Pentraxin 3 Levels Research Articles

Study on Serum Pentraxin-3 Levels in Vasculitis with Hypertension.

Pentraxin-3 (PTX-3) is derived from the secretion of macrophages, neutrophils, endothelial cells, epithelial cells, and vascular smooth muscle cells, which can regulate the immune activity of macrophages. The objectives of our study were to investigate the serum PTX-3 levels and analyze this correlation with vasculitis (Vas), with hypertension. A total of 155 cases consisting 51 patients with Vas [including 7 cases of takayasu arteritis (TA), 24 cases of polyarteritis nodosa (PAN), and 20 cases of antineutrophil cytoplasmic antibody-associated Vas (AAV)] were screened by angiography and/or biopsy; 46 patients with essential hypertensions (PH) and 58 healthy controls (HC) were enrolled in this study from January 2013 to December 2016. Serum PTX-3 levels were determined by enzyme-linked immunosorbent assay. Compared with the HC and PH, the serum PTX-3 levels in systemic Vas were significantly higher (both P < 0.001, 4.42 ± 0.95 vs. 2.67 ± 0.92 and 4.42 ± 0.95 vs. 2.95 ± 0.60), and there was no significant difference between HC and essential hypertension (P = 0.886, 2.67 ± 0.92 vs. 2.95 ± 0.60). There was no significant difference of PTX-3 levels among TA, PAN, and AAV, as well as active and inactive groups, and renal and nonrenal groups even if they had a significant difference from EH and HC, respectively. There was no significant correlation between PTX-3 levels and blood pressure, erythrocyte sedimentation rate, or Birmingham Vasculitis Activity Score. Receiver operating characteristic analysis has shown that the best cutoff point was at 3.618 ng/μL; the sensitivity and specificity were calculated as 84.3% and 93.5% for the diagnosis of Vas from heath control, and the best cutoff point was at 3.425 ng/μL, The sensitivity and specificity were calculated as 88.2% and 82.6% for the diagnosis of Vas from essential hypertension. Serum PTX-3 levels were significantly higher in patients with Vas than essential hypertension or health control, and elevated PTX-3 levels can help identify Vas patients from healthy or essential hypertensive populations.

SUN-270 Atherosclerotic vascular disease and inflammation in CKD patients in South Africa

Chronic inflammation is a known risk factor for cardiovascular disease (CVD) among chronic kidney disease (CKD) patients. Current evidence supports the pivotal role of inflammation in atherosclerosis, which is reinforced by the association between traditional inflammatory markers, such as the high sensitivity C-reactive protein (hs-CRP), and CVD. We evaluated the association between inflammatory markers and atherosclerotic vascular disease (AsVD) in stage 3 CKD, end-stage kidney disease (ESKD) patients on dialysis and kidney transplant recipients (KTRs). This was a cross-sectional study of 40 adult (aged 18-65 years) non-diabetic stage 3 CKD patients, 40 peritoneal dialysis (PD) patients, 40 haemodialysis (HD) patients, 41 KTRs and 41 age- and sex-matched healthy controls. Serum was analysed for creatinine, albumin, lipid profile and inflammatory markers including hs-CRP, pentraxin-3, tumour necrosis factor alpha (TNF-α) and the ligand of the receptor for advanced glycation end-products (EN-RAGE). Echocardiography was performed on all patients and carotid intima media thickness (CIMT) was assessed in both right and left carotid arteries at 1 cm proximal to the carotid bulb. The levels of all the inflammatory markers assessed were elevated in CKD patients compared to controls. Pentraxin-3 levels were significantly higher in stage 3 CKD, PD, HD and KTRs (p < 0.05) compared to controls, while hs-CRP levels were significantly increased in stage 3 CKD, PD and HD patients, (p < 0.05). Tumour necrosis factor-alpha levels were significantly higher in PD patients compared to controls, (p < 0.001). EN-RAGE levels were significantly higher among KTRs compared to controls, (p < 0.05). Age, increased WHR and low HDL-C levels were associated with AsVD. Pentraxin-3 correlated positively with other inflammatory markers (except hs-CRP) and negatively with serum albumin levels (r = -0.316, p = 0.004). Hypertension, elevated total cholesterol, TNF-α and EN-RAGE levels were predictors of high pentraxin-3 levels while age (> 40 years) [OR 5.18, p < 0.001], the male gender [OR 2.45, p = 0.031] and low HDL-C [OR 2.93, p = 0.009] independently predicted AsVD. Inflammation is present in all the kidney disease groups and persists in the post-transplant period. Age (> 40 years), male gender and low HDL-C independently predicted AsVD. Aggressive treatment of lipid disorders and eradication of inflammation may be beneficial in reducing the burden of CVD in CKD.

