Pentraxin 3 Levels Research Articles

Relationship Between Plasma Pentraxin 3 Concentration and Platelet Indices in Patients With Stable Coronary Artery Disease.

Few reports have analyzed the effect of pentraxin 3 (PTX3) on platelets and their activation. We explored the association between plasma PTX3 and platelet indices. Forty-nine patients with stable coronary artery disease (CAD) were enrolled. Based on median PTX3, the study population was divided into group 1 (n = 25; PTX3 ≤ 0.98 ng/mL) and group 2 (n = 24; PTX3 > 0.98 ng/mL). Platelet indices investigated included mean platelet volume (MPV), platelet distribution width (PDW), platelets and large cell ratio (P-LCR), MPV to platelet count ratio (MPV/PC), platelet to lymphocyte ratio (PLR), and MPV to lymphocyte ratio (MPVLR). Patients with lower PTX3 had a higher lymphocyte count. Platelet count was similar in both groups. Notwithstanding, patients with higher PTX3 concentrations had elevated MPV (8.3 vs 10.0 fL; P < .001) and PDW (9.4 vs 12.4 fL; P < .001). However, the MPV/PC ratio was similar in both groups. Thromboinflammatory biomarkers (PLR, MPVLR) were also elevated in group 2. Pentraxin 3showed a strong, positive correlation with MPV ( r = .75, P < .01) and PDW ( r = .80, P < .01), and weak to moderate correlation with MPVLR. In conclusion, PTX3 is associated with larger platelet size as assessed by platelet volume indices. There is a strong correlation between plasma PTX3 level and MPV and PDW.

Circulating levels of pentraxin-3 (PTX3) in patients with liver cirrhosis

BackgroundDespite the circulating levels of PTX3 were related to the severity of various diseases, there are no studies investigating its role in patients with liver cirrhosis. We aimed to study PTX3 levels in patients with liver cirrhosis. Material and methodsA prospective cohort study included 130 patients hospitalized for acute decompensation of liver cirrhosis, 29 stable cirrhotic outpatients and 32 healthy controls evaluated in a tertiary hospital in Southern Brasil. ResultsThe median PTX3 level was significantly higher in stable cirrhotic patients compared to controls (2.6 vs. 1.1 ng/mL; p < 0.001), hospitalized cirrhotic patients compared to controls (3.8 vs. 1.1 ng/mL; p < 0.001), and hospitalized cirrhotic patients compared to stable cirrhotic patients (3.8 vs. 2.6 ng/ mL; p = 0.001). A positive correlation was found between PTX3 and serum creatinine (r = 0.220; p = 0.012), Chronic Liver Failure -Sequential Organ Failure Assessment score (CLIF-SOFA) (r = 0.220; p = 0.010), MELD (r = 0.279; p = 0.001) and Child-Pugh score (r = 0.224; p = 0.010). Significantly higher levels of PTX3 were observed in patients on admission with ACLF (8.9 vs. 3.1 ng/mL; p < 0.001) and MELD score ≥ 20 (6.6 vs. 3.4 ng/mL; p = 0.002). Death within 90 days occurred in 30.8% of patients and was associated with higher levels of PTX3 (5.3 vs. 3.4 ng/mL; p = 0.009). The probability of Kaplan-Meier survival was 77.0% in patients with PTX-3 < 5.3 ng mL (upper tercile) and 53.5% in those with PTX3 ≥ 5.3 ng/mL (p = 0.002). ConclusionThese results indicate the potential for use of PTX3 as an inflammatory biomarker for the prognosis of patients with hepatic cirrhosis.

Pentraxin 3 Gene Polymorphisms and Pulmonary Aspergillosis in Chronic Obstructive Pulmonary Disease Patients.

