Search Results (77)

Chronic inflammation plays a key role in cancer pathogenesis. Aggressive thyroid cancer is associated with immune infiltration and systemic inflammation. Long pentraxin 3 (PTX3) is an inflammatory protein implicated in tumor progression. This study evaluates PTX3 plasma levels in patients with non-medullary thyroid cancer (TC) compared to benign thyroid disease and investigates its tissue expression. We prospectively included 55 TC patients: 42 papillary, 3 follicular, 4 oncocytic, 4 anaplastic (ATC), and 2 poorly differentiated (PDTC). The control group consisted of 32 patients with benign thyroid disease. PTX3 plasma concentrations were measured by ELISA, and tissue expression of PTX3 and CD68 was analyzed using immunohistochemistry. PTX3 plasma levels did not significantly differ between TC and controls, but patients with PDTC and ATC had markedly higher concentrations. Tissue analysis showed strong PTX3 expression in three of four ATC cases in tumor and stromal cells, whereas benign and differentiated thyroid tissues exhibited minimal staining. CD68 expression was positive in ATC, indicating tumor-associated macrophage infiltration, but a few cells were double-positive for PTX3 and CD68. Our findings suggest a possible association between PTX3 and aggressive TC, particularly ATC. Further studies are needed to validate these findings and elucidate the cellular origin and functional role of PTX3. Full article

Human cleft lip morphopathogenesis is a complicated process involving multiple genes and proteins. Certain factors like muscle segment homeobox 1 (MSX1) and 2 (MSX2) as well as receptor-like tyrosine kinase (RYK) are important during lip embryogenesis, while others like nuclear factor kappa-B protein 65 (NFκB p65), C-C motif chemokine ligand 4 (CCL4), and pentraxin 3 (PTX3) regulate local inflammation and immunomodulation. The exact role of these factors in human cleft morphopathogenesis remains uncertain and limits the opportunity to improve cleft treatment and possible prophylaxis. Immunohistochemistry (IHC) for MSX1, RYK, NFκB p65, and CCL4 proteins and chromogenic in situ hybridization (CISH) for MSX2, RYK, and PTX3 genes were used to analyze postnatal human cleft lip tissue (15 patients) and control tissue (6 patients). The semiquantitative counting method was used to assess factor/gene-signal-containing cells. Statistical analysis was performed. IHC findings showed decreased MSX1, NFκB p65, and CCL4 proteins in cleft lip connective tissue and endothelium, while RYK protein was decreased only in cleft connective tissue. CISH showed increases in MSX2 and RYK gene-signal-containing cells in cleft lip tissue while PTX3 did not differ from controls. Multiple statistically significant correlations were calculated. The findings are discussed in detail to determine their significance in cleft lip morphopathogenesis. Full article

Background: Septic arthritis is an orthopedic emergency. However, optimal biomarkers and diagnostic criteria remain unclear. The study aimed to evaluate the diagnostic performance of routinely used and novel biomarkers, including serum C-reactive protein (CRP), synovial white blood cells (WBC), pentraxin-3 (PTX3), interleukin-6 (IL-6), and presepsin, in distinguishing septic from non-septic arthritis. Methods: Thirty-one patients undergoing arthrocentesis were included. Patients were categorized into septic and non-septic arthritis groups. Synovial fluid and serum samples were analyzed for five biomarkers. Diagnostic performance was assessed by calculating the area under the curve (AUC), accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). Results: Synovial WBC demonstrated the highest diagnostic performance among single biomarkers (AUC = 0.837, p = 0.012). Among novel biomarkers, PTX3 showed the highest accuracy and sensitivity. The serum CRP and synovial WBC combination yielded an AUC of 0.853, with 100% sensitivity, 68.0% specificity, 42.9% PPV, and 100% NPV. Adding all three novel biomarkers to this combination increased the AUC to 0.887 (p = 0.004), maintaining 100% sensitivity and NPV. When individually added, PTX3 achieved 100% sensitivity and NPV, while presepsin showed the highest specificity (96.0%), PPV (75.0%), and accuracy (87.1%). Conclusions: Serum CRP and synovial WBC remain essential biomarkers for diagnosing septic arthritis; however, combining them with PTX3, IL-6, and presepsin improved diagnostic accuracy. PTX3 is best suited for ruling out septic arthritis due to its high sensitivity and NPV, whereas presepsin is more useful for confirmation, given its specificity and PPV. These results support a tailored biomarker approach aligned with diagnostic intent. Full article