Inflammatory markers: Pentraxin 3, Interleukin10 and Interleukin18 in children with Chronic Kidney Disease

Background Inflammation is a major risk factor for cardiovascular (CV) complications and mortality in patients with ESRD. Patients with end stage renal disease (ESRD) strongly exhibit higher serum levels of inflammatory cytokines compared to healthy individuals. Patients & Methods The serum levels of proinflammatory cytokine IL-18, and anti-inflammatory IL-10 and of Pentraxin 3 were studied in sixty pediatric patients, aiming to compare the inflammatory status of children with end-stage renal disease on hemodialysis and those on conservative treatment; and to study the effect of vascular access and cardiac disease on those cytokines. Thirty patients had end stage renal disease on regular hemodialysis in Pediatric Nephrology Unit, Cairo University Children’s Hospital, fifteen patients had chronic kidney disease, on conservative therapy, in addition to fifteen healthy matched controls. Results The mean age of patients and duration of dialysis for the hemodialysis group was 11.93 ±3.79 and 6.03±2.46 years respectively while the other group was 8.46±3.63 years. Hemodialyzed patients had significantly higher post dialysis levels of Pentraxin3 and interleukin18 compared to pre dialysis levels with p value of 0.044 and 0.001 respectively. There was no difference regarding pre and post dialysis levels of interleukin10. Hemodialyzed patients had higher levels of Pentraxin3 and interleukin18 than conservative patients with P value of 0.006 and 0.01 respectively. Pentraxin3 and interleukin18 were higher in patients who dialyzed via central venous catheters than via Arteriovenous fistula with P value of 0.04, 0.002 respectively; while interleukin10 was lower with P value of 0.03. Conclusion Children with ESRD had higher post dialysis levels of inflammatory cytokines such as PTX3 and IL 18 than pre-dialysis levels. Also, they had higher levels than conservative patients. No significant difference as regard IL10 in both hemodialysis and conservative patients. IL10 was negatively correlated with cardio-vascular complications. Fourty percent of patients had cardio-vascular lesions proved by ECHO. The use of central venous catheter in HD patients is associated with increase in inflammatory markers. PTX3, IL18 were significantly higher in patients who dialyzed via CVC than those via A-V fistula.

Cancer cell-derived long pentraxin 3 (PTX3) promotes melanoma migration through a toll-like receptor 4 (TLR4)/NF-κB signaling pathway.

Cutaneous melanoma is one of the most aggressive cancers characterized by a high plasticity, a propensity for metastasis, and drug resistance. Melanomas are composed of phenotypically diverse subpopulations of tumor cells with heterogeneous molecular profiles that reflect intrinsic invasive abilities. In an attempt to identify novel factors of the melanoma invasive cell state, we previously investigated the nature of the invasive secretome by using a comparative proteomic approach. Here, we have extended this analysis to show that PTX3, an acute phase inflammatory glycoprotein, is one such factor secreted by invasive melanoma to promote tumor cell invasiveness. Elevated PTX3 production was observed in the population of MITFlow invasive cells but not in the population of MITFhigh differentiated melanoma cells. Consistently, MITF knockdown increased PTX3 expression in MITFhigh proliferative and poorly invasive cells. High levels of PTX3 were found in tissues and blood of metastatic melanoma patients, and in BRAF inhibitor-resistant melanoma cells displaying a mesenchymal invasive MITFlow phenotype. Genetic silencing of PTX3 in invasive melanoma cells dramatically impaired migration and invasion in vitro and in experimental lung extravasation assay in xenografted mice. In contrast, addition of melanoma-derived or recombinant PTX3, or expression of PTX3 enhanced motility of low migratory cells. Mechanistically, autocrine production of PTX3 by melanoma cells triggered an IKK/NFκB signaling pathway that promotes migration, invasion, and expression of the EMT factor TWIST1. Finally, we found that TLR4 and MYD88 knockdown inhibited PTX3-induced melanoma cell migration, suggesting that PTX3 functions through a TLR4-dependent pathway. Our work reveals that tumor-derived PTX3 contributes to melanoma cell invasion via targetable inflammation-related pathways. In addition to providing new insights into the biology of melanoma invasive behavior, this study underscores the notion that secreted PTX3 represents a potential biomarker and therapeutic target in a subpopulation of MITFlow invasive and/or refractory melanoma.