Pentraxin 3 (PTX3) plays an important role in resistance to Aspergillus infections. Previous studies have suggested that PTX3 polymorphisms influence the risk of invasive aspergillosis among transplantation recipients. This study investigated the association between PTX3 gene polymorphisms and pulmonary aspergillosis in a chronic obstructive pulmonary disease (COPD) population. We included 173 consecutive inpatients with COPD. Thirty-six case patients were finally diagnosed with pulmonary aspergillosis. Among these, 25 case patients had invasive pulmonary aspergillosis (IPA), and 11 case patients had chronic pulmonary aspergillosis (CPA). Three single nucleotide polymorphisms (SNPs; rs2305619, rs3816527, and rs1840680) in the PTX3 gene were detected by polymerase chain reaction direct sequencing, and their associations with aspergillosis were evaluated. Plasma PTX3 levels were measured by enzyme-linked immunosorbent assay. Three SNPs were consistent with Hardy-Weinberg equilibrium. The recessive model for SNP rs1840680 suggests that the AA homozygote is associated with a higher risk for pulmonary aspergillosis (both IPA and CPA) in COPD patients. However, for genotypic and allele frequencies of rs2305619 and rs3816527, no association was observed. The distribution of haplotypes (rs2305619 and rs3816527) also showed no significant differences. Plasma PTX3 levels significantly increased in IPA patients. In the IPA group, the rs1840680 AA genotype subjects showed lower plasma PTX3 levels than those harboring AG and GG genotypes. This study showed a significant association between PTX3 rs1840680 polymorphisms and the susceptibility of pulmonary aspergillosis in patients with COPD. Plasma PTX3 levels may be potentially used as indicators for the diagnosis of IPA in COPD patients.

The relationship of pentraxin-3 levels with IL-17, fetuin-A, insulin in patients with Behçet's disease

Abstract Background Pentraxin (PTX) 3 is synthesized by leukocytes, dendritic cells, endothelial cells and monocytes in response to IL-1 and tumor necrosis factor (TNF)-α, and it might be informative regarding local inflammation. In additionally, pentraxin (PTX)-3, produced by endothelial cells in atherosclerotic plaques, acts as a modulator of inflammatory processes and is involved in the development of atherosclerotic lesions. Objective This study aimed to identify the levels of proteins, such as PTX and fetuin-A, which are thought to play a role in the progression of atherosclerotic and cardiovascular disorders in patients with BD, and to investigate the relationship of these protein levels with BD activity, inflammatory cytokines, insulin resistance and dyslipidaemia. Patients and methods This study included 58 patients (36 females, 22 males) with BD and 20 healthy controls. Serum PTX-3, fetuin-A, interleukin (IL)-17 and insulin concentrations were determined. Homeostasis model of insulin resistance (HOMA-IR) values were calculated, and disease activity was assessed using BD Current Activity Form (BDCAF) scores. Results The levels pentraxin-3, fetuin-A, IL-17, insulin and HOMA-IR in patients with BD were found to be higher than control subjects (p 0.05). Conclusions Similar to CRP, PTX-3 is an acute-phase reactant that is considered an inflammatory and atherosclerotic biomarker. This study showed that PTX-3 levels can increase, similar to IL-17, but no relationship was detected between disease activity and coronary risk factors such as serum lipids, glucose intolerance and obesity. This was a cross-sectional study; therefore, the patients should be followed in long-term studies to determine whether higher PTX levels in BD patients are associated with a higher incidence of cardiovascular disease.

The clinical value of inflammatory biomarkers in coronary artery disease: PTX3 as a new inflammatory marker

ObjectivePrevious experiments have demonstrated that several inflammatory biomarkers, including pentraxin 3 (PTX3), matrix metalloprotein 9 (MMP9), interleukin-6 (IL-6), and the neutrophil to lymphocyte ratio (NLR), are differentially elevated in coronary artery disease (CAD). This study aims to compare the associations between plasma levels of these biomarkers and CAD, identifying the best biomarker that has the most powerful association with CAD. MethodsBlood samples were collected from 64 patients admitted to the Department of Cardiology, 31 of whom had CAD and 33 of whom were CAD-free. Plasma levels of PTX3, MMP9, and IL-6 were measured via ELISA. The coronary Gensini score was used to evaluate the severity of coronary artery lesions. ResultsPTX3 levels and NLR levels between the CAD group and the CAD-free group were statistically significant (P<0.05). Stepwise multiple linear regression analysis showed that PTX3 levels and NLR levels were independently associated with CAD (r=1.3, P<0.05; r=1.8, P<0.05). Only PTX3 was associated with the severity of coronary artery stenosis. A PTX3 threshold of 4.38ng/mL maximized true-positive and false-negative results. PTX3 displayed a greater area under the receiver operating characteristic curve (AUC) than NLR, MMP9, and IL-6 (0.733 versus 0.612 versus 0.725 versus 0.518). ConclusionsCompared to NLR, MMP9, and IL-6, PTX3 displayed greater AUC and association with CAD. PTX3 may become a potentially powerful inflammatory biomarker for CAD.

