PTX3 Levels Research Articles

Pentraxin 3 level in acute migraine attack with aura: Patient management in the emergency department

ObjectivesWe investigated the state of inflammation, PTX3 level and other routine inflammatory markers (high sensitivity C-reactive protein [hsCRP], and white blood cells [WBC]), in patients who presented to the emergency department (ED) with migraine. We also investigated the relationship between the clinical presentation, PTX3 level, and other routine inflammatory markers in the emergency management of these patients. MethodsThe study included 44 patients (group 1) who presented to the ED due to a migraine attack with aura and 44 controls (group 2) with similar demographic characteristics. ResultsThe WBC count was 8.82 ± 2.10 × 109/L in group 1 and 7.85 ± 2.04 × 109/L in group 2. The mean PTX3 level was 11.57 ± 3.99 ng/mL in patients who presented at the ED with a migraine attack, and 4.59 ± 1.28 ng/mL in controls. The differences values of WBC and PTX3 between the two groups were significant (respectively; P = 0.031, P < 0.001). ROC analyses indicated significant results for PTX3 as a marker for acute migraine attack. It had a sensitivity of 93% and specificity of 84% at a cut-off value of 5.80 ng/mL. ConclusionThis is the first study to investigate plasma levels of PTX3 in patients with acute migraine. PTX3 as a biomarker may be used as an additional examination to the current subjective criteria to support the diagnosis of patients presenting to the ED with an acute migraine attack.

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.

Pentraxin-3 and inflammatory biomarkers related to posterolateral thoracotomy in Thoracic Surgery.

Objective:Posterolateral thoracotomy is the most frequently used operation in thoracic surgery, and may initiate an inflammatory process. We aimed to evaluate inflammatory response of the body to posterolateral thoracotomy.Methods:This study was conducted between January 2013 and June 2014. Blood samples were drawn from 36 patients who underwent posterolateral thoracotomy preoperatively, and on postoperative days one, three and seven The levels of PTX-3, CRP and WBC in the serums of the patients were identified. All the results were recorded and analyzed.Results:PTX-3 levels were found statistically significantly higher in patients with lung cancer and/or aged above 65 years. There were significant differences in WBC and CRP levels between preoperative levels and on those on postoperative days one, three and seven but not for PTX-3. The area under the curve(AUC) levels in the receiver operating characteristics(ROC) analysis, which was performed to estimate the strength of PTX-3 in the differentiation of malignant and benign patients was found statistically significant(p<0.05).Conclusions:The present study suggests that the novel inflammatory marker PTX-3 may be used in the diagnosis and follow-up of prognosis as a biomarker of inflammatory response in patients with lung cancer. However, it showed that PTX-3 levels are insignificant to identify the levels of inflamatuar response due to posterolateral thoracotomy in thoracic surgery.

Periodontitis is associated with systemic inflammation and vascular endothelial dysfunction in patients with lacunar infarct.

Periodontitis has been associated with lacunar infarct (LI), a type of cerebral small vessel disease. The objective of this study was to ascertain whether periodontitis is associated with increased circulating levels of systemic inflammation and endothelial dysfunction biomarkers in patients with LI. One hundred twenty patients with LI and 120 healthy controls underwent a full-mouth periodontal examination. The periodontal inflamed surface area (PISA) was calculated for each participant. Demographic, medical, and neurological information were recorded from all of them. In addition, blood samples were collected in order to investigate differences in terms of interleukin (IL)-6, IL-10, pentraxin (PTX) 3, soluble fragment of tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and amyloid-beta (Aβ) peptides (i.e., Aβ1-40 , and Aβ1-42 ) measured in serum. Periodontitis was independently associated with increased levels of IL-6 (R2 =0.656, P<0.001), PTX3 (R2 =0.115, P<0.001), sTWEAK (R2 =0.527, P<0.001), and Aβ1-40 (R2 =0.467, P<0.001) in patients with LI. Within patients with poor outcome, PISA positively correlated with IL-6 (r=0.738, P<0.001), PTX3 (r=0.468, P=0.008), sTWEAK (r=0.771, P<0.001), and Aβ1-40 (r=0.745, P<0.001). Our data suggest a link between periodontitis, systemic inflammatory response, and disruption of the vascular endothelial function in patients with LI. Experimental studies are needed to elucidate possible pathways through which periodontitis could lead to this systemic inflammatory state with impairment of the endothelial function in LI. Further longitudinal studies with large samples are warranted to confirm our findings.