Background and Objectives: Acute ulcerative colitis is characterized by excessive mucosal inflammation and epithelial disruption, often driven by dysregulated cytokine and immune signaling. Indoximod (1-methyl-DL-tryptophan), although not a direct enzymatic inhibitor, modulates the indoleamine 2,3-dioxygenase (IDO) pathway and has been reported to exert immunoregulatory effects in various models of inflammation. This study aimed to evaluate the protective effects of Indoximod in an acetic acid-induced colitis model in rats, focusing on histopathological changes and inflammatory mediators. Materials and Methods: Thirty male Wistar albino rats were randomly assigned to three groups (n = 10 per group): Group 1 (Control) received 0.9% saline oral gavage; Group 2 (Colitis) received intrarectal 4% acetic acid to induce colitis and were then treated with saline; Group 3 (Colitis + Indoximod) received 4% acetic acid followed by oral gavage administration of Indoximod (30 mg/kg) for 15 consecutive days. Histopathological evaluation of colonic tissues was performed using hematoxylin and eosin (H&E) staining. Colonic expression of Toll-like receptor 4 (TLR4) and plasma levels of tumor necrosis factor-alpha (TNF-α), pentraxin-3 (PTX-3), and platelet-activating factor (PAF) were quantified using enzyme-linked immunosorbent assay (ELISA). Results: Acetic acid-induced colitis significantly increased mucosal damage, TLR4 expression, and circulating levels of TNF-α, PTX-3, and PAF compared with controls (p < 0.001). Indoximod treatment markedly reduced histological injury and significantly suppressed TLR4 and TNF-α levels (p < 0.01), along with partial reductions in PTX-3 (p < 0.05). However, PAF levels remained elevated despite treatment, indicating limited efficacy in PAF-associated pathways. Conclusions: Indoximod exhibited anti-inflammatory effects in this acute colitis model, likely by downregulating key proinflammatory mediators. Full article

Background/Objectives: Hypercholesterolemia, accompanied by vascular inflammation, leads to the premature initiation and progression of atherosclerosis, and both are considered nowadays as well-established cardiovascular (CV) risk factors. For several years, proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9is), drugs that reduce the degradation of the receptors for low-density lipoprotein cholesterol (LDLRs), have appeared to be a very efficient lipid-lowering therapy among patients with complications resulting from atherosclerotic cardiovascular disease (ASCVD). Previous studies showed that drugs used to fight hypercholesterolemia (predominantly statins) have significant pleiotropic effects, including anti-inflammatory effects. To date, data on the potential impact of PCSK9 inhibitors, especially inclisiran, on the course of inflammation is still lacking. Therefore, we conceived a study to evaluate the effects of inclisiran on the markers of subclinical inflammation (e.g., pentraxin 3 (PTX3), interleukin-18 (IL-18), and soluble cluster of differentiation 40 ligand (CD40L)) and compared their magnitude in patients at high CV risk, with and without established heterozygous familial hypercholesterolemia (HeFH). Methods: A total of 24 patients at high cardiovascular risk, according to European Society of Cardiology (ESC) guidelines, with or without concomitant HeFH diagnosed using Dutch Lipid Clinic Network (DLCN) criteria, were enrolled in this study. Lipid concentrations and levels of subclinical inflammatory markers of atherosclerosis were measured at the beginning and after 3 months of therapy. Results: After three months of therapy with inclisiran, a statistically significant reduction included total cholesterol (TC): study group 1: from 287.6 ± 94.15 to 215.2 ± 89.08 [mg/dL], p = 0.022 and study group 2: from 211.71 ± 52.72 to 147.64 ± 55.44 [mg/dL], p < 0.001, and low-density lipoprotein cholesterol (LDL-c): study group 1: from 180.79 ± 73.33 to 114.65 ± 71.54 [mg/dL], p = 0.031 and study group 2: from 129.62 ± 46.75 to 63.39 ± 43.6 [mg/dL], p < 0.001. Moreover significant drops were observed in concentrations of PTX3: study group 1: from 1336.33 ± 395.15 to 1121.75 ± 351.17 [pg/mL], p = 0.013 and study group 2: from 1610.76 ± 537.78 to 1376.92 ± 529.19 [pg/mL], p = 0.017), and IL-18: study group 1: from 11.89 (9.72–13.98) to 9.15 (8.62–10.06) [pg/mL], p = 0.005 and study group 2: from 11.58 (10.87–16.97) to 9.65 (8.43–10.95) [pg/mL], p = 0.003). There were no significant changes in the levels of sCD40L. Conclusions: This study confirmed the ability of inclisiran to reduce LDL-c levels in patients at high cardiovascular risk just after one dose of the drug. Furthermore, it appeared that beyond its lipid-lowering effect, the drug may also affect some inflammatory processes involved in the initiation and progression of atherosclerosis. Full article