Abstract 4773: Dysregulated expression of pentraxin-3 in glioblastoma (GBM) stem cells: Implications for GBM invasion and progression

Abstract Glioblastoma multiforme (GBM) is highly invasive and resistant to current therapies. The aggressiveness of brain tumor is attributed to GBM stem cells (GSC) that release inflammatory cytokines, and exacerbate inflammation in tumor microenvironment, critically affecting GBM survival and invasiveness. The glycoprotein pentraxin-3 (PTX3), a modulator of tumor-associated inflammation, is known to be correlated with tumor grade and severity of malignancies of some cancers. However, little is known about the role of PTX3 in GBM growth and invasion. In this study, we examined the role of PTX3 in GSCs exhibiting various degree of invasiveness. From patient brain tumors, our team has isolated the small subsets of glioblastoma stem cells (GSCs) and are validated for their self-renewal and multi-lineage potential. Our studies have shown that these GSCs efficiently form orthotopic brain tumors in immune-deficient mice. Our results show that conditioned media from GSCs promote pro-angiogenic tube formation from endothelial cells. GSCs that are grown in the absence of growth factors EGF and bFGF, formed efficient xenografts in immune-deficient mice and showed increased dispersal in the mice brain. Interestingly, polymerase chain reaction (RT-PCR) and immunofluorescence staining showed upregulated expression of PTX3 in these GSCs, and correlated with the degree of invasiveness. Differentiation of GSC into astrocytes in vitro, lead to decreased expression of PTX3. In support of this, recent histochemical study has shown that PTX3 levels correlate with GBM grade and is a candidate biomarker for cancer progression. Thus, PTX3 may represent a new target and marker of inflammation for glioma malignancy. Citation Format: Umadevi V. Wesley, Paul Clark, John S. Kuo, Robert J. Dempsey. Dysregulated expression of pentraxin-3 in glioblastoma (GBM) stem cells: Implications for GBM invasion and progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4773. doi:10.1158/1538-7445.AM2017-4773

Examination of levels pentraxin-3, interleukin-6, and C-reactive protein in rat model acute and chronic exercise.

Different types of exercise occurs damage at the cellular level in the muscles. Muscle damage caused by exercise is determined creatine kinase, myoglobin, and increase in levels of acute phase protein and interleukin in blood. The purpose of this study was investigated the levels of pentraxin-3 (PTX-3), interleukin-6 (IL-6), and C-reactive protein (CRP) following acute and chronic exercising in rats. Twenty-six Wistar Albino male rats were divided in to three groups. A treadmill exercise was performed 3 days/week, 10 min/day for 1 week in acute groups. In chronic group, exercise performed 7 days/week, 60 min/day for 4 weeks. At the end of the experiment, plasma PTX-3, IL-6, and CRP levels were measured. In current study, the PTX-3, IL-6, and CRP levels not observed statistically significant difference among control, acute, and chronic groups. The levels IL-6 and CRP were not significantly different between acute and chronic exercise groups (P>0.05). However, the level of PTX-3 was found to be higher in the chronic group compared to the acute group (P<0.05). The PTX-3 level increase on chronic exercise-induced muscle damage. Accorting to our results, we think that PTX-3 may have a protect role on muscle damage during chronic exercises.

Aqueous humor pentraxin-3 levels in patients with diabetes mellitus.

PurposeTo evaluate aqueous humor (AH) pentraxin-3 (PTX3) levels in diabetic patients with and without diabetic retinopathy (DR).MethodsIn this prospective study, patients undergoing cataract surgery were enrolled. The study group was composed of 26 type-2 diabetic patients without DR (group 1), 32 diabetic patients with DR (group 2) and 29 age-matched subjects without any systemic disease (group 3). Fifteen proliferative DR (PDR) and 17 non-proliferative DR (NPDR) patients were enrolled in Group 2. HbA1c levels and duration of diabetes were noted. AH samples were obtained from anterior chamber at the beginning of cataract surgery and PTX3 levels were analyzed with Elisa kit.ResultsBaseline demographic characteristics were similar between groups. The mean duration of diabetes was 11.9±7.9 years in group 1 and 15.8±7.8 years in group 2 (P=0.11). The mean plasma HbA1c levels in group 1 was 9.1±2.6 and 8.2±2.4 in group 2 (P=0.36). PTX3 levels were 5.75±0.41 in group 1, 6.11±1.47 in group 2 and 4.93±0.84 ng/ml in group 3 (P=0.01). PTX3 levels in group 2 were higher than in group 1 and 3 (P=0.06 and P=0.01, respectively). There was no correlation between HbA1c and PTX3 levels (P=0.06 r=0.57, P=0.19 r=0.3, respectively). The mean PTX3 was 6.6±0.3 in PDR group and 5.6±0.5 ng/ml in NPDR group (P=0.04).ConclusionsPTX3 is an important marker especially for vascular endothelial damage. Since diabetic vascular changes are dependent on endothelial cell damage, high levels of AH PTX3 of DR patients may indicate the importance of PTX3 protein in the pathogenesis of DR.

