Search Results (3,551)

Background/Objective: With rising per capita sugar consumption, skin glycation-related issues including dullness, homeostasis disruption and accelerated wrinkling have gained widespread attention. However, globally standardized and rigorous evaluation criteria for anti-glycation efficacy remain lacking. This study aimed to establish stage-specific glycation injury cell models and elucidate the stage-dependent molecular mechanisms of glycation-induced fibroblast damage, providing a standardized reference for anti-glycation efficacy assessment. Methods: Three glycation injury models were constructed in human foreskin fibroblasts (HFF-1): early-stage (glucose-induced), intermediate-stage (glyoxal-induced), and late-stage (advanced glycation end products (AGEs)-induced). Core biomarkers including Nε-(carboxymethyl)lysine (CML), collagen type I (Col I) and elastin (ELN) were used to optimize modeling conditions via Cell Counting Kit-8 (CCK-8) and enzyme-linked immunosorbent assay (ELISA). Untargeted metabolomics based on ultra-high-performance liquid chromatography (UHPLC)-Q Exactive Orbitrap was applied to identify differential metabolites and perturbed pathways, following Metabolomics Standards Initiative (MSI) Level 2 identification criteria. Results: Optimal conditions were determined as 50 mmol/L glucose for 48 h, 0.5 mmol/L glyoxal for 48 h, and 200 μg/mL AGEs for 24 h. A total of 319, 34 and 148 differential metabolites were identified in the three groups, respectively. Six key pathways were significantly perturbed. Early and intermediate models shared similar mechanisms (purine metabolism disturbance), while the late model showed distinct alterations in pyrimidine, nicotinate, arachidonic acid and steroid hormone metabolism. Conclusions: Three stable stage-specific glycation models were successfully established in HFF-1 cells. Significant differences in metabolic profiles and mechanisms exist across the three stages, providing a rational basis for model selection and theoretical support for anti-glycation efficacy evaluation. Full article

Epidermal hyperinnervation is a major cause of intractable itch in barrier dysfunction conditions such as atopic dermatitis. Keratinocyte-derived semaphorin 3A (Sema3A) suppresses epidermal hyperinnervation, but its expression is markedly reduced in barrier-disrupted skin. Although konjac ceramide (kCer) has been reported to act as a Sema3A-like ligand, the mechanisms by which it regulates Sema3A expression in keratinocytes remain unclear. Normal human epidermal keratinocytes (NHEKs) were treated with kCer, konjac glucosylceramide (kGlcCer), or C24 ceramide. Sema3A mRNA and protein levels were assessed by quantitative real-time PCR and enzyme-linked immunosorbent assay, respectively. The involvement of intracellular signaling was examined using mitogen-activated protein kinase (MAPK) inhibitors, activator protein-1 (AP-1) inhibitors, retinoic acid-related orphan receptor alpha (RORα) inverse agonists, and siRNAs targeting c-Jun, c-Fos, and RORα. kCer induced Sema3A expression in NHEKs more potently than kGlcCer or C24 ceramide and promoted Sema3A protein secretion. Pharmacological inhibition or genetic knockdown of MEK1/2, JNK, AP-1 components, or RORα significantly attenuated kCer-induced Sema3A expression, indicating involvement of the MAPK/AP-1 signaling axis and RORα. kCer upregulates Sema3A expression in human keratinocytes through MAPK/AP-1 signaling and RORα, suggesting it may represent a promising antipruritic agent for epidermal hyperinnervation associated with skin barrier dysfunction. Full article