Serum Pentraxin 3 level as a recent biomarker of diabetic retinopathy in Egyptian patients with diabetes

IntroductionSerum Pentraxin3 Level As A recent Biomarker Of Diabetic Retinopathy In Egyptian patients with diabetes. ObjectiveTo evaluate the association between elevated levels of plasma pentraxin 3 and the development and/or progression of diabetic retinopathy. Subjectsand methods: This case control study was carried out in internal medicine department, outpatient clinic of internal medicine and outpatient clinic of ophthalmology, at Zagazig university Hospital, 2018. Serum PTX3 level, HsCRP, HbA1c, lipid profile, serum creatinine were determined in 20 normal subjects, 20 patients with prediabetes, 20 patients with diabetes without diabetic retinopathy (DR), 20 patients with non-proliferative diabetic retinopathy (NPDR) and 20 patients with proliferative diabetic retinopathy (PDR). ResultsSerum PTX3 level significantly increased in patients with DR more than patients without DR with cut off point 1150 pg/ml, sensitivity 93.3%and specificity 72%. Serum HsCRP level significantly increased in patients with DR more than patients without DR with cut off point of 7.60 pg/ml has sensitivity 93.3% and specificity 68%.. Combined use of PTX3 and HsCRP decreases sensitivity to 76.7%, but combined use increases specificity to 90%.Significant relation between poor glycemic control and development of DR and its severity as showed by HbA1c. ConclusionSerum PTX3 levels mayt have significant role in the development of DR and its severity. Serum HsCRP increased with DR progression. Poor glycemic control significantly associated with high incidence of diabetic retinopathy and its severity. Longer diabetes duration is associated with progression of DR.

PS1570 PENTRAXIN-3 LEVEL AS A NOVEL VASCULAR ENDOTHELIAL MARKER IN NEWLY DIAGNOSED AND MULTI-TRANSFUSED PATIENTS WITH B-THALASSEMIA MAJOR: RELATION TO OXIDATIVE STRESS AND SUB-CLINICAL ATHEROSCLEROSIS

Background: It is suggested that PTX-3 increases oxidant stress and can be used as an early diagnostic marker for inflammation. PTX3 is a sensitive and specific biomarker for the diagnosis of cardiovascular diseases such as acute coronary syndrome (ACS) and also in coronary artery disease patients with inflammatory rheumatic disease (IRD). On this basis, PTX-3 can be an indicator of vascular endothelial damage occurring with oxidative stress, and the evaluation of endothelial function can serve as a prognostic factor for cardiovascular diseases. Recently, it has been shown that vascular endothelial damage in thalassemia patients can be evaluated through the serum PTX-3 level Aims: This study assessed the level of pentraxin-3 as a potential early marker for oxidative stress and its relation to markers of hemolysis, iron overload, lipid peroxidation and subclinical atherosclerosis in newly diagnosed and multi-transfused thalassemia patients. Methods: Sixty β-TM patients (30 newly diagnosed cases and 30 chronic transfusion dependent ones) without symptoms of heart disease were compared to 30 healthy controls and studied stressing on splenectomy, transfusion history, chelation therapy and mean serum ferritin in last year prior to the study. PTX-3 and MDA levels were assessed. Carotid intima media thickness (CIMT) was measured using Doppler ultrasound. Results: Serum MDA, PTX-3 and CIMT were significantly higher in all the studied β-TM patients than the control group (p < 0.05). MDA and PTX-3 levels were significantly higher in both newly diagnosed and chronic β-TM patients compared with healthy controls with the highest levels found among chronic transfusion-dependent patients (p < 0.05). CIMT was significantly higher in chronic transfusion-dependent β-TM patients compared with newly diagnosed and healthy controls (p < 0.05) while no significant difference between the latter two groups (p>0.05). PTX-3levels were significantly elevated in splenectomized patients (p = 0.047). Chronic β-TM patients with good compliance to chelation had lower PTX-3levels than non-compliant patients (p = 0.036). Both MDA and PTX-3 were positively correlated. Multivariable linear regression analysis revealed that lactate dehydrogenase, serum ferritin, MDA and CIMT were the significant independent variables related to increasedPTX-3levels in patients with β-TM. Summary/Conclusion: Conclusion: We suggest that oxidative stress starts early in pediatric patients with β-TM even in newly diagnosed ones as defined by high levels of PTX-3 and MDA. This process aggravates in chronic transfusion-dependent patients. PTX-3 is a promising marker of oxidative stress in β-TM patients. Good selection of chelation therapy based on the patients’ compliance, iron overload status is needed in order to decrease oxidative stress and the incidence of endothelial dysfunction among β-TM patients and consequently, lower PTX-3 levels.