Severe dental pulp inflammation can lead to tissue lysis and destruction, underscoring the necessity for effective treatment of pulpitis. N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac⁴C) modification has recently emerged as a key regulator in inflammatory processes. However, whether NAT10 affects the inflammatory response in human dental pulp stem cells (hDPSCs) remains unelucidated. In this study, elevated NAT10 expression was observed in pulpitis tissues and LPS-stimulated hDPSCs. Knockdown of NAT10 led to reduced inflammatory gene expression and lower reactive oxygen species (ROS) production in LPS-stimulated hDPSCs, while the chemotactic migration of macrophages was also suppressed. Similar results were observed when hDPSCs were treated with Remodelin, an inhibitor of NAT10. Differentially expressed genes identified through RNA sequencing were significantly enriched in inflammatory signaling pathways after NAT10 depletion. Among the differential genes, pentraxins 3 (PTX3) was identified as the potential target gene due to the presence of the ac⁴C modification site and its known ability to regulate dental pulp inflammation. The mRNA and protein levels of PTX3 were reduced in NAT10-deficient cells, along with a decrease in its mRNA stability. Exogenous PTX3 supplementation partially reversed the inflammatory inhibition induced by NAT10 knockdown. Further evidence in vivo revealed that Remodelin treatment attenuated the severity of dental pulp inflammation in rats with pulpitis. In summary, these data indicated that NAT10 deficiency inhibited the stability of PTX3 mRNA and further inhibited hDPSC inflammation, while Remodelin might be a potential therapeutic agent for pulp capping. Full article

Background and Objectives: The purpose of this study was to evaluate potential protective effects of suramin on inflammation, oxidative stress, and histopathological damage a rat model of acute colitis created with acetic acid. Materials and Methods: Wistar albino (male) rats were randomly assigned to three groups: control (n = 10), colitis + saline (n = 10), and colitis + suramin (n = 10). Rectal instillation of 4% acetic acid was used to induce acute colitis. Suramin (10 mg/kg/day) or saline was administered intraperitoneally for 15 days. Plasma concentrations of pentraxin 3 (PTX3), tumor necrosis factor-alpha (TNF-α), neutrophil extracellular traps (NETs), and malondialdehyde (MDA) were determined using enzyme-linked immunosorbent assay (ELISA) and spectrophotometric methods. In addition, vascular endothelial growth factor (VEGF) and TNF-α levels in colonic tissue were also measured. Histopathological evaluations were conducted using hematoxylin and eosin staining. Results: Significant increases in plasma and tissue inflammatory markers, oxidative stress parameters, and histopathological scores were observed when compared to control group; values were higher in colitis group. Suramin treatment significantly reduced plasma PTX3, TNF-α, NETs, and MDA levels, and colonic TNF-α and VEGF concentrations compared to the untreated colitis group. Histological analysis showed reduced epithelial injury and leukocyte presence in rats receiving suramin. Conclusions: Our findings demonstrate that suramin significantly attenuates inflammatory and oxidative damage in an experimental model of acute colitis. These results suggest that suramin may possess therapeutic potential in intestinal inflammation; however, this effect requires further support through advanced experimental and clinical studies. Full article

