OBJECTIVE To demostrate the possibility to quantify C1q intrathecal synthesis by using the IgM reibergram. MATERIAL AND METHODS 64 paired cerebrospinal fluid (CSF) and serum samples from normal healthy people without blood-brain dysfunction were obtained. CSF and serum C1q was quantified by immunoenzimatic assay. All the results were plotted in the reibergram employed to determine IgM intrathecal synthesis. RESULTS The concentrations of C1q in CSF were two orders of magnitude lower than those in serum. C1q values increased with the increment of CSF/serum albumin concentration quotient (QAlb) (Figure 1) as a measure of the function ability of the blood-CSF barrier and the velocity of CSF flow suggesting diffusion of C1q from blood to CSF. Because the C1q molecular weight (400 kDa) is similar than IgM´s (800 kDa) the CSF and serum C1q values was plotted in IgM reibergram (Figure 2). CONCLUSIONS The strong positive correlation of C3 with QAlb suggests that a substantial portion of C1q in CSF originates from blood and the C1q complement system could be synthesized in the CSF and its quantities could be calculate by the corresponding IgM reibergram.

Serum Complement C1q Activity Is Associated With Obstructive Coronary Artery Disease.

Background: Complement C1q plays a dual role in the atherosclerosis. Previous studies showed inconsistent results about the association of serum C1q levels and coronary artery disease (CAD). Here, we explored the associations of serum C1q activity with CAD, coronary stenosis severity, cardiovascular biomarkers, and 1-year restenosis after coronary artery revascularization.Methods: We enrolled 956 CAD patients and 677 controls to evaluate the associations of serum complement C1q activity to the presence and severity of obstructive CAD and non-obstructive CAD. Serum C1q activity and the concentrations of laboratory markers were measured in all subjects. All the data were analyzed using SPSS22.0 software.Results: Serum C1q activity in Obstructive CAD and Non-Obstructive CAD groups was significantly higher than the control group (195.52 ± 48.31 kU/L and 195.42 ± 51.25 kU/L vs. 183.44 ± 31.75 kU/L, P < 0.05). Greater C1q activity was significantly correlated with higher total cholesterol (TC) and triglyceride (TG) levels. C1q activity was associated with an increased Odds Ratio (OR) of CAD (OR = 1.322, 95% CI 1.168–1.496, P < 0.05) and 1-year restenosis after revascularization (the highest OR = 3.544, 95% CI 1.089–12.702, P < 0.05). Complement C1q activity was not correlated with Gensini score in the Obstructive CAD group after adjustment for confounders. C1q activity has low value in predicting the incidence of CAD.Conclusion: Serum complement C1q activity is associated with obstructive CAD.

Elevated Serum C1q Levels in Children With Sepsis.

Objective: To analyze the serum complement C1q levels in children with sepsis, and explore the suggestive effect of serum C1q levels on the condition of children with sepsis.Methods: The clinical and laboratory data of children with sepsis (n = 95) and healthy children (n = 71) in Renmin Hospital of Wuhan University from January 2019 to October 2019 were collected, and each index of the two groups was compared. Then we divided children with sepsis into three subgroups based on the Pediatric Critical Illness Score (PCIS): non-critical group, critical group, and extremely critical group. The serum C1q and PCT levels of the three subgroups were analyzed, and the correlation analysis was carried out between the levels of serum C1q and PCT levels as well as PCIS among children with sepsis. Finally, we analyzed the serum C1q levels of septic children infected by different pathogens.Results: The serum C1q levels of children with sepsis were significantly higher than those of healthy children (median 198.4 vs. 186.2 mg/L, P < 0.001). In the analysis of subgroups, the serum C1q levels of non-critical group, critical group, and extremely critical group septic children were 182.80 (166.75, 195.85) mg/L, 219.90 (209.10, 246.40) mg/L and 249.95 (239.10, 272.25) mg/L, respectively, which were correlated with the severity of the disease. At the same time, we also found that serum C1q in children with sepsis was positively correlated with PCT levels (r = 0.5982, P < 0.001), and negatively correlated with PCIS score (r = −0.6607, P < 0.001). The serum C1q levels of septic children with bacterial infections, mycoplasma infections, viral infections, and co-infection were higher than those of the control group (P < 0.05).Conclusion: The serum levels of C1q in children with sepsis were increased and related to the severity of sepsis, suggesting that C1q may be involved in the occurrence and development of sepsis, which had reference value for the preliminary diagnosis and severity classification of sepsis.