SP562Association of serum Pentraxin-3 level and Cardiovascular risk in Hemodialysis Patients

SP562Association of serum Pentraxin-3 level and Cardiovascular risk in Hemodialysis Patients

Severe periodontitis is linked with increased peripheral levels of sTWEAK and PTX3 in chronic migraineurs

Periodontitis (PD) and chronic migraine (CM) have been recently linked, and inflammatory processes and vascular endothelial changes are hypothesized as potential mediators of this relationship. The aim of this cross-sectional analysis was to investigate the potential association of PD with vascular systemic inflammation and complement activation in patients with CM. Ninety-four chronic migraineurs underwent a full-mouth periodontal evaluation and a measure of PD activity and severity, namely the periodontal inflamed surface area (PISA) was calculated for each patient. We divided CM patients according to their periodontal status: mild PD (N = 14), moderate PD (N = 22), severe PD (N = 19), and non-PD (N = 39). Serum levels of C-reactive protein (CRP), pentraxin 3 (PTX3), soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK), and complements C3 and C4 were measured outside of migraine attacks. We found that severe periodontal patients had significantly higher circulating levels of PTX3 and sTWEAK compared with those without PD (2475.3 ± 1646.8pg/mL vs. 516.6 ± 1193.8pg/mL, P < 0.0001 and 672.4 ± 118.2pg/mL vs. 485.7 ± 112.2pg/mL, P < 0.0001; respectively). For the remaining biomarkers, no significant differences were found between groups. Severe PD was independently associated with higher levels of PTX3 (β = 1997.6, P < 0.0001) and sTWEAK (β = 187.1, P < 0.0001) but not with CRP, C3, and C4. PISA positively correlated to PTX3 (r = 0.475, P < 0.0001) and sTWEAK (r = 0.386, P < 0.0001). Based on these preliminary results, severe PD was linked with vascular systemic inflammation in patients with CM. However, further longitudinal studies should be performed to confirm these findings. sTWEAK and PTX3 measured in serum could be used as biomarkers in the PD-CM link.

Evaluating Serum Levels of Pentraxin-3, von Willebrand Factor and C-X-C Motif Chemokine Ligand 13 as Inflammatory Markers of Unstable Angina Pectoris

Unstable angina pectoris (USAP) is a complex condition in which widespread coronary inflammatory processes have important implications for clearer understanding of its pathogenesis and also its treatment. This study aimed at evaluating the diagnostic as well as prognostic value of serum inflammatory markers of pentraxin-3 (PTX-3), Von Willebrand Factor (vWf) and C-X-C Motif Chemokine Ligand 13 (CXCL13) in such patients. Out of sixty-nine patients, thirty-nine had USAP, thirty had stable angina pectoris (SAP), and thirty-nine were healthy controls. For all participants, serum PTX-3, vWf and CXCL13 levels were measured using ELISA. For each patient with USAP, the Thrombolysis in Myocardial Infarction (TIMI) and the scores of Global Registry of Acute Coronary Events (GRACE) were calculated to determine the severity of the disease. We, then, analyzed the relation of PTX-3, vWf and CXCL13 levels with TIMI and GRACE scores in patients with USAP. Serum PTX-3, vWf and CXCL13 levels were significantly higher in USAP group than those in either SAP or control groups (p˂0.001). Strong correlation was observed between CXCL13 level and TIMI risk score (p=0.019). In receiver operating characteristic (ROC) curves, area under the curve (AUC) values of PTX3, vWf and CXCL13 for detection of USAP were 0.755, 0.751, and 0.906, respectively. The levels of serum PTX3, vWf and CXCL13 increased in patients with USAP. The notable correlation implied that CXCL13 might be a sensitive and specific biomarker for the diagnosis of USAP as well as its severity. It might also show additional diagnostic values when measured in combination with vWf.