Levels and prognostic impact of circulating markers of inflammation, endothelial activation and extracellular matrix remodelling in patients with lung cancer and chronic obstructive pulmonary disease

BackgroundThe development of both chronic obstructive pulmonary disease (COPD) and lung cancer (LC) is influenced by smoking related chronic pulmonary inflammation caused by an excessive innate immune response to smoke exposure. In addition, the smoking induced formation of covalent bonds between the carcinogens and DNA and the accumulation of permanent somatic mutations in critical genes are important in the carcinogenic processes, and can also induce inflammatory responses.How chronic inflammation is mirrored by serum markers in COPD and LC and if these markers reflect prognosis in patients with LC is, however, largely unknown.MethodsSerum levels of 18 markers reflecting inflammation, endothelial activation and extracellular matrix remodelling were analysed in 207 patients with non-small lung carcinoma (NSCLC) before surgery and 42 COPD patients. 56% of the LC patients also suffered from COPD. The serum samples were analysed by enzyme immunoassays.ResultsSerum levels of OPG, PTX3, AXL, ALCAM, sCD163, CD147, CatS and DLL1 were significantly higher in patients with COPD as compared to patients with LC. High sTNFR1 levels were associated with improved progression free survival (PFS) and overall survival (OS) in LC patients with (PFS hazard ratio (HR) 0.49, OS HR 0.33) and without COPD (OS HR 0.30). High levels of OPG were associated with improved PFS (HR 0.17) and OS (HR 0.14) for LC with COPD. CRP was significantly associated with overall survival regardless of COPD status.ConclusionSeveral markers reflecting inflammation, endothelial activation and extracellular matrix remodelling are elevated in serum from patients with COPD compared to LC patients. Presence of COPD might influence the levels of circulating biomarkers. Some of these markers are also associated with prognosis.

Diagnostic Value of Plasma Pentraxin3- Level For Diagnosis of Erectile Dysfunction.

Erectile dysfunction (ED) is a sexual dysfunction described as the inability to develop or maintain an erection of the penis adequate for sexual intercourse, and its prevalence increases with age. Seen as a common sexual disorder worldwide, organic causes are the underlying reason for 80 percent of ED cases, with the most characteristic pathology responsible for organic ED being atherosclerosis. This study investigates the diagnostic value of plasma PTX-3 levels in arterial ED. This study included a total of 45 patients who were admitted to the urology and cardiologyoutpatient clinics of the Medical Faculty of Canakkale Onsekiz Mart University (COMU) and consented to participate in this study. Patients were categorized into three equal groups in number: (1) patients with ED diagnosed with coronary artery disease (CAD) (15 patients in total); (2) patients with ED not having coronary artery disease or any other equivalent diseases (diabetes mellitus, hypertension and hyperlipidemia) (15 patients in total);and (3) ordinary patients with no ED (15 patients in total). An interview was conducted at the andrology polyclinic with each patient in order to ascertain detailed information on their medical and sexual history and on demographic characteristics. All patients were also administered the International Index of Erectile Function (IIEF) questionnaire. The findings from this study investigating the diagnostic value of plasma PTX-3 levels in ED were statistically significant for two comparisons: the differences between the peripheral blood and cavernous blood values of the patient groups (group 1 and 2) and the control group (group 3), and the differences between the peripheral blood and cavernous blood values of group 2 (patients with ED who do not have CAD) and the control group (group 3). As PTX-3 is more specific than the formerly recognized biochemical markers in endothelial dysfunction, it can be used in the diagnosis of vascular originated ED.

MicroRNA-150 restores endothelial cell function and attenuates vascular remodeling by targeting PTX3 through the NF-κB signaling pathway in mice with acute coronary syndrome.