Background/Objectives: Polycystic ovary syndrome (PCOS) is a common endocrine disorder associated with chronic low-grade inflammation. Interleukin-39 (IL-39), a newly identified cytokine, has been implicated in immune regulation; however, its role in PCOS remains unclear. This study aimed to evaluate serum IL-39 levels in patients with PCOS and its potential as an adjunctive inflammatory biomarker candidate. Methods: This case–control study included 44 patients with PCOS diagnosed according to the Rotterdam criteria and 44 age-matched in the control group. Serum IL-39 levels were measured using enzyme-linked immunosorbent assay (ELISA). Clinical and laboratory parameters were recorded. Group comparisons were performed using appropriate parametric and non-parametric tests. Correlation analysis was conducted using Spearman’s coefficient. Multivariable logistic regression analysis was performed to identify independent predictors of PCOS. Receiver operating characteristic (ROC) analysis was used to assess discriminative performance. Results: Serum IL-39 levels were significantly higher in the PCOS group compared to control group (p < 0.001). No significant correlations were observed between IL-39 and other clinical or laboratory parameters. In multivariable analysis, IL-39 was independently associated with PCOS. ROC analysis showed that IL-39 had moderate discriminative ability (AUC = 0.74), with 68% sensitivity and 70% specificity. The combined model including IL-39, body mass index (BMI), luteinizing hormone (LH), and age demonstrated improved performance (AUC = 0.78), with higher sensitivity (86%) and negative predictive value (81%). Conclusions: IL-39 levels are elevated in PCOS and may represent a potential adjunctive inflammatory biomarker candidate. Its diagnostic performance improves when combined with other clinical parameters, supporting a multivariable approach in PCOS evaluation. Full article

Mucosal immunity, including antibodies like immunoglobulin A (IgA), function as the body’s first line of defense in the respiratory tract, particularly against viruses. An anti-rS protein IgA enzyme-linked immunosorbent assay (ELISA) was developed using the Omicron XBB.1.5 subvariant of SARS-CoV-2 and was validated to demonstrate the suitability of the method for testing saliva from SARS-CoV-2 vaccine clinical trials. This assay successfully met acceptance criteria for inter-/intra-assay precision, specificity, selectivity, linearity, lower/upper limits of quantitation, and assay robustness. The IgA in saliva was stable for up to 7 freeze/thaw cycles, for up to 48 h at 24 °C, up to 7 days at 4 °C, up to 3 weeks at −20 °C, and up to 1 year at −80 °C. After validation using Omicron XBB.1.5 rS protein, cross-reactivity was demonstrated with the SARS-CoV-2 variant JN.1. This validated IgA assay can be a valuable tool to assess mucosal IgA levels in SARS-CoV-2 clinical trials. Full article

Alzheimer’s disease (AD) is increasingly recognized as a biological continuum characterized by early neuropathological and molecular changes that precede the onset of clinical symptoms. Fluid biomarkers have transformed the diagnostic landscape by enabling the in vivo detection of core AD pathologies, particularly amyloid-β deposition and tau-related neurodegeneration. Despite the rapid expansion of candidate biomarkers, however, only a limited number have successfully translated into clinical practice. Discovery-phase approaches, primarily driven by mass spectrometry-based proteomics, enable the unbiased identification of novel biomarker candidates across multiple biological pathways. Research-phase methods, including immunoassays such as enzyme-linked immunosorbent assay (ELISA), electrochemiluminescence immunoassays (ECLIA), microfluidic platforms, and ultrasensitive technologies such as single-molecule array (SIMOA), support analytical and clinical validation in well-characterized cohorts. Clinical implementation has been advanced by fully automated platforms, including Lumipulse and Elecsys, which have obtained regulatory approval for cerebrospinal fluid biomarkers and, more recently, blood-based biomarkers. These developments represent a paradigm shift toward minimally invasive and scalable diagnostic strategies that may reduce dependence on neuroimaging techniques. Nevertheless, major challenges remain, including assay standardization, inter-platform variability, demonstration of clinical utility, and barriers to widespread clinical adoption. This review provides a comprehensive overview of analytical methods used to measure AD fluid biomarkers in cerebrospinal fluid and plasma, structured according to the biomarker development pipeline from discovery to clinical implementation. Overall, the review highlights a fit-for-purpose approach to biomarker development and emphasizes the complementary roles of diverse analytical technologies across the different phases of biomarker translation. Full article