Evaluation of pentraxin-3 levels in sera and plasma of multiple sclerosis patients

Evaluation of pentraxin-3 levels in sera and plasma of multiple sclerosis patients

Pentraxin 3 in Noninvasively Obtained Cervical Fluid Samples from Pregnancies Complicated by Preterm Prelabor Rupture of Membranes

Problem: To determine the changes of pentraxin 3 (PTX3) level in noninvasively obtained cervical fluid samples from women with preterm prelabor rupture of membranes (PPROM) based on the presence of microbial invasion of the amniotic cavity (MIAC) and/or intra-amniotic inflammation (IAI), and intra-amniotic infection (the presence of both MIAC and IAI). Methods of Study: A total of 160 women with PPROM were included. Cervical fluid samples were obtained using a Dacron polyester swab and amniotic fluid samples were obtained by transabdominal amniocentesis. Cervical fluid PTX3 levels were assessed using enzyme-linked immunosorbent assay. Results: PTX3 was found in all the cervical fluid samples and its levels were higher in women with MIAC, IAI, and intra-amniotic infection than in women without these conditions. When the women were categorized into four subgroups based on the presence of MIAC and/or IAI, women with intra-amniotic infection had higher cervical fluid PTX3 levels than those with sterile IAI (IAI alone), colonization (MIAC alone), or no MIAC or IAI. A cervical fluid PTX3 level of 11 ng/mL was the best value for identifying the presence of intra-amniotic infection in women with PPROM. Conclusions: PTX3 is a constituent of cervical fluid of women with PPROM. Cervical fluid PTX3 level reflects the situation in the intra-amniotic compartments of women with PPROM. Cervical fluid PTX3 is a potential marker for the noninvasive identification of intra-amniotic infection in PPROM.

Increased Left Ventricular mRNA Levels of the Inflammatory Biomarkers Pentraxin‐3 and Interleukin 1 Receptor‐Like 1 are Correlated with Diastolic Dysfunction in a Pre‐Clinical Swine Model of HFpEF

Approximately 50% of heart failure cases are diagnosed as heart failure with preserved ejection fraction (HFpEF). HFpEF is challenging to accurately diagnose given traditional biomarkers, such as natriuretic peptide levels, have shown reduced prognostic value for HFpEF patients. Thus, the purpose of this study was to identify biomarkers considered potentially relevant to HFpEF in a new pre‐clinical Ossabaw swine model of heart failure. We hypothesized female Ossabaw swine fed a Western Diet and subject to chronic cardiac pressure‐overload would display physiologic features and biomarkers relevant to HFpEF. Animals were assigned into control (CON, n=5) and Western Diet‐fed aortic‐banded heart failure (WD‐AB, n=4) groups. WD‐AB animals were fed a Western Diet for 10 months started at 2 months of age, and subject to aortic‐banding for 6 months beginning at 6 months of age. Terminal studies were conducted at 12 months of age. Echocardiography was used to examine left ventricular (LV) mechanics (2‐dimensional speckle tracking) the week of terminal studies. RNA‐seq was performed on LV samples and Module Enrichment Analysis was performed on all expressed and varying genes, with networks generated using Ingenuity Pathway Analysis (IPA). qRT‐PCR was used to confirm RNA‐seq data, and group comparisons were made using a student's t‐test with significance reported at the P &lt; 0.10 and P &lt; 0.05 levels. IPA found enrichment of inflammatory and immune gene networks with significance to heart failure in WD‐AB animals. Gene interactions within these lists indicated activation of Pentraxin‐3 (PTX3) and interleukin 1 receptor‐like 1 (IL1RL1), which were chosen for validation given their potential relevance to HFpEF as inflammatory biomarkers. The approximate 5‐fold increase in PTX3 reported by RNA‐seq in WD‐AB compared to CON animals was confirmed separately using qRT‐PCR, as was an increase in IL1RL1 mRNA level. Both PTX3 and IL1RL1 mRNA levels (X‐axis) showed a significant negative correlation with LV apical early diastolic rotation rate (i.e. LV untwisting; Y‐axis), a 2D speckle tracking measure of diastolic function. Group means reflected a right and downward shift along the regression line for both PTX3 and IL1RL1 versus LV untwisting in the WD‐AB group compared to CON, indicating an increase in LV levels of these biomarkers is associated with a decline in LV diastolic mechanical function. In conclusion, WD‐AB animals express increased LV mRNA levels of the inflammatory biomarkers PTX3 and IL1RL1 that are significantly correlated with diastolic function. These data suggest studies in this Ossabaw pre‐clinical model may be useful for elucidating and testing biomarkers with diagnostic value potentially relevant to HFpEF.Support or Funding InformationHL112998 (CAE); VA‐Merit I01BX003271 (RSR); HL125503 (JP); HL136292 (TLD); HL122737, HL123295, &amp; HL129639 (YW).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Enhancement of Tissue Factor Expression in Monocyte-Derived Dendritic Cells by Pentraxin 3 and Its Modulation by C1 Esterase Inhibitor