MicroRNAs (miRNAs) have been known to function as important regulators in the vascular system, with various physiopathological effects such as vascular remodeling and hypertension modulation. We aimed to explore whether microRNA-150 (miR-150) regulates endothelial cell function and vascular remodeling in acute coronary syndrome (ACS), and the involvement of PTX3 and NF-κB signaling pathway. Ten normal mice and sixty ApoE-/- mice were chosen, and their coronary artery tissues and endothelial cells were extracted. ApoE-/- mice were injected with a series of inhibitor or mimic for miR-150, or siRNA against PTX3. The miR-150 expression, NF-κB1, RELA, and PTX3 mRNA expression were assessed by reverse transcription quantitative polymerase chain reaction, and pentraxin-3, p-P50, and p-P65 protein expression by Western blot analysis. Cell viability and migration were assessed by MTT assay and scratch test. Matrigel tube formation assay was employed to determine vascular remodeling of endothelial cells. The dual-luciferase reporter assay verified that PTX3 was a target of miR-150. Mice with ACS presented with decreased miR-150 but increased PTX3. It was observed that the miR-150 mimic and siRNA against PTX3 reduced levels of PTX3, NF-κB1, and RELA in mice, and the miR-150 inhibitor reversed the tendency. The in vitro cell experimentation proved that miR-150 might facilitate endothelial cell proliferation, migration, and restrain vascular remodeling via inhibiting PTX3 expression. On the basis of the results of this study, it was hypothesized that miR-150 could possibly maintain endothelial cell function and suppress vascular remodeling by inhibiting PTX3 through the NF-κB signaling pathway in mice with ACS.

The effect of periodontal disease treatment in patients with continuous ambulatory peritoneal dialysis.

Chronic inflammation is an obvious risk factor of atherosclerotic diseases, and the presence of periodontal disease is one of the important sources of chronic inflammation in patients with chronic kidney disease (CKD) and diabetes mellitus (DM). Thus, we aimed to investigate the effects of non-surgical periodontal therapy of the patients undergoing CAPD due to diabetic nephropathy, diabetic patients without CKD, and healthy controls on inflammation exponents. Thirty-two CAPD patients due to diabetic nephropathy (group III), 31 diabetic patients without nephropathy (group II), and 38 healthy subjects (group I) were enrolled to the study. All patients enrolled to the study (to all groups) suffered from chronic periodontitis. Plaque index, Gingival index, pocket depth (PD) measurements were recorded before and after periodontal therapy. All blood samples for biochemical parameters were measured by using standard laboratory techniques with an automatic analyser. Blood samples for TNF-α, IL-6, and PTX-3 were centrifuged, and separated serum and plasma samples were stored at - 80 °C until analysis. All inflammatory markers were significantly higher in group III than the other two at baseline. TNF-α levels were significantly decreased after periodontal treatment at 3-month visit in all groups. PTX-3, IL-6, and Hs-CRP levels were significantly reduced after periodontal treatment at 3months in group III. Periodontal disease is an important source of inflammation in diabetic CAPD patients and treatment of periodontal disease can be monitored by inflammatory markers including TNF-alpha, PTX-3, IL-6, and Hs-CRP. TNF-alpha may be useful and more sensitive monitoring inflammation in healthy patients and diabetic patients after periodontal treatment.

Pro-Inflammatory Biomarkers in Stable Versus Acutely Decompensated Heart Failure With Preserved Ejection Fraction.

BackgroundUnderlying inflammation has been increasingly recognized in heart failure with a preserved ejection fraction (HFpEF). In this study we tested the hypothesis that pro‐inflammatory biomarkers are elevated in patients with acutely decompensated HFpEF (AD‐HFpEF) compared with patients with stable HFpEF (S‐HFpEF).Methods and ResultsUsing a post hoc analysis the serum biomarkers tumor necrosis factor‐alpha, high‐sensitivity C‐reactive protein interleukin 6 and pentraxin 3 (PTX3) and clinical, demographic, echocardiographic‐Doppler and clinical outcomes data were analyzed in HFpEF patients enrolled in NHLBI Heart Failure Research Network clinical trials which enrolled patients with either AD‐HFpEF or S‐HFpEF. Compared to S‐HFpEF, AD‐HFpEF patients had higher levels of PTX3 (3.08 ng/mL versus 1.27 ng/mL, P<0.0001), interleukin‐6 (4.14 pg/mL versus 1.71 pg/mL, P<0.0001), tumor necrosis factor‐alpha (11.54 pg/mL versus 8.62 pg/mL, P=0.0015), and high‐sensitivity C‐reactive protein (11.90 mg/dL versus 3.42 mg/dL, P<0.0001). Moreover, high‐sensitivity C‐reactive protein, interleukin‐6 and PTX3 levels were significantly higher in AD‐HFpEF compared with S‐HFpEF patients admitted for decompensated HF within the previous year. PTX3 was positively correlated with left atrial volume index (r=0.41, P=0.0017) and left ventricular mass (r=0.26, P=0.0415), while tumor necrosis factor‐alpha was inversely correlated with E/A ratio (r=−0.31, P=0.0395).ConclusionsLevels of pro‐inflammatory biomarkers are strikingly higher in AD‐HFpEF compared with S‐HFpEF patients. PTX3 and tumor necrosis factor‐alpha are correlated with echocardiographic‐Doppler evidence of diastolic dysfunction. Taken together these data support the concept that a heightened pro‐inflammatory state has a pathophysiologic role in the development of AD‐HFpEF.