Objective: In this study, Dehydroepiandrosterone (DHEA-induced Polycystic Ovary Syndrome (PCOS) mice were used as models to evaluate the improvement effect of Vitexin (Vit) on ovarian fibrosis and explore the mechanism of action of the NR4A1/NLRP3 signaling pathway. Method: Sixty 4-week-old female ICR mice of the same batch number were selected and their systems were divided into 6 groups (n = 10): normal (Control, Ctrl) group, model (Polycystic Ovary Syndrome, PCOS) group, treatment (Vitexin, The Vit group, normal NR4A1 gene silencing group (Ctrl NR4A1^-/-), NR4A1 gene silencing model group (PCOS NR4A1^-/-), and NR4A1 gene silencing treatment group (Vit NR4A1^-/-). Silencing gene modeling was performed by tail vein injection of adeno-associated virus (serotype AAV-8), and the mouse genotypes were detected by qRT-PCR technology 14 days after injection. After the genotype was determined, the PCOS group and the PCOS NR4A1^-/- group were administered dehydroepandrosterone (6 mg/100 g/d) by gavage for 28 consecutive days for modeling, while the Vit group and the Vit NR4A1^-/- group were treated with dehydroepandrosterone + vitexin (10 mg/kg/d) by gavage for 28 consecutive days. All mice were raised with pure water and regular maintenance food. After 4 weeks of drug intervention, the mice were euthanized and samples were collected. The pathological changes in ovarian tissue were observed by H&E staining, and the degree of ovarian tissue fibrosis was observed by Masson staining. The levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) in mouse serum were detected by biochemical kits. The levels of inflammatory factors (IL-1β, IL-6, IL-18, TNF-α) in mouse serum were determined by enzyme-linked immunosorbent assay. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect oxidative kinase (Gsta4, Prdx3, Mgst1, Gpx3, Gsr), inflammatory factors (Nlrp3, Caspase-1, Asc, Il-1β, Il-18, Tnf-α) and fibrotic pathway-related genes (Tgf-β1, Smad3, Collagen1, CTGF, α-SMA, Mmp-13, and β-catenin) in ovarian tissues. The levels of inflammatory factors (NLRP3, Caspase-1, ASC, IL-1β, IL-18, TNF-α, IκBα) and fibrosis in mice were determined by Western blot method, and statistical description and analysis were performed using SPSS software. Result: In the wild-type genotype group, compared with the PCOS group, Vit treatment could effectively regulate the metabolic abnormalities of PCOS mice, including inhibiting excessive weight gain, restoring normal glucose tolerance, and reducing body fat content. After Vit treatment, the levels of MDA, TC, TG, LDL, IL-1β, IL-6, IL-18 and TNF-α in the serum of PCOS mice were significantly reduced, while the levels of SOD and HDL in the serum of PCOS mice were increased. The staining results indicated that Vit treatment could significantly inhibit the process of ovarian fibrosis in PCOS mice. The results of WB and PCR demonstrated that after Vit gavage treatment in mice, inflammatory and fibrotic factors such as Nlrp3, Caspase-1, Asc, Il-1β, Il-18, Tgf-β1, Smad3, Collagen1, CTGF, and α-SMA in ovarian tissues could be significantly down-regulated, and the fibrotic level of ovarian tissues could be reduced. Among the same measurement indicators, the silenced NR4A1 group showed a certain degree of increase compared with the wild genotype group, but there was no significant difference. Conclusions: Vit intervention can restore the sex hormone levels and follicular development in ovarian tissues of PCOS mice, regulate reproductive endocrine disorders and abnormal lipid metabolism levels, and regulate the expression of Collagen I, a-SMA and CTGF in the ovaries by inhibiting the NR4A1/NLRP3 signaling pathway, thereby improving the ovarian fibrosis level of PCOS mice. It is suggested that it may play a key role in the treatment of PCOS and the prevention and delay of its long-term complications. Full article