Pentraxin 3 as a New Cardiovascular Marker in Adrenal Adenomas

Pentraxin 3 (PTX3) is an acute-phase glycoprotein, which is increased in patients with cardiovascular disease (CVD) and considered as a predictor of CVD in the general population. Both functional and nonfunctional adrenal tumors are associated with a higher risk of cardiovascular events and mortality. We aimed to investigate plasma PTX3 levels in patients with functioning and nonfunctioning adrenal tumors and determine its relationship with cardiovascular risk factors. Twenty-one patients with functional adrenal tumors (11 pheochromocytomas, 9 Cushing syndrome, and 1 primary hyperaldosteronism), 28 patients with nonfunctional adrenal incidentalomas, and 40 healthy controls were enrolled in the study. Serum PTX3 levels were measured using a human PTX3 enzyme-linked immunosorbent assay. PTX3 concentrations were significantly higher in the adrenal tumor group compared with the control group (3,001.64 ± 374.64 pg/mL vs. 1,173.59 ± 168.89 pg/mL; P<.001). PTX3 concentrations were positively correlated with carotid intima media thickness (CIMT) (r2, 0.464; P<.001), high-sensitivity C-reactive protein (hsCRP) (r2, 0.551; P<.001), diastolic blood pressure (r2, 0.334; P = .003), systolic blood pressure (r2, 0.312; P = .006), and urinary metanephrine concentrations (r2, 0.320; P = .041). Serum PTX3 concentrations in patients with functional adrenal tumors and comorbidities including hypertension, diabetes mellitus, or CVD were higher than in those without comorbidities (3,654.54 ± 447 pg/mL vs. 1,026.96 ± 447.97 pg/mL; P = .008). We found that serum PTX3 concentrations increased in both functional and nonfunctional adrenal tumors. PTX3 levels were correlated with cardiovascular risk factors such as CIMT, hsCRP, and blood pressure. BMI = body mass index; CIMT = carotid intima-media thickness; CRP = C-reactive protein; CT = computed tomography; CVD = cardiovascular disease; FGF2 = fibroblast growth factor 2; hsCRP = high-sensitivity C-reactive protein; PA = primary hyperaldosteronism; PTX3 = pentraxin 3.

Can Pentraxin-3 be a Candidate Marker in the Follow-Up of the Patients With Behçet's Disease?

This study aims to assess the level of pentraxin-3 (PTX-3) as an inflammatory marker and compare it with C-reactive protein (CRP) levels in patients with Behçet's disease (BD). Forty-two patients with BD (15 males, 27 females; mean age 39.7±8.6 years; range 20 to 64 years) and 42 age- and sex- matched healthy controls (14 males, 28 females; mean age 40.8±8.2 year; range 25 to 60 years) were included in the study. Serum CRP and plasma PTX-3 levels were measured. Subgroup analyses were performed according to clinical manifestations of patients with BD. Both PTX-3 and CRP levels were significantly higher in patients with BD than controls (1.33±0.29 vs 0.85±0.12, p<0.05 for PTX-3 and 0.71±0.13 vs 0.27±0.03, p<0.001 for CRP, respectively). Area under the curve was 0.633±0.062 vs 0.729±0.05, respectively. Mean PTX-3 and CRP levels were 1.1 vs 1.5, p=0.5; 0.5 vs 0.9, p=0.5; respectively, in patients with mucocutaneous involvement alone and with other involvements, whereas they were 0.9 vs 1.6, p=0.1; 0.5 vs 0.8, p=0.3; respectively, in patients with and without peripheral arthritis, and were 1.7 vs 0.9, p=0.06; 1.0 vs 0.5, p=0.07; respectively, in patients with and without uveitis. Although PTX-3 levels were higher in patients with BD than healthy controls, sensitivity and specificity of PTX-3 was not different than CRP in patients with BD.