Abstract A039: FGF/PTX3 crosstalk in bladder cancer: novel prognostic and therapeutic implications

Abstract Bladder cancer is one of the most common cancers in the world. Although most of urothelial carcinomas (UCs) are low-grade papillary tumors, their propensity to recur and to progress to become invasive with a poor survival rate represents a major challenge. Different members of the Fibroblast growth factor (FGF) family are expressed by human bladder cancer cells, and aberrant expression of FGF receptors (FGFRs) is a typical feature of bladder cancer compared to normal urothelium. High expression levels of FGFR1 are associated with poor survival and FGFR3 is frequently dysregulated in UC. Thus, the FGF/FGFR system may represent a promising therapeutic target in invasive and noninvasive bladder cancer. Long-pentraxin 3 (PTX3) acts as a natural FGF trap by binding FGFs and hampering their biologic activity in various tumor models. Preliminary observations have shown that low-grade UCs express PTX3 while high-grade/invasive UCs lose PTX3 expression. Accordingly, bladder cancer cell lines share an overall presence of FGFRs and FGFs but express different levels of PTX3 in vitro and in vivo. Of note, high-grade/invasive cells express very low or undetectable levels of PTX3, whereas low-grade, papilloma-like cells express high levels of PTX3. Indeed, invasive bladder cancer cell xenografts grow faster in nude mice and express much lower levels of PTX3 than low grade-derived lesions, thus confirming an inverse correlation between UC grade and PTX3 expression. This hypothesis is reinforced by a preliminary case study performed on a small cohort of biopsies from UC patients confirming that the presence of PTX3 is a common feature of low-grade samples while PTX3 is poorly expressed or absent in aggressive/invasive cases. These data point to PTX3 as a natural FGF trap that could play a role in modulating bladder cancer progression and invasiveness and indicate that inhibition of the FGF/FGFR system by natural and synthetic FGF traps may represent a promising target for the therapy of UCs. Citation Format: Sara Matarazzo, Federica Maccarinelli, Gaia Cristina Ghedini, Laura Melocchi, Mattia Bugatti, William Vermi, Marco Presta, Roberto Ronca. FGF/PTX3 crosstalk in bladder cancer: novel prognostic and therapeutic implications [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2017 Oct 26-30; Philadelphia, PA. Philadelphia (PA): AACR; Mol Cancer Ther 2018;17(1 Suppl):Abstract nr A039.

Effects of MiR-375-BMPR2 as a Key Factor Downstream of BMP15/GDF9 on the Smad1/5/8 and Smad2/3 Signaling Pathways