Epimedium is a traditional Chinese tonic used to tonify the kidneys, enhance sexual function, and strengthen muscles and bones. However, the potential effects of Epimedium on the semen quality of Bama boars remain incompletely elucidated. The objective of this study was to evaluate the effects of dietary Epimedium ultrafine powder (EP) supplementation on the semen quality of Bama boars and to explore the underlying mechanisms. The objective of this study was to evaluate the effects of dietary EP supplementation on the semen quality of Bama boars and to explore the underlying mechanisms. Eighteen healthy, sexually mature adult male Bama boars were randomly divided into three groups (n = 6) and fed either a basal diet (CON) or the basal diet supplemented with 0.3% (EP3) or 0.5% (EP5) Epimedium ultrafine powder for five weeks. This study employed enzyme-linked immunosorbent assay (ELISA), 16S RNA gene sequencing, non-targeted metabolomics (CON and EP5), and Spearman correlation analysis, among other methods. The results indicated that dietary Epimedium (0.3% and 0.5%) increased the levels of serum TP, FSH, and SOD and decreased the abnormal sperm rate and the levels of serum TBA, TNF-α, and IL-6. Among them, adding 0.5% Epimedium in the diet increased sperm motility and the levels of serum T, LH, and IgG. 16S rRNA gene sequencing analysis revealed that both 0.3% and 0.5% Epimedium supplementation reduced the abundance of Streptococcus. Specifically, the 0.3% dose decreased Prevotella abundance, while the 0.5% dose reduced Escherichia-Shigella abundance. PICRUSt2 analysis revealed that the pathways of phenylalanine, butanoate, biotin, and arachidonic acid metabolism were significantly enriched in the Epimedium group. A non-targeted metabolomics analysis identified that indole-3-acrylic acid, DL-tryptophan, 2-hydroxyphenylalanine, and propionylcarnitine showed significant upregulation after Epimedium supplementation. Spearman correlation analysis indicated that Streptococcus was negatively correlated with sperm motility and serum-related parameters (TP, T, LH, IgM, and IgG). Streptococcus and Escherichia-Shigella were negatively correlated with indole-3-acrylic acid, DL-tryptophan, and biotin. In conclusion, Epimedium has a positive impact on the seminal quality, reproductive hormones, and immune–antioxidant levels of Bama boars by regulating the composition and metabolites of the intestinal microbiota. Full article

Objectives: An infectious trigger can initiate a systemic inflammatory response, which in turn activates immune cells and causes the release of various mediators. Local mediators, such as resolvin D1 (RvD1), actively interact with immune cells to promote the resolution of inflammation. This study aimed to determine the impact of RvD1 on the inflammatory response mediated by monocytes in response to LPS. Methods: To investigate the mechanism by which RvD1 affects the monocyte-mediated inflammatory response to LPS, human THP-1 monocytic cells were treated with LPS, RvD1, or vehicle for 24 h. Inflammatory cytokines, interleukin-1β (IL-1β) and tumor necrosis factor (TNF-α), were measured using enzyme-linked immunosorbent assay (ELISA). RNA sequencing (RNA-seq) was used to identify differentially expressed genes (DEGs). The NF-κB and MAPK p38 signaling pathways were validated using real-time quantitative PCR (RT-qPCR) and Western blotting (WB). Results: RvD1 diminished the levels of IL-1β and TNF-α in LPS-induced inflammation. RvD1 significantly enhanced the mRNA expression of CREB, NRF2, and BCL-2. In addition, RvD1 significantly decreased the mRNA expression of CASP3. RvD1 regulated the inflammatory process in human monocytic THP-1 cells via the NF-κB p65 (MyD88, p65) and p38 MAPK signaling pathways (p38, BCL-2) and further suppressed the expression of apoptotic factors (PI3K, caspase-3). Conclusions: RvD1 has been shown to exert pro-resolving effects by regulating the anti-apoptotic gene BCL-2 and activating the NF-κB p65 and MAPK p38 signaling pathways. Full article