Vaccination with a live attenuated Acinetobacter baumannii deficient in thioredoxin provides protection against systemic Acinetobacter infection

Multi-drug resistant Acinetobacter baumannii (MDR-Ab), an opportunistic pathogen associated with nosocomial and combat related infections, has a high mortality due to its virulence and limited treatment options. Deletion of the thioredoxin gene (TrxA) from a clinical isolate of MDR-Ab resulted in a 100-fold increase in 50% lethal dose (LD50) in a systemic challenge murine model. Thus, we investigated the potential use of this attenuated strain as a live vaccine against MDR-Ab. Mice were vaccinated by subcutaneous (s.c.) injection of 2×105 CFU of the ΔtrxA mutant, boosted 14days later with an equivalent inoculum, and then challenged 30days post-vaccination by i.p. injection with 10 LD50 of the wild type (WT) Ci79 strain. Efficacy of vaccination was evaluated by monitoring MDR-Ab specific antibody titers and cytokine production, observing pathology and organ burdens after WT challenge, and measuring levels of serum pentraxin-3, a molecular correlate of A. baumannii infection severity, before and after challenge. Mice vaccinated with ΔtrxA were fully protected against the lethal challenge of WT. However, minimal immunoglobulin class switching was observed with IgM predominating. Spleens harvested from vaccinated mice exhibited negligible levels of IL-4, IFN-γ and IL-17 production when stimulated with UV-inactivated WT Ci79. Importantly, tissues obtained from vaccinated mice displayed reduced pathology and organ burden compared to challenged non-vaccinated mice. Additionally, serum pentraxin-3 concentrations were not increased 24h after challenge in vaccinated mice, correlating with reduction of WT MDR-Ab infection in ΔtrxA immunized mice. Furthermore, passive immunization with ΔtrxA-immune sera provided protection against lethal systemic Ci79 challenge. Collectively, the defined live attenuated ΔtrxA strain is a vaccine candidate against emerging MDR Acinetobacter infection.

Inflammatory Long Pentraxin 3 is Associated with Leukocyte Telomere Length in Night-Shift Workers.

Aging is an emerging worldwide threat to public health, even in the workplace, as it links with risk of illness and death. Bewildered inflammatory responses and stressful conditions associate with age-related disorders. Additionally, circadian rhythm disruption, a critical health issue in night-shift workers, correlates with premature aging. We investigated the hypothesis of a link between altered inflammatory response, detected by plasmatic long pentraxin 3 (PTX3), and biological aging, measured by leukocyte telomere length (LTL), attrition, and possibly induced by night-shift work. Within the framework of a cross-sectional study, such possible relationships were appraised by simultaneous equation model (SEM) technique among day and night-shift hospital workers. PTX3 levels, modulated by several aging conditions [i.e., body mass index (BMI) (beta = −0.22; p = 0.022), C-reactive protein (CRP) (beta = −0.07; p = 0.000), and cardiovascular diseases with hypertension included (CVD) (beta = −0.12; p = 0.000)], positively associate with LTL (coefficient = 0.15; p = 0.033). LTL, in turn is reduced by CVD (beta = −0.15; p = 0.000), binge drinking (beta = −0.10; p = 0.004), and CRP (beta = −0.05; p = 0.026). On the other hand, night-shift work, found to be remarkably free from aging risk factors [i.e., age (beta = −0.13; p = 0.017), BMI (beta = −0.17; p = 0.030), CVD (beta = −0.14; p = 0.000), and binge drinking (beta = −0.13; p = 0.000)], does associate almost significantly with reversed PTX3 (coefficient = −0.09; p = 0.089) and even with CRP (beta = 0.17; p = 0.000). In conclusion, the SEM analysis indicates that PTX3 is positively linked to LTL. The finding suggests a possible new role of this long pentraxin that, by orchestrating an efficient governance of inflammatory processes, may protect telomere from attrition, ensuring therefore the genetic stability of cells. The higher CRP levels among night-shift workers suggest that night-shift work is associated with increased systemic inflammation. This would make nocturnal workers more susceptible to premature aging.