The clinical role of combined serum C1q and hsCRP in predicting coronary artery disease

ObjectiveC1q has been shown to be associated with coronary heart disease (CAD) and can co-deposit with C-reactive protein (CRP) in atherosclerotic plaques. However, few studies have been conducted between C1q, CRP parameters and CAD. The aim of this study is to explore the relationship between C1q and CRP parameters and assess their clinical significance in CAD. Methods238 total patients who underwent coronary artery angiography were enrolled and divided into control group (n = 65), stable CAD group (n = 47) and unstable angina group (UA group, n = 126). Patients’ data were collected from self-administered questionnaires and electrical medical records. The severity of coronary stenosis was presented by Gensini score. The relationship between C1q, CRP parameters and CAD were evaluated by multivariate regression analysis and their predicting performance were assessed by ROC analysis and odds ratio analysis. ResultsCompared with control group, C1q was showed significantly lower in stable CAD (P = 0.004) and UA groups (P = 0.008), while hsCRP was higher in UA group (P = 0.024). Serum C1q was weakly positively associated with hsCRP (r = 0.24, P < 0.001) but not correlated with Gensini score. Logistic regression identified C1q (OR: 0.87 per 10 mg/L, 95% CI: 0.79–0.95, P = 0.001) and hsCRP (OR: 1.08 mg/L, 95% CI: 1.01–1.15, P = 0.032) as independent determinants of CAD. Furthermore, combined C1q and hsCRP level showed higher discriminatory accuracy in predicting CAD than C1q (AUC: 0.676 vs 0.585, P = 0.101; NRI: 10.4%, P = 0.049; IDI: 3.9%, P < 0.001) or hsCRP (AUC: 0.676 vs 0.585, P = 0.101; NRI: 16.7%, P = 0.006; IDI: 5.8%, P < 0.001). ConclusionsReduced serum C1q and increased hsCRP are independently associated with CAD and could be potential predictors for CAD diagnosis. Furthermore, combined C1q and hsCRP showed better performance in predicting CAD than using single one.

Clinical Evaluation of Serum Complement Component 1q and Cystatin C in the Diagnosis of Early Diabetic Kidney Disease

IntroductionTo investigate the diagnostic value of serum complement components 1 q (C1q), neutrophil gelatinase-associated lipocalin (NGAL), cystatin C (CysC), creatinine (SCr) and urea (SUr) for early diabetic kidney disease (EDKD)Material and methodsIndividuals with type 2 diabetes mellitus (DM) and healthy subjects at Mianyang Central Hospital from March, 2017 to November, 2017 were enrolled according to the inclusion and exclusion criteria. Serum SUr, SCr, CysC, C1q and NGAL were detected. Diagnostic values were evaluated by ROC.ResultsTotally, 546 individuals were enrolled, including 136 patients in simple DM group (SDM group), and 109 patients in EDKD group and 301 healthy controls (HC group). Compared with SDM group and HC group, serum SUr, SCr, C1q, CysC and NGAL in EDKD group were significantly increased (P&lt;0.01). C1q, CysC, and NGAL were significantly related to EDKD and they were risk factors for EDKD. Diagnostic performance of CysC (AUC=0.813, 0.777~0.845), C1q (AUC=0.797, 0.761~0.830) or NGAL (AUC=0.770, 0.732~0.805) was much higher than that of SCr (AUC=0.681, 0.640~0.720) or SUr (AUC=0.650, 0.608~0.690) (p &lt; 0.05). C1q +CysC (AUC=0.896, 0.867~0.920; Se=77.98%, 74.27% - 81.39%; Sp=89.4%, 86.59% - 91.92%; YI=0.675) had the optimal diagnostic performance. However, combination of C1q+CysC+NGAL (AUC=0.909, 0.882~0.932; Se=88.99%, 86.06% - 91.49%; Sp=80.32%, 76.73% - 83.57%; YI=0.693) or C1q+CysC+NGAL+SCr (AUC=0.912, 0.885~0.934; Se=87.16%, 84.06% - 89.85%; Sp=83.98%, 80.63% - 86.96%; YI=0.711) did not further improve diagnosis performance for EDKD (p&gt;0.05).ConclusionsC1q, CysC and NGAL have similar diagnostic performances, which is superior to SCr, in diagnosis of EDKD. Moreover, C1q +CysC combination has the optimal diagnostic performance for EDKD.