Introduction: Orthobiologics such as Platelet-Rich Plasma (PRP) and Injectable Platelet-Rich Fibrin (i-PRF) have emerged as promising tools in regenerative medicine. However, the lack of methodological standardization and the still limited comparative characterization between these products represent significant barriers to their optimized clinical application. This comparative laboratory study aimed to characterize and differentiate PRP and i-PRF, focusing on their cellular composition, obtained volume, and total Platelet-Derived Growth Factor (PDGF-BB) content. Materials and Methods: This study was conducted with 34 individuals meeting standard blood donation criteria. Peripheral blood samples were collected from all participants. PRP was obtained using a modified double-spin centrifugation protocol, whereas i-PRF was prepared using a modified low-speed centrifugation technique. Cellularity (platelet and leukocyte counts), final produced volume, and total PDGF-BB content were assessed using complete blood count analysis and an enzyme-linked immunosorbent assay (ELISA), respectively. Statistical analysis was performed using Linear Mixed Models (LMMs). Results: Both protocols resulted in significant increases in platelet and leukocyte concentrations compared to baseline values. PRP showed significantly higher platelet and leukocyte concentrations compared with i-PRF, as well as markedly higher PDGF-BB levels. In contrast, i-PRF yielded a substantially greater final volume and enabled a higher absolute delivery of total leukocytes, whereas PRP delivered a greater absolute number of platelets. In exploratory analyses, female sex, the presence of comorbidities, and increased abdominal circumference were associated with variations in product volume and cellular composition. Discussion: These findings indicate that PRP and i-PRF exhibit distinct biological profiles in terms of cellularity, volume, and total PDGF-BB content. Whether these laboratory differences translate into distinct clinical outcomes remains unknown. The results should therefore be viewed as hypothesis-generating: they suggest that PRP and i-PRF may not be interchangeable, and that future randomized clinical trials are needed to define product-specific indications based on the target tissue and desired biological mechanism. Full article

Background: Diabetic foot infection (DFI) is a serious complication of diabetes mellitus associated with chronic inflammation, impaired wound healing, endothelial dysfunction, and oxidative stress. Sirtuin (SIRT) signaling and the apelinergic system have been implicated in these processes. This study aimed to evaluate serum SIRT1, SIRT3, apelin, and elabela (ELA) levels in patients with DFI and to examine their cross-sectional associations with clinical indicators, inflammatory markers, osteomyelitis, and glycemic control. Methods: This cross-sectional study included 47 patients with DFI and 42 healthy controls. Serum biomarker levels were measured using enzyme-linked immunosorbent assay (ELISA). Clinical and laboratory data, including the infection component of the PEDIS classification, were recorded. Group comparisons, Spearman correlation analyses, receiver operating characteristic (ROC) curve analysis, and logistic regression were performed. Results: Patients with DFI exhibited higher inflammatory and glycemic markers and lower hemoglobin and lipid levels compared with controls (p < 0.05). Serum SIRT1, SIRT3, apelin, and ELA levels were significantly lower in the DFI group and showed inverse correlations with HbA1c, PEDIS stage, disease duration, osteomyelitis, and inflammatory markers. Among these biomarkers, SIRT1 showed the highest discriminative ability within this cohort (AUC = 0.820). In an exploratory multivariable model, age and SIRT1 were independently associated with the presence of DFI. Conclusions: Serum SIRT1, SIRT3, apelin, and ELA levels were lower in patients with DFI and were associated with clinical and biochemical indicators of disease burden. Among these biomarkers, SIRT1 demonstrated the strongest discriminative ability within this cohort. These findings suggest that sirtuin signaling and the apelinergic system may be relevant in the biological context of DFI; however, they should be interpreted cautiously. The observed differences may reflect not only DFI but also underlying diabetes, glycemic burden, age, and systemic inflammation. Further prospective studies including appropriate diabetic comparator groups are required to clarify the clinical relevance and potential utility of these biomarkers. Full article