Pentraxin 3 levels in bronchoalveolar lavage fluid of lung transplant recipients with invasive aspergillosis

Invasive aspergillosis is the most common invasive fungal infection in lung transplant recipients. The use of galactomannan testing in bronchoalveolar lavage (BAL) fluid has improved diagnosis of invasive aspergillosis; however, false-positive results can lead to overdiagnosis and unnecessary treatment. The use of proinflammatory markers such as pentraxin 3 (PTX3) may help differentiate between Aspergillus colonization and disease. BAL PTX3 concentrations were measured by enzyme-linked immunosorbent assay in 151 lung transplant recipients and 9 healthy control subjects. Patients were characterized as having Aspergillus colonization or invasive disease according to International Society of Heart and Lung Transplantation criteria. Concomitant PTX3values were compared using Mann-Whitney U and Kruskal-Wallis tests. We analyzed 322 BAL stored samples and identified 15 invasive aspergillosis events, 38 Aspergillus colonizations, and 17 positive galactomannan with negative Aspergillus cultures. Median BAL PTX3 level was significantly higher in patients with invasive aspergillosis compared with patients with Aspergillus colonization and healthy control subjects (439.20 pg/ml [interquartile range (IQR) 168.18-778.90], 68.93 pg/ml [IQR 13.67-156.74], and 13.67 pg/ml [IQR 13.67-121.18]; p < 0.001). Patients with BAL PTX3 value >319 pg/ml with positive galactomannan and patients with BAL PTX3 value >312 pg/ml with positive Aspergillus culture were 4.5 and 5.5 times more likely to have invasive pulmonary aspergillosis, respectively. Our study shows that PTX3 measurements in BAL samples were significantly higher among patients with invasive aspergillosis and may help to identify patients with Aspergillus colonization and false-positive galactomannan in BAL samples.

Synergistic Cardioprotective Effects of Combined Chromium Picolinate and Atorvastatin Treatment in Triton X-100-Induced Hyperlipidemia in Rats: Impact on Some Biochemical Markers

Hyperlipidemia is one of the major risk factors for atherosclerosis and ischemic heart disease. Chromium (Cr) mineral is playing a crucial role in glucose and lipid homeostasis. The aim of this study was to evaluate the protective effects of combined chromium picolinate (CrPic) and atorvastatin treatment against hyperlipidemia-induced cardiac injury. Seventy-five male albino rats were divided into five groups (15 rats each). Hyperlipidemia was induced by intraperitoneal injection of a single dose of Triton X-100 (300mg/kg body weight (b.w) (group ІІ). Treatment of hyperlipidemic rats was induced by daily administration of CrPic at a dose of 200μg/kg b.w/day (group ІІІ), atorvastatin at a dose of 10 mg/kg/day (group IV), and combined treatment with both (group V) by gavage for 7days. At the end of experiment, serum and heart tissues were obtained. Hyperlipidemia was confirmed by histopathology of heart tissues, marked serum dyslipidemia, increased atherogenic indices, and values of ischemia-modified albumin. In addition to increased values of proprotein convertase subtilisin/kexin type 9, activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase enzyme and high relative expression levels of pentraxin-3 were observed. However, paraoxonase-1 activity was markedly decreased in the hyperlipidemic group. Significant improvement in all assessed parameters was observed in the rat group treated with both CrPic and atorvastatin. It can be concluded that combined CrPic and atorvastatin treatments had synergistic cardioprotective effects against hyperlipidemia which may be through modulating atherosclerosis as well as cardiac and aortic damage and/or activation of anti-inflammatory and anti-oxidant pathways, thus reversing endothelial dysfunction.

Study of the relationship between APOA-II −265T>C polymorphism and HDL function in response to weight loss in overweight and obese type 2 diabetic patients

It has been reported that people may respond differently to the same environmental changes because of genome variations. The main purpose of the present study is to determine gene-diet interactions between-265T>C apolipoprotein A-II polymorphisms and evaluate the effect of weight loss on parameters related to HDL function. In the present study, 56 overweight and obese type 2 diabetic patients were chosen from 697 genotype-specified subjects. After matching for gender, age and BMI, an equal number of patients were chosen for each genotype of APOA-II (TT/TC and CC group). After six-week calorie restriction programme, 44 patients completed the study. Serum paraoxonase-1 (PON1), paraoxonase-3 (PON3), pentraxin-3 (PTX3), and PTX3 gene expression in peripheral blood mononuclear cells were compared between two genotypes and also before and after the intervention separated in each genotype. The mean differences of PON enzymes and PTX3 between groups were not significant at the baseline. After weight loss, the mean weight, BMI and serum concentration of PON1 and PON3 decreased significantly and PTX3 increased in total population. Although, the mean differences of PON enzymes and PTX3 between two groups were not significant. However, in comparison of mean differences within the groups, decreased PON3 and increased PTX3 have been observed only in TT group. A comparison of the mean differences in PON3 and PTX3 within two genotype groups showed that T allele carriers are more sensitive to lifestyle modification, and serum PON3 and PTX3 levels significantly changed only in the TT/TC group.