Background: We have previously shown that human monocyte-derived dendritic cells (moDCs) may participate in immune system-mediated hypercoagulable state through enhanced tissue factor (TF) expression and that the complement system may be involved in this process. Objectives: The aim of this study was to explore the role of pentraxin 3 (PTX3) and the complement system in enhanced TF expression in moDCs. Methods: moDCs were generated from isolated human monocytes. PTX3 levels in whole human blood supplemented with moDCs were determined after lipopolysaccharide (LPS) stimulation. PTX3 release by the generated moDCs upon LPS stimulation was also assessed. The effect of PTX3 on whole blood coagulation was investigated using thromboelastometric analysis. TF expression in stationary moDCs treated with LPS and/or PTX3 was determined by measuring TF activity. The effect of complement inhibitors on TF activity in moDCs treated with LPS and/or PTX3 under low-shear conditions was evaluated. Results: PTX3 levels were higher in whole blood supplemented with moDCs than in the presence of monocytes and were further elevated by LPS stimulation. PTX3 release from generated moDCs was also increased by LPS stimulation. PTX3 reduced whole blood coagulation time in a dose-dependent manner. However, PTX3 did not increase TF expression in stationary moDCs. Under low-shear conditions, PTX3 increased TF expression in moDCs. C1 esterase inhibitor (C1-inh) suppressed this effect. Conclusions: PTX3 might have a thrombophilic activity and enhance TF expression in moDCs under low-shear conditions. Furthermore, suppression of moDC-associated hypercoagulability by C1-inh might be partly ascribed to its inhibitory effect on PTX3.

The Long Pentraxin 3 Contributes to Joint Inflammation in Gout by Facilitating the Phagocytosis of Monosodium Urate Crystals.

The purpose of this study was to investigate the role of pentraxin 3 (PTX3), a pivotal component of the innate immune system, in gout. Levels of PTX3 and IL-1β in human samples were evaluated by ELISA. Development of murine gout was evaluated through the levels of cytokines (PTX3, CXCL1, and IL-1β) and neutrophil recruitment into the joint cavity. Phagocytosis of monosodium urate (MSU) crystals and caspase-1 activation were determined by flow cytometer. Acute gout patients showed elevated concentration of PTX3 in plasma and synovial fluid as compared with healthy and osteoarthritic subjects. Moreover, there was a positive correlation between intra-articular PTX3 and IL-1β levels. PTX3 was induced in the periarticular tissue of mice postinjection of MSU crystals. Importantly, Ptx3-deficient mice showed reduced inflammation in response to MSU crystal injection compared with wild-type mice, including reduction of neutrophil recruitment into the joint cavity and IL-1β and CXCL1 production. Interestingly, addition of PTX3 in vitro enhanced MSU crystal phagocytosis by monocytes and resulted in higher production of IL-1β by macrophages. This contribution of PTX3 to the phagocytosis of MSU crystals and consequent production of IL-1β occurred through a mechanism mainly dependent on FcγRIII. Thus, our results suggest that PTX3 acts as a humoral pattern recognition molecule in gout facilitating MSU crystal phagocytosis and contributing to the pathogenesis of gouty arthritis.

Pentraxin-3 Levels Relate to the Wells Score and Prognosis in Patients with Acute Pulmonary Embolism.

Objective To investigate the value of the PTX-3 test in evaluating the prognosis of acute pulmonary embolism (APE). Method 117 APE patients were selected and divided into two groups according to plasma PTX-3 levels, including the group in which PTX − 3 ≥ 3.0 ng/mL (n = 42) and the group in which PTX − 3 < 3.0 ng/mL (n = 75). Patients were stratified into high-risk, medium-risk, and low-risk groups according to the Wells scores, and the PTX-3 levels were compared among the groups. Patients had been followed-up as well. Results According to the Wells scores, 11 patients were classified as high-risk (9.4%) and 68 were medium-risk (58.1%), while 38 were low-risk (32.5%). The PTX-3 levels in different risk groups were statistically different (all P < 0.05). During the follow-up period, 6 deaths occurred in the group with elevated PTX-3 (≥3.0 ng/mL), while 2 deaths occurred in the group with nonelevated PTX-3 (<3.0 ng/mL). The difference between the two groups was statistically significant (P < 0.01). 13 patients were hospitalized due to recurrent pulmonary embolism, of which 12 were in the group with elevated PTX-3 (≥3.0 ng/mL), while 1 patient was in the group with nonelevated PTX-3 (<3.0 ng/mL). The difference was statistically significant (P < 0.01). Conclusion The plasma PTX-3 level in APE patients is correlated with PE risk stratification. There is a significant correlation between PTX-3 levels and PE-related cardiac deaths, as well as the prognosis of recurrent PE. PTX-3 can be used as a clinical indicator of PE prognosis.