Canine leishmaniosis can cause a variety of signs. The detailed assessment of disease severity lacks a standardized, validated scoring system. This prospective study aimed to develop and validate an objective scoring system (“Total Leishmania Score”, TLS) combining clinical and laboratory parameters for monitoring dogs with Leishmania (L.) infantum infection. Fifty-one L. infantum-infected dogs were examined every 3 months over 1 year. Evaluations included physical examination, complete blood count, serum biochemistry, urinalysis including protein-to-creatinine ratio, and a L. infantum antibody Enzyme-Linked Immunosorbent Assay (ELISA). At each visit, 2 veterinarians applied the TLS, comprising 10 clinical and 8 laboratory parameters graded on a four-point severity scale (0–3) and weighted according to their estimated prognostic relevance values. Interobserver agreement was assessed using intraclass correlation coefficients (ICCs) and Bland–Altman analysis. Longitudinal changes were analyzed using robust linear mixed-effects models. In total, 488 scores were evaluated. Interobserver reliability was excellent (ICC: 0.998; CI_95%: 0.997–0.998; p < 0.001) with no relevant systematic bias. Reliability remained excellent at all time points (ICC: 0.996–0.999). The TLS increased significantly before and during relapse (p < 0.001) and decreased significantly within 3 months after leishmanicidal treatment (p < 0.001). The TLS demonstrated excellent reliability and responsiveness, supporting its use for the longitudinal monitoring of dogs with leishmaniosis. Full article

Circulating immune complexes (CICs) are frequently detected in the sera of patients with myeloperoxidase (MPO)–antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (MPO-AAGN) and their role in activating the classical complement pathway has been suggested. However, the precise composition and functional characteristics of CICs in AAGN remain poorly understood. We analyzed serum samples from four patients with MPO-AAGN and confirmed CICs. An immunoadsorbent column was prepared using a monoclonal rheumatoid factor antibody that binds to CICs, enabling extraction via immunoprecipitation. CICs were analyzed by Western blotting to detect MPO and IgG. Their capacity to activate complement was assessed in vitro by measuring complement activation products using the enzyme-linked immunosorbent assay following incubation with normal human serum. Western blotting revealed distinct bands for both MPO and IgG in all samples. Incubation of extracted CICs with normal human serum resulted in elevated levels of complement activation products, including C5a and C5b-9. This increase was completely inhibited by the addition of EDTA or EGTA. In conclusion, CICs in the serum of patients with MPO-AAGN contain MPO and IgG (presumably MPO-ANCA). These CICs can activate the complement system, likely through the classical pathway. Our findings support the hypothesis that CICs composed of MPO and MPO-ANCA contribute to complement activation via the classical pathway and play a significant role in AAGN pathogenesis. Full article

Background/Objectives: Coronary artery disease is a chronic inflammatory disorder characterized by progressive atherosclerosis and heterogeneous clinical presentations ranging from acute coronary events to stable ischemic conditions. Galectin-3 is a β-galactoside-binding lectin involved in inflammatory responses, fibrosis, and tissue remodeling, and has been investigated as a potential biomarker in cardiovascular diseases. However, its diagnostic significance across different clinical stages of coronary artery disease remains unclear. Methods: This prospective study included 180 participants who underwent coronary angiography and were classified into three groups: control (n = 60), acute coronary syndrome (n = 60), and chronic coronary syndrome (n = 60). Serum Galectin-3 concentrations were measured using an enzyme-linked immunosorbent assay. Group comparisons were performed using non-parametric statistical tests. Correlation analysis, receiver operating characteristic curve analysis, and multivariable logistic regression were conducted to evaluate diagnostic performance and independent associations. Results: Galectin-3 concentrations were significantly higher in both acute coronary syndrome and chronic coronary syndrome groups compared with the control group (p < 0.001), whereas no significant difference was observed between the two disease groups. Receiver operating characteristic analysis demonstrated limited diagnostic performance for identifying acute coronary syndrome (area under the curve 0.617, sensitivity 96.7%, specificity 43.3%, p = 0.027) and poor diagnostic performance for chronic coronary syndrome (area under the curve 0.541, sensitivity 91.7%, specificity 30.0%, p = 0.436). In multivariable analysis, Galectin-3 was not identified as an independent predictor of either clinical condition. Age and smoking were independently associated with acute coronary syndrome, while age and male sex were independently associated with chronic coronary syndrome. Conclusions: Galectin-3 levels are elevated in patients with coronary artery disease and appear to reflect the inflammatory burden associated with atherosclerosis. However, its diagnostic discrimination between different clinical stages of coronary artery disease remains limited. Larger prospective studies are required to clarify its clinical value. Full article