Background/Aims: Bone morphogenetic protein 15 (BMP15) and growth differentiation factor 9 (GDF9), which are secreted by oocytes, are important regulators of follicular growth and development and ovarian function. These two factors can regulate the proliferation and apoptosis of cumulus cells via modulation of the Smad signaling pathway. Studies have shown that BMP15 and GDF9 can affect the level of miR-375, whereas the target gene of miR-375 is BMPR2, the type II receptor of BMP15 and GDF9. However, whether or how the BMP15/ GDF9-miR-375-BMPR2 pathway affects the proliferation and apoptosis of bovine cumulus cells through regulation of the Smad signaling pathway remains unclear. Methods: In this study, cumulus cells were first obtained from cumulus-oocyte complexes (COCs). Appropriate concentrations of BMP15 and GDF9 were added during the in vitro culture process. Cell Counting Kit-8 (CCK-8) analyses and flow cytometry were used to determine the effects of BMP15/GDF9 on bovine cumulus cells proliferation and apoptosis. Subsequently, miR-375 mimics, miR-375 inhibitor and BMPR2 siRNA were synthesized and used for transfection experiments. Western Blot analysis was used to detect changes before and after transfection in the expression levels of the BMP15/GDF9 type I receptors ALK4, ALK5 and ALK6; the phosphorylation levels of Smad2/3 and Smad1/5/8, which are key signaling pathway proteins downstream of BMP15/GDF9; the expression levels of PTX3, HAS2 and PTGS2, which are key genes involved in cumulus cells proliferation; and Bcl2/Bax, which are genes involved in apoptosis. Results: The addition of 100 ng/mL BMP15 or 200 ng/mL GDF9 or the combined addition of 50 ng/mL BMP15 and 100 ng/mL GDF9 effectively inhibited bovine cumulus cell apoptosis and promoted cell proliferation. BMP15/GDF9 negatively regulated miR-375 expression and positively regulated BMPR2 expression. High levels of miR-375 and inhibition of BMPR2 resulted in increased expression of ALK4 and decreased expression of PTX3, HAS2 and PTGS2, whereas miR-375 inhibition resulted in the opposite results. BMP15 and GDF9 significantly activated the levels of p-Smad2/3 and p-Smad1/5/8, whereas miR-375 inhibited the levels of p-Smad2/3 and p-Smad1/5/8 by negatively regulating BMPR2 and also led to apoptosis. Conclusion: BMP15 and GDF9 have synergistic effects and can act through miR-375 to affect the expression levels of type I receptor ALK4 and type II receptor BMPR2 and the activation of Smad signaling pathway, which subsequently affected the proliferation, spread and apoptosis of cumulus cells.

Bronchoscopic characteristics of mycoplasma pneumoniae in children and the level of inflammatory factors in bronchoalveolar lavage fluid

Objective To investigate the specpfic electric fiberobronchoscopic manifestations of refractory Mycoplasma pneumoniae pneumonia(RMPP) and explore the level of IL-17, IL-18, PTX3 in bronchoalveolar lavage fluid(BALF)and their clinical sigfinance. Methods To select patients who were diagnosed as MPP and examined by fiberobronchoscopy in acute stage.Dividing them into groups: (1) RMPP group (60cases): dividing RMPP patients into three groups according to if they were treated by systemic corticosteroids or immunoglobulin before the examination of fiberbronchoscope, ① RMPP-A group: both are not used.②RMPP-B group: use systemic corticosteroids.③ RMPP-C: both are used.(2)general MPP group(35 cases).15 children with foreign body in bronchus were enrolled as control group.Firstly, to analysis the electric fiberobronchoscopic manifestations of all the cases.Secondly, the cases who had BALF samples in all group were selected, the levels of IL-17, IL-18 and PTX3 are detected by ELISA. Results Under electric fiberobronchoscopy, that the proportions of RMPP group with mucosal erosion, necrotic mucous membrane peeling, sputum bolt blockage in bronchial lumen or moulding are higher than general MPP group.The levels of IL-17, IL-18 and PTX3 in BALF of all MPP cases are higher than control group(P<0.05), but only the difference of IL-18 between RMPP group and general MPP group has statistical significance (P<0.05). The levels of IL-17, IL-18 and PTX3 in BALF of RMPP-B group are all higher than RMPP-A group (P<0.05). Conclusion Mucosal erosion, necrotic mucosa peeling and sputum bolt, moulding are the characteristic manifestations of RMPP, and can help identify RMPP.IL-17, IL-18 and PTX3 all participated in the pathogenesis of RMPP.Only the level of IL-18 in BALF can be the predictive marker of RMPP.Systemic corticosteroids may inhibit the levels of IL-17, IL-18 and PTX3 of RMPP patients. Key words: Refractory Mycoplasma pneumoniae pneumonia; Bronchoscopy; Inflammatory factor

55 The Role of Poly (ADP-Ribose) Polymerases in Porcine Cumulus - Oocyte Complex During In Vitro Maturation and Embryonic Development