Background: The implantation process is complex and involves numerous factors that can affect its success. In artificial reproductive treatments (ARTs), chronic inflammation seems to be associated with implantation failure, largely contributing to reproductive dysfunction. Pentraxin 3 (PTX3) is overexpressed in several pathological conditions by exerting a pivotal role both as a regulator and indicator of inflammatory response. Some literature data have shown that PTX3 could have an impact on follicle growth and development, influencing women’s fertility. This study aimed to detect PTX3 in follicular fluids collected during an ART protocol in relation to implantation outcomes. Methods: The PTX3/NF-kB/TLR4 pathway and other cytokines were assessed in the follicular fluid of 169 subjects, under the age of 40 years, undergoing IVF cycles, including females without achieved implantation (n = 98) and those with implantation (n = 71). Furthermore, subgroup analyses were performed to evaluate PTX3 values according to age difference. Results: From our data, PTX3 emerged as a strong predictor, more than TNFα and IL-1β, of implantation failure and related inflammatory follicular state. Overall, the results point to PTX3 as a potential biomarker for ART success, and their testing may be helpful in women whose successful implantation remains unexplained. Conclusions: Therefore, PTX3 could constitute a reliable biomarker and a valuable target to improve ART outcomes. Full article

Background: Oral ulcerative mucositis (OUM) is a painful, inflammatory mucosa lesion that impairs quality of life. Despite available treatments, effective agents that promote faster healing and modulate inflammation are still needed. Oxytocin (OT), a neuropeptide with anti-inflammatory and antioxidant properties, may aid wound healing by regulating the remodeling of the extracellular matrix (ECM). This study investigates the effects of OT on oral ulcer healing in rats, focusing on its modulation of the MMP-2/TIMP-2 pathway. Methods: Acetic acid 70% was used as the oral mucosal ulcer inducer. Thirty-six Wistar albino rats were divided into control, oral ulcer + saline, and oral ulcer + OT (intraperitoneally for 15 days) groups. Histopathological, biochemical, and molecular analyses were performed. Buccal mucosa tissue was examined for TNF-α, TIMP-2, and MMP-2 levels via ELISA, while oxidative stress markers and pentraxin-3 (PTX3) were also assessed. Results: OT significantly preserved epithelial integrity and reduced fibrosis compared to the saline group (p < 0.001). TNF-α, MMP-2, PTX3, and malondialdehyde levels were significantly lower, while TIMP-2 levels were elevated in the OT-treated group (p < 0.01). Histopathological analysis confirmed reduced inflammation and enhanced tissue organization. Conclusions: OT accelerates oral ulcer healing by modulating inflammation, oxidative stress, and ECM remodeling via the MMP-2/TIMP-2 pathway. These findings highlight its potential as a therapeutic agent for managing mucosal injuries. Further clinical studies are warranted. Full article

Diabetes mellitus (DM) is a multifactorial metabolic disorder associated with systemic inflammation and vascular complications. Pentraxin-3 (PTX3) has emerged as a key biomarker of inflammation and endothelial dysfunction in DM. We aimed to examine the role of PTX3 in DM and assesses the impact of pharmacological interventions on its expression. The review included studies analyzing PTX3 modulation by antidiabetic therapies, such as sodium-glucose cotransporter-2 inhibitors (SGLT-2i), glucagon-like peptide-1 agonists (GLP-1a), and dipeptidyl peptidase-4 inhibitors (DPP-4i), as well as the effects of lifestyle interventions. Clinical and experimental studies demonstrated a strong correlation between PTX3 levels and DM progression. Elevated PTX3 levels were associated with diabetic complications, including nephropathy, retinopathy, and cardiovascular diseases. Antidiabetic drugs showed differential effects on PTX3 expression, with GLP-1a and DPP-4i significantly reducing PTX3 levels, while SGLT-2i displayed a paradoxical increase. Lifestyle interventions, including dietary modifications and weight loss, yielded inconsistent effects, suggesting genetic and metabolic factors influence PTX3 regulation. While pharmacological therapies, particularly GLP-1a and DPP-4i, demonstrate anti-inflammatory effects, further research is needed to standardize PTX3 measurement and explore its potential as a therapeutic target. Personalized treatment strategies incorporating genetic profiling may optimize inflammation control and disease management in DM patients. Full article