Interferon-α coincides with suppressed levels of pentraxin-3 (PTX3) in systemic lupus erythematosus and regulates leucocyte PTX3 in vitro.

Dysfunctional elimination of cell debris, and the role of opsonins such as pentraxins, is of interest regarding systemic lupus erythematosus (SLE) pathogenesis. Interferon (IFN)-α is typically elevated during SLE flares, and inhibits hepatocyte production of the pentraxin 'C-reactive protein' (CRP), partly explaining the poor correlation between CRP levels and SLE disease activity. The extrahepatically produced 'pentraxin 3' (PTX3) shares waste disposal functions with CRP, but has not been studied extensively in SLE. We analysed serum PTX3 in SLE, and assessed its interference with IFN-α in vitro. Serum samples from 243 patients with SLE and 100 blood donors were analysed regarding PTX3. Patient sera were analysed for IFN-α, and genotyped for three PTX3 single nucleotide polymorphisms reported previously to associate with PTX3 levels. Stimulated PTX3 release was assessed in the presence or absence of IFN-α in blood donor neutrophils and peripheral blood mononuclear cells (PBMC). Serum PTX3 was 44% lower in patients with SLE compared to blood donors (P < 0·0001) and correlated with leucocyte variables. Patients with undetectable IFN-α had 29% higher median PTX3 level than patients with detectable IFN-α (P = 0·01). PTX3 production by PBMC was inhibited by IFN-α, whereas neutrophil degranulation of PTX3 was increased. No differences in PTX3 levels were observed between the SNPs. In conclusion, median serum PTX3 is lower in SLE (especially when IFN-α is detectable) compared to blood donors. In addition to its potential consumption during waste disposal, it is plausible that IFN-α also attenuates PTX3 by inhibiting synthesis by PBMC and/or exhausting PTX3 storage in neutrophil granules.

Serum Pentraxin 3 is associated with signs of arterial alteration in women with preeclampsia

BackgroundPreeclampsia (PE) in pregnancy is a state of exaggerated inflammation and is associated with an increased risk of cardiovascular disease (CVD) later in life. Levels of pentraxin 3 (PTX3), a novel inflammation marker, are increased during PE and in individuals with CVD. The primary aim of this study was to assess whether serum PTX3 in women with PE is associated with adverse arterial effects; a thicker intima and higher intima/media (I/M) ratio in the common carotid artery (CCA). MethodsSerum PTX3 levels were measured using commercially available enzyme-linked immunosorbent assay kits, and individual CCA intima and media thicknesses were estimated by 22MHz non-invasive ultrasound in 55 women at PE diagnosis and 64 women with normal pregnancies at a similar gestational age, and about one year postpartum. A thick intima, thin media and high I/M ratio indicate a less healthy artery wall. ResultsDuring pregnancy serum PTX3 correlated positively with intima thickness and I/M ratio but negatively with media thickness (all p<0.0001), indicating adverse arterial effects. About one year postpartum, PTX3 levels had decreased in both groups and there remained no significant group difference or significant correlation with CCA wall layers. ConclusionsHigher levels of serum PTX3 in women with PE were significantly associated with signs of adverse arterial effects during pregnancy, but not one year postpartum, supporting the rapid dynamics of PTX3.

Pentraxin-3 levels are associated with vasculitis and disease activity in childhood-onset systemic lupus erythematosus.