Poly(ADP-ribosyl)ation (PARylation) is related to DNA repair, chromatin modification, and apoptosis and is catalyzed by PARylation polymerases (PARP). Previous studies have shown that PARylation regulates pre-implantation development and participates autophagy mechanism in mouse and pig. However, the involvement of PARylation and pro-survival autophagy in pre-implantation development from cumulus–oocyte complexes (COC) to the blastocyst stage has not yet been documented. Thus, we investigated the role of PARylation during in vitro maturation (IVM) of porcine COC and their embryonic development. To study the effect of PARylation, COC were cultured with 3-aminobenzamide (3-ABA, PARP inhibitor) during IVM. Nuclear maturation rates of oocytes were showed no significant differences between 2 groups in all stages (from GV to MII). However, the expansion rates of cumulus cells were significantly decreased in 3-ABA–treated COC compared with control (11.05 ± 1.09 v. 48.40 ± 0.67%). When we analysed mRNA levels of maturation- and expansion-related genes in cumulus cells, levels of PTX3, CX43, and COX-2 were increased but levels of HAS2 and TNFAIP6 were decreased in treatment group. In addition, expression levels of GDF9 and BMP15 in oocytes were up-regulated in treated group. Then, we examined the development of IVF embryos from IVM oocytes in the presence and absence of 3-ABA and their quality at the blastocyst stage. We found that the developmental rates of embryos were significantly decreased in 3-ABA-treated group. In particular, the proportion of expanded blastocysts was lower in the treated embryos (2.65 ± 1.53) compared with control embryos (12.27 ± 3.05). Furthermore, the transcript levels of autophagy-related genes (ATG5, BECLIN1, and LC3) in 3-ABA-treated embryos were lowered in all stages. In addition, we found a higher rate of apoptosis in treated blastocysts compared with the control (total apoptosis index; 15.65 ± 2.73 v. 4.89 ± 0.67). Finally, SQSTM1/p62 aggregate increased in 3-ABA-treated blastocysts, indicating that the inhibition of PARylation regulates selective autophagy pathways to utilise SQSTM1/p62. Therefore, these results indicate that PARylation by PARPs during IVM of COC is deeply involved in the pro-survival autophagy and influences the development and quality of porcine embryos. This research was supported by a Grant from the Bio &amp; Medical Technology Development Program (2015M3A9C7030091) of the National Research Foundation (NRF) funded by the Korean government.

Diagnostic Value of Plasma Pentraxin-3 in Acute Appendicitis

ABSTRACTPurpose: To measure serum PTX3 levels in patients admitted with right lower quadrant pain to emergency department and to investigate whether this parameter will be helpful for the diagnosis of acute appendicitis.Materials and methods: This study was conducted with a group of 89 patients over 17 years of age who were admitted with the complaint of right lower quadrant pain to ED and had a preliminary diagnosis of acute appendicitis clinically and the control group of 31 healthy volunteers in a tertiary university hospital for 3 months.Results: Median PTX3 levels were 3.28 (1.08-30.24) ng/mL in the acute appendicitis groups and 0.97 (0.34-2.62) ng/mL in the control group. A significant difference was observed between acute appendicitis groups and the control group (p < 0.05).Conclusion: PTX3 was found to be significantly higher in patient with acute appendicitis compared to the control group and the patients with non-specific abdominal pain. PTX3 can be used as an aid in the diagnosis of acute appendicitis.

Serum levels of PTX3 and SFLT-1 predict the outcomes of frozen-thawed euploid embryo transfer cycles

Serum levels of PTX3 and SFLT-1 predict the outcomes of frozen-thawed euploid embryo transfer cycles

Possible effects of lipoprotein-associated phospholipase A2 single-nucleotide polymorphisms on cardiovascular risk in patients with preeclampsia

Purpose: Lipoprotein lipase-associated phospholipase A2 (Lp-PLA2) is a vascular inflammatory marker associated with cardiovascular diseases (CVD). Women with preeclampsia (PE) have elevated vascular inflammation and at higher CVD risk in the later life. We hypothesize that vascular inflammation related genetic variations increase the risk for developing future cardiovascular disease in women with PE. To test this hypothesis, we studied PLA2G7 gene polymorphisms, Lp-PLA2 mass, activity, index, and other cardiovascular risk factors in women with preeclampsia.Methods: A total of 200 pregnant women were included into the study. We stratified the PE group: early (28.7 ± 3.0 weeks) and late onset (36.0 ± 1.4 weeks). Serum Lp-PLA2 mass in the early PE and the late PE group were significantly higher than the control group (p = .000). Lp-PLA2 index, Hs-C-reactive protein (CRP), serum amyloid A (SAA), calprotectin, and PTX3 levels were higher in early and late PE (p = .000). Single-nucleotide mutations of PLA2G7 rs1805017 (r = −0.228, p < .05) and rs9381475 (r = 0.216, p < .05) were correlated with LpPLA2 mass for the early PE group. Logistic regression analysis showed that LP-PA2 mass an independent risk factor for early PE with rs1805017 and rs9381475 carriers.Conclusions: Lp-PLA2 genetic variability with vascular inflammatory markers might contribute the incidence of future cardiovascular events.