Background/Objectives: Primary Sjögren’s disease is a systemic autoimmune disease characterized by chronic inflammation of exocrine glands and heterogeneous clinical manifestations. There remains a need for objective, non-invasive biomarkers that reflect local glandular involvement and disease-related immune activity. Methods: This observational cross-sectional case–control study included 34 patients fulfilling the 2016 ACR/EULAR classification criteria for primary Sjögren’s disease and 34 healthy controls between December 2024 and February 2025. Unstimulated whole-saliva samples were collected in the morning using the passive drool method, and salivary galectin-9 concentrations were measured via the enzyme-linked immunosorbent assay. Disease activity and symptom burden were assessed using validated indices, and receiver operating characteristic analysis was performed to evaluate discriminatory performance. Results: Salivary galectin-9 levels were significantly higher in patients with primary Sjögren’s disease compared with healthy controls. However, no significant associations were observed between salivary galectin-9 levels and disease activity scores after correction for multiple comparisons, nor with patient-reported symptoms, autoantibody profiles, Schirmer test results, or minor salivary gland biopsy findings. Salivary galectin-9 demonstrated limited discriminative ability between patients and controls. Conclusions: Salivary galectin-9 levels were elevated in primary Sjögren’s disease and may be associated with local glandular immune processes. Further prospective studies are needed to determine their clinical relevance. Full article

Background: Asthma is a heterogeneous chronic inflammatory airway disease characterized by recurrent exacerbations and variable airflow limitation. Epithelial-derived alarmins, particularly interleukin-33 (IL-33) and its receptor ST2, play key roles in type 2 inflammation. The soluble form of ST2 (sST2) acts as a decoy receptor regulating IL-33 signaling. Vitamin D is an important immunomodulator influencing airway inflammation, but its interaction with the IL-33/ST2 pathway remains unclear. Objective: To evaluate the association between serum IL-33, sST2, and 25-hydroxyvitamin D [25(OH)D] levels with asthma severity and exacerbation status, and to assess their potential as clinical biomarkers. Methods: This study enrolled 52 adult asthma patients (27 experiencing exacerbation and 25 in remission) and 28 healthy controls. Serum levels of IL-33 and sST2 were measured using enzyme-linked immunosorbent assays, while 25(OH)D concentrations were determined via electrochemiluminescence immunoassay. Results: Serum sST2 levels were significantly higher and 25(OH)D levels significantly lower in asthma patients compared with controls (p < 0.000 for both). Serum IL-33 levels did not differ significantly between groups (p > 0.05). During exacerbation, sST2 levels were markedly elevated compared with remission (p < 0.001), whereas vitamin D levels were significantly reduced (p = 0.038). A significant negative correlation was identified between sST2 and 25(OH)D (r = −0.333, p = 0.016). Conclusions: The presence of asthma and the severity of exacerbations are associated with elevated circulating sST2 levels and reduced vitamin D levels. These findings suggest a regulatory interaction between vitamin D and the IL-33/ST2 axis in airway inflammation and indicate that targeting this axis could be a potential therapeutic strategy. Full article