One of the most dangerous and difficult side effects to treat after total hip arthroplasty (THA) is periprosthetic or superficial site infection. Blood and synovial fluid biomarkers have recently come into focus in addition to conventional systemic indicators of inflammation in order to assess their potential utility in the diagnosis of infections. Long pentraxin 3 (PTX3) appears to be a sensitive biomarker of acute-phase inflammation. The purpose of this study is to determine plasma PTX3 in patients undergoing THA and compare its trend with other common serum markers, such as CRP, D-dimer, procalcitonin, and ESR up to 30 days post-operatively. Patients with hip arthritis or avascular necrosis of the femoral head were consecutively enrolled in a single-center study. Each patient underwent blood testing for ESR, CRP, procalcitonin, D-dimer, and PTX3 levels before surgery and at 1, 3, 5, 15, and 30 days after THA. PTX3 was measured using the ELISA method. Other markers’ values and trends were compared with PTX3’s. A total of 50 patients met our inclusion criteria. When different trends were evaluated, PTX3 was found to have a trajectory and sensitivity comparable to other inflammatory markers. Notably, PTX3 changed more quickly than the other markers, with a sharp increase immediately post-operatively, followed by normalization at the 5-, 15-, and 30-day follow-ups, corresponding to the resolution of the inflammatory condition. However, 30 days post surgery, no patients exhibited signs or symptoms of early prosthetic infection. PTX3 is confirmed as a reliable and promising serum biomarker for tracking the level of inflammation in patients undergoing total hip replacements. Blood PTX3 values rise even more rapidly than CRP and procalcitonin and then quickly return to normal values when the inflammatory process resolves. One of the primary barriers to PTX3’s inclusion in routine studies on early periprosthetic infections is the waiting period for PTX3 sample analysis. Full article

Background: Medical history, ECG findings and cardiac markers are used in the diagnosis of myocardial infarction (MI). Biomarkers used especially for the diagnosis of MI include high-sensitivity troponins (hsTns), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), myoglobin, cardiac myosin-binding protein C and new cardiac biomarkers. This study evaluated the levels of serum thrombomodulin (TM), heart-type fatty-acid-binding protein (H-FABP), pentraxin-3 (PTX-3) and galectin-3 (Gal-3) to determine their utility in distinguishing between ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI). Methods: This study included a total of 180 patients (90 patients with acute STEMI and 90 patients with NSTEMI) who presented to the Gaziosmanpaşa Training and Research Hospital, Cardiovascular Surgery and Emergency Department, with ischemic chest pain lasting longer than 30 min. Ninety healthy volunteers were included as the control group. Results: Serum levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), TM, H-FABP, PTX-3 and Gal-3 were significantly different across the STEMI, NSTEMI and control groups (p < 0.001). Strong positive correlations were observed between NT-proBNP and TM, H-FABP, PTX-3 and Gal-3 in the STEMI group. ROC analysis demonstrated excellent diagnostic accuracy for these biomarkers in distinguishing STEMI from NSTEMI and control groups. Conclusions: Vascular inflammation plays an important role in the pathophysiology of STEMI and NSTEMI. A comprehensive cardiac biomarker panel enhances diagnostic accuracy and risk stratification, particularly when distinguishing between STEMI and NSTEMI. The biomarkers hs-TnI, CK-MB, NT-proBNP, TM, H-FABP, PTX-3 and Gal-3 offer complementary information when used together as a panel. Further research and validation are essential to establish standardized protocols for their widespread use. Full article