The effects of ozone therapy on periodontal therapy: A randomized placebo-controlled clinical trial.

The aim of this randomized split-mouth clinical trial was to evaluate the effects of ozone therapy on clinical and biochemical parameters of moderate to severe generalized periodontitis patients after non-surgical periodontal therapy. A total of 36 moderate to severe generalized periodontitis patients were included in the study. The patients were systemically healthy and 18 to 64years of age. Periodontal parameters, including plaque index (PI), gingival index (GI), probing depth (PD), percentage of bleeding on probing, percentage of pockets deeper than 5mm and clinical attachment level (CAL), and percentage of ≥3mm CAL, were evaluated at baseline and 3months following periodontal therapy. All participants were treated non-surgically. Topical gaseous ozone was applied into periodontal pockets twice a week for 2weeks during active periodontal therapy. Gingival crevicular fluid pentraxin-3 (PTX-3), interleukin-1β (IL-1β), and high sensitivity C-reactive protein (Hs-CRP) were evaluated. All statistical data were analyzed using SPSS software. Total of 36 participants completed the study (18 males, 18 females). PI, GI, PD, percentage of bleeding on probing, percentage of pockets deeper than 5mm and CAL, and percentage of ≥3mm CAL were improved, and there were no significant differences between the two sides. All inflammatory parameters, PTX-3, Hs-CRP, and IL-1, were reduced at 3-month follow-up. Only the decrease in PTX-3 levels between baseline and 3-month follow-up was statistically significant. Ozone therapy did not have any additional effect on periodontal parameters. All cytokines were reduced after periodontal therapy. Only PTX-3 levels were significantly lower at ozone sites compared to those at the control sites.

Atrial contractility and fibrotic biomarkers are associated with atrial fibrillation after elective coronary artery bypass grafting

ObjectiveNew-onset postoperative atrial fibrillation is common after cardiac surgery. Less has been reported about the relationship among fibrosis, inflammation, calcium-induced left atrial and right atrial contractile forces, and postoperative atrial fibrillation. We sought to identify predictors of postoperative atrial fibrillation. MethodsFrom August 2016 to February 2018, we evaluated 229 patients who had preoperative sinus rhythm before elective primary coronary artery bypass grafting. Of 229 patients, 191 maintained sinus rhythm postoperatively, whereas 38 patients developed atrial fibrillation. Preoperative tissue inhibitor of metalloproteinase-1, pentraxin-3, matrix metallopeptidase-9, galectin-3, high-sensitivity C-reactive protein, growth differentiation factor 15, and transforming growth factor-ß were measured. Clinical and echocardiographic findings (tricuspid annular plane systolic excursion for right heart function) and calcium-induced force measurements from left atrial and right atrial–derived skinned myocardial fibers were recorded. ResultsPatients with atrial fibrillation were older (P = .001), had enlarged left atrial (P = .0001) and right atrial areas (P = .0001), and had decreased tricuspid annular plane systolic excursion (P = .001). Levels of matrix metallopeptidase-9 and pentraxin-3 were decreased (P < .05), whereas growth differentiation factor 15 was increased (P = .001). We detected lower left atrial force values at calcium-induced force measurements 5.5 (P < .05), 5.4 (P < .01), and 5.3 to 4.52 (P = .0001) and right atrial force values at calcium-induced force measurements 5.0 to 4.52 (P < .05) in patients with postoperative atrial fibrillation. Multivariable analysis showed that advanced age (P = .033), decreased left atrial force value at calcium-induced force measurement of 5.5 (P = .033), enlarged left atrial (P = .013) and right atrial (P = .081) areas, and reduced tricuspid annular plane systolic excursion (P = .010) independently predicted postoperative atrial fibrillation. ConclusionsAdvanced age, decreased left atrial force value at calcium-induced force measurement of 5.5, enlarged left atrial and right atrial areas, and reduced tricuspid annular plane systolic excursion were identified as independent predictors for postoperative atrial fibrillation.

Elevated Systemic Pentraxin-3 Is Associated With Complement Consumption in the Acute Phase of Thrombotic Microangiopathies.