Acute ethanol intoxication suppresses pentraxin 3 expression in a mouse sepsis model involving cecal ligation and puncture.

Acute ethanol intoxication impairs immunological reactions and increases the risk of sepsis; however, the underlying mechanism remains unclear. Pentraxin (PTX) 3 is a humoral pattern recognition receptor whose levels rapidly increase in response to inflammation. PTX3 production is triggered by tumor necrosis factor (TNF)-α and is mediated by c-Jun N-terminal kinase (JNK). As PTX3 exerts protective effects against sepsis as well as acute lung injury, we investigated whether acute ethanol exposure exacerbates sepsis by altering PTX3 expression. Sepsis was induced in C57/BL6 mice by cecal ligation and puncture (CLP) after ethanol/saline administration. Survival rates were significantly lower in ethanol-treated than in saline-treated mice. Increased vascular permeability and attenuation of PTX3 expression were observed in the lungs of ethanol-treated mice 4h after CLP. Concomitant with a delayed increase of plasma TNF-α in ethanol-treated mice, plasma PTX3 was also suppressed in the early phase of sepsis. Although TNF-α level in ethanol-treated mice exceeded that in saline-treated mice 16h after CLP, PTX3 levels were still suppressed in the former group. JNK phosphorylation in lung tissue was suppressed in both groups 4 and 16h after CLP. Furthermore, JNK phosphorylation in ethanol-treated human umbilical vein endothelial cells was suppressed even in the presence of exogenous TNF-α, resulting in inhibition of PTX3 mRNA and protein expression. Our results suggest that ethanol suppresses de novo PTX3 synthesis via two mechanisms - i.e., suppression of TNF-α production and inhibition of JNK phosphorylation. PTX3 suppression may therefore contribute to exacerbation of sepsis in acute ethanol intoxication.

Diagnostic value of Pentraxin-3 in patients with sepsis and septic shock in accordance with latest sepsis-3 definitions

BackgroundPentraxin-3 (PTX-3) is an acute-phase protein involved in inflammatory and infectious processes. This study assesses its diagnostic and prognostic value in patients with sepsis or septic shock in a medical intensive care unit (ICU).MethodsThe study includes 213 ICU patients with clinical criteria of sepsis and septic shock. 77 donors served as controls. Plasma levels of PTX-3, procalcitonin (PCT) and interleukin-6 were measured on day 1, 3 and 8.ResultsPTX-3 correlated with higher lactate levels as well as with APACHE II and SOFA scores (p = 0.0001). PTX-3 levels of patients with sepsis or septic shock were consistently significantly higher than in the control group (p ≤ 0.001). Plasma levels were able to discriminate sepsis and septic shock significantly on day 1, 3 and 8 (range of AUC 0.73–0.92, p = 0.0001). Uniform cut-off levels were defined at ≥5 ng/ml for at least sepsis, ≥9 ng/ml for septic shock (p = 0.0001).ConclusionPTX-3 reveals diagnostic value for sepsis and septic shock during the first week of intensive care treatment, comparable to interleukin-6 according to latest Sepsis-3 definitions.Trial registrationNCT01535534. Registered 14.02.2012

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.

Prenatal Exposure to Lipopolysaccharide Induces PTX3 Expression and Results in Obesity in Mouse Offspring

This study tested the hypothesis whether inflammation will directly lead to obesity. This study was designed to investigate the relationship between inflammation and obesity by intraperitoneally injecting pregnant mice with lipopolysaccharide (LPS) (75 μg kg−1). The results showed that inflammation during pregnancy could lead to a significant increase in the levels of the inflammatory factor PTX3. The offspring of the LPS-treated mice displayed abnormal levels of fat development, blood lipids, and glucose metabolism, and fat differentiation markers were significantly increased. Our study also confirmed that PTX3 can increase the susceptibility to obesity by regulating the expression of adipogenic markers; this regulatory role of PTX3 is most likely caused by MAPK pathway hyperactivation. Our study is the first to find strong evidence of inflammation as a cause of obesity. We determined that PTX3 was an important moderator of obesity, and we elucidated its mechanism, thus providing new targets and theories for obesity therapy. Moreover, our study provides new ideas and directions for the early intervention of anti-inflammation in pregnancy.