Objectives Childhood-onset systemic lupus erythematosus (cSLE) is a multisystemic autoimmune disease characterized by inflammatory organ damage by means of vasculitis. Pentraxin-3 (PTX3) is expressed locally at the sites of inflammatory processes, predominantly from endothelial cells. In adult studies, PTX3 has shown to be an indicator of active vasculitis both in large-vessel and small-vessel vasculitides, as well as in SLE. Moreover, in SLE it has found to be correlated with disease activity, and with some of the clinical manifestations and laboratory parameters. We aimed to ascertain if PTX3 might be a significant mediator in cSLE and if it might indicate active vasculitis during the course of the disease. Methods Serum PTX3 levels were measured in 76 patients with cSLE and 41 healthy subjects. We have investigated its relation with disease activity, damage, clinical features, laboratory parameters and medications. Results Serum levels of PTX3 were found to be increased in cSLE compared to healthy controls (mean ± SD; 10.6 ± 8.2 ng/mL vs 2.7 ± 1.3 ng/mL, p < 0.001). PTX3 concentrations were also in correlation with SLEDAI-2K ( r = 0.57, p < 0.001). When viewed from the clinical perspective, serum PTX3 levels were significantly higher only in patients with active vasculitis ( p < 0.001), Raynaud phenomenon ( p = 0.006) and mucocutaneous manifestations ( p < 0.001). However, an association between PTX3 and age, age at disease onset, disease duration, complement levels, PedSDI score (pediatric version of the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index), ESR, CRP, procalcitonin levels, anti-ds DNA antibody, anticardiolipin antibodies was not detected. Conclusions Patients with cSLE have increased levels of serum PTX3 compared to healthy controls. Thus, serum PTX-3 level might be a significant mediator in cSLE. Apart from these, the results support that PTX3 reflects active cutaneous vasculitis in cSLE and correlates with disease activity.

Role of interleukin-6 and pentraxin 3 as an early marker in Peyronie’s disease

Inflammation is mechanistically involved in the development of Peyronie’s disease (PD). The aim of this study is to assess the relevance of serum pentraxin 3 (PTX3) and interleukin-6 (IL-6) concentrations in PD. The study enrolled 40 patients with PD in the acute phase and 40 healthy controls. Plasma PTX3 and IL-6 concentrations were evaluated in 40 patients in the acute phase of PD and 40 healthy controls by enzyme-linked immunosorbent assay. Serum concentrations of both PTX3 and IL-6 were significantly higher in the PD patients than in the control group (p=0.001 and p=0.001, respectively). There was a significant correlation between concentration of PTX3 and painful erections. IL-6 concentrations were significantly higher in patients with erectile dysfunction. IL-6 and PTX3 levels showed no correlation with age, serum C-reactive protein, degree of curvature, and disease duration. IL-6 trans-signaling and PTX3 amplification at the site of inflammation could have a role in pathophysiological mechanisms of PD. Biological drugs may be used for treatment during the acute phase of the disease based on this mechanism.

Pentraxin 3 as a new indicator of cardiovascular‑related death in patients with advanced chronic kidney disease.

INTRODUCTION Pentraxin3 (PTX3) play an important role in the inflammatory response, taking part in recognizing pathogens and damaged tissues. OBJECTIVES The aim of the study was to assess the relationship between PTX3 levels and all-cause and cardiovascular (CV) mortality in chronic kidney disease (CKD) patients during five-year observation period. PATIENTS AND METHODS The study comprised 78 patients (51 hemodialyzed, 27 predialysis). The examined parameters included PTX3, calcium, phosphate, iPTH, interleukin-6 (IL-6), fibroblast growth factor 23 (FGF-23), osteopontin (OPN), osteoprotegerin (OPG), osteocalcin (OC), osteopontin (OPN), osteoprotegerin (OPG), osteocalcin, tumor necrosis factor receptor II (TNF-R II), transforming growth factor-β (TGF-β), hepatocyte growth factor (HGF), stromal cell-derived factor α (SDF1α), and thrombomodulin (TM). In a subgroup of 45 patients, fragments of radial artery obtained during creation of hemodialysis access were stained for calcifications. In 51 patients, ultrasonography was performed to assess intima-media thickness (CCA-IMT). RESULTS Median serum concentration of PTX3 was 1.43 (0.74-2.50) ng/ml. Higher concentrations of fibrinogen, CRP, IL-6, TNF-R II, TGFβ1, HGF, OPN, OPG, FGF-23, TM, SDF1α, lower albumin and uric acid levels were observed in patients with PTX3 above the median. During follow-up, 27 patients (35%) died, including 25 due to CV causes. In contrast to CRP, baseline PTX3 predicted CV mortality independently of classical CV risk factors. Also, PTX3 concentrations significantly predicted mortality after adjustment for age, baseline dialysis status, serum OPG and CRP, radial artery calcifications, and CCA-IMT. CONCLUSIONS We postulate that PTX3 might be an early marker of CV mortality in patients with advanced CKD yet before the increase of specific marker for systemic inflammation like hsCRP.