Pentraxin-3 (PTX3) and C-reactive protein (CRP) have been shown to regulate complement activation in vitro, but their role has not been investigated in complement consumption in vivo. Thrombotic microangiopathies (TMA) are often accompanied by complement overactivation and consumption, therefore we analyzed the relation of the systemic pentraxin levels to the complement profile, laboratory parameters and clinical outcome of TMA patients. We determined the PTX3 and CRP levels, complement factor and activation product concentrations in blood samples of 171 subjects with the diagnosis of typical hemolytic uremic syndrome (STEC-HUS) (N = 34), atypical HUS (aHUS) (N = 44), secondary TMA (N = 63), thrombotic thrombocytopenic purpura (TTP) (N = 30) and 69 age-matched healthy individuals. Clinical data, blood count and chemistry were collected from medical records. To determine the in vitro effect of PTX3 on alternative pathway (AP) activation, sheep red blood cell-based hemolytic assay and AP activity ELISA were used. We found that PTX3 levels were elevated in the acute phase of STEC-HUS, aHUS and secondary TMA, whereas PTX3 elevation was exceptional is TTP. Conversely, a significantly higher median CRP was present in all patient groups compared to controls. PTX3, but not CRP was associated with signs of complement consumption in vivo, and PTX3 significantly decreased the AP hemolytic activity in vitro. Our results provide a detailed description of acute phase-TMA patients' complement profile linked to changes in the systemic pentraxin levels that may support further molecular studies on the function of PTX3 in disease pathogenesis and add to the laboratory assessment of complement consumption in TMA.

Urinary excretion of pentraxin-3 correlates with the presence of renal scar following acute pyelonephritis in children.

Acute pyelonephritis is associated with considerable morbidity and potential for renal scarring. Pentraxin3 (PTX3) is a recently discovered mediator of inflammation. The objective of this study was to investigate the changes in serum and urine PTX3 levels in children who had a history of pyelonephritis and were diagnosed with renal parenchymal scar (RPS) and/or vesicoureteral reflux (VUR). The study included 88 children (31 males, 57 females) aged between 3months and 18years. The children included in the study were divided into four groups: VUR with RPS (Group 1), RPS without VUR (Group 2), VUR without RPS (Group 3), and healthy children without a history of hydronephrosis or UTI history (Group 4). After the initial evaluation, the participants were further divided into two more groups and re-evaluated: Children with RPS (Group 1 + 2), children without RPS (Group 3 + 4), children with VUR (Group 1 + 3), and children without VUR (Group 2 + 4). We found that urine pentraxin 3 (uPTX3) and uPTX3/Creatinine levels were significantly higher in the groups with renal scar with or without VUR than the ones without RPS [mean uPTX3, 3.5pg/ml (min-max 0.0022-12.3668) vs. 2.2pg/ml (min-max 0.0022-18.5868) and uPTX3/creatinine, 10.5pg/mg (min-max 0.0035-51.1) vs. 5.8pg/mg (min-max 0.0004-78.7), p < 0.01]. uPTX3 levels were not different among the groups with and without VUR. In addition, serum PTX3 levels were not different among the groups. We showed that urinary PTX3 increased only in patients with scarred kidneys. These results might be helpful to predict RPS due to past pyelonephritis.

The association of inflammatory markers and echocardiographic parameters in Behçet’s disease

Background: The main objective of the current study is to find out if any association exists between specific inflammatory markers such as homocysteine (Hcy) and pentraxin-3 (PTX-3) and cardiac involvement determined by means of echocardiographic parameters in patients with Behçet disease (BD).Methods: From January 2011 to January 2012, a total of 62 Behçet’s patients were enrolled in the study. Thirty-two healthy subjects constituted the control group. The diagnosis of BD was made as proposed by International Study Group of BD.Results: The mean PTX-3, Hcy, and C-reactive protein levels were significantly higher in patients with BD compared to the control group. The electromechanical delay (EMD) times were found to be prolonged in patients with BD. Also, the aortic stiffness index (SI) and elastic modulus (Ep) were significantly higher, while the aortic dispensibility was significantly lower in patients with BD. The left atrial volume, left atrial volume index, E/A ratio, E/E’ septal, IRight-EMD, PA’-ML, PA’-MS, PA’-TL, SI, and Ep were correlated with PTX-3 levels. In addition, the E/A, PA’-ML, PA’-MS, SI, and Ep displayed correlation with Hcy levels in patients having BD.Conclusion: Elevated levels of PTX-3 and Hcy were found to be correlated with cardiac involvement determined by means of echocardiographic parameters in patients with BD.