Background/Objectives: Pentraxin 3 (PTX3), a member of the pentraxin superfamily, plays diverse roles in immunity and inflammation. Its dual role in tumorigenesis, exhibiting both protumoral and antitumoral effects, has been the subject of conflicting reports. High PTX3 expression levels in serum and tumor tissues have been associated with poor prognosis in various malignancies, suggesting its potential as a prognostic biomarker. Through this meta-analysis, we aim to comprehensively assess the prognostic significance of PTX3 protein expression in human malignancies and evaluate its potential as a pan-cancer prognostic marker. Methods: A systematic literature search was conducted across the PubMed, Embase, Web of Science, MEDLINE, and Cochrane Library databases. Studies were included if they assessed the association between PTX3 protein expression and overall survival (OS) in cancer patients. Hazard ratios (HRs) were pooled using a random-effects model. Subgroup analyses were performed based on the method of PTX3 assessment, and publication bias was evaluated using Egger’s and Begg’s tests. Results: Nine studies encompassing 1215 patients were included in the analysis. High PTX3 expression was significantly associated with poorer OS (HR = 1.89, 95% CI = 1.55–2.32, p < 0.01) with no significant heterogeneity (I² = 0%). Subgroup analysis revealed consistent results across different assessment methods (immunohistochemistry: HR = 1.93, p < 0.01; immunoassay: HR = 1.86, p < 0.01). However, publication bias was detected (Egger’s test, p = 0.03). Conclusions: High PTX3 protein expression is associated with a poor prognosis in various malignancies, supporting its potential as a prognostic biomarker. Full article

Ovarian torsion (OT) is a rare gynaecological emergency that requires a prompt diagnosis for optimal patient management. To determine whether there were any biomarkers suitable for the non-invasive detection of OT, two independent reviewers performed systematic searches of five literature databases (PubMed, Medline, Scopus, Cochrane, and CINAHL) from inception until October 1st, 2023. Following the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines, the search included patients with OT that had quantified biomarker expression with no age, geographical location, publication date, language, or setting restrictions. Articles were excluded if OT was found incidentally, was based on qualitative analyses, or were not primary research articles. Full texts of 23 selected articles were assessed for risk of bias and quality assurance using a modified Newcastle–Ottawa Scale (NOS) for clinical studies and SYRCLE’s risk of bias tool for the assessment of pre-clinical (animal) studies. A total of 11 articles described studies on animals and all described serum biomarkers comparing results between OT versus a sham operation, a control group, or readings before and after OT. Ischaemia-modified albumhumin (IMA), serum D-dimer (s-DD), heat shock protein-70 (hsp-70), Pentraxin-3 (PTX3), and c-reactive protein (CRP) each showed the most promise, with p-values for the difference between OT and control groups achieving ≤ 0.001. In studies of humans, the biomarkers ranged from 16.4 to 92.3% sensitivity and 77–100% specificity. The most promising biomarkers for the early prediction of OT in patients included s-DD, interleukin-6 (IL-6), IMA, and tumour necrosis factor-alpha (TNF-α). Signal peptide, CUB domain, and EGF-like domain-containing 1 (SCUBE1) had a high specificity at 93.3%, second only to s-DD and a positive likelihood ratio (LR) > 10. IMA was the only other biomarker that also had a positive LR > 10, making it a promising diagnostic biomarker. The studies identified by this systematic literature review each analysed small patient groups but IMA, DD, and SCUBE1 nevertheless showed promise as serum biomarkers with a pooled LR > 10. However, further well-designed studies are needed to identify and evaluate individual markers or diagnostic panels to help clinicians manage this important organ-threatening condition. Full article

Pentraxin 3 [PTX3] is an acute-phase protein playing an important role in the regulation of the humoral arm of immune response. As one of the molecules from the conservative family of pentraxins, PTX3 is a soluble mediator involved in the transduction of pro-inflammatory signals between immunocompetent cells. Additionally, recognizing damage-associated molecular patterns (DAMPs) during tissue injury mediates wound healing; therefore, its concentration potentially correlates with the severity of fibrosis. The aim of our study was to evaluate the value of the PTX3 measurement as a phenotypic marker of the stenotic form of Crohn’s disease. The research covered 63 patients, 35 with the narrowing type (B2) and 28 with the inflammatory type (B2) of CD. The mean concentrations of PTX3 in the study were as follows: 3.06 ng/mL (95% CI: 1.27–6.99) for the B1 phenotype, 4.89 ng/mL (95% CI: 2.98–13.65) for the B2 phenotype, and 3.04 ng/mL (95% CI: 1.01–4.97) for the control group. PTX3 concentrations reached the highest values in the B2 group and the lowest in the control group. The differences between the B1 and B2 groups were statistically significant at p < 0.001. The presented studies indicate the potential role of PTX3 in the monitoring of tissue remodeling and the development of fibrosis in CD. Full article