Search Results (263)

Precision fermentation (PF) yields single, well-characterized recombinant proteins, such as dairy and egg white proteins, at an industrial scale, and several products have reached the market. Numerous PF-derived proteins, including ovomucoid and β-lactoglobulin, are known allergens designed as exact structural copies of their native homologs; hence, assessments center on equivalence rather than novel hazards. Therefore, the current tiered scheme of allergen database comparison, digestibility testing, and serum immunoglobulin E binding assays is applicable. Nevertheless, residual host cell proteins, altered host-dependent enzymatic glycosylation, and process-related impurities render PF-derived products imperfect replicas, and thermal and high-pressure processing, enzymatic hydrolysis, and non-enzymatic glycation can modify linear or conformational epitopes, thereby reducing IgE binding or generating neoepitopes. Because these effects depend on structural attributes acquired during production, including folding stability, disulfide bonding, glycosylation, and proteolytic resistance, PF-derived proteins and native proteins may respond differently to identical processing. This review explores the molecular attributes acquired at each stage of PF production and the epitope changes originating during processing, reevaluates the current assessment scheme, and outlines considerations for a premarket safety framework reflecting realistic processing and consumption conditions. Full article

Severe COVID-19 is characterized by immune dysregulation, yet reliable biomarkers associated with adverse outcomes remain limited. Immunoglobulin G (IgG) N-glycosylation modulates antibody effector function and reflects the immune system’s inflammatory state. In this study, we investigated whether specific IgG glycosylation profiles are associated with COVID-19 severity, mortality, and clinical course in patients without known prior SARS-CoV-2 infection. Of the 806 admitted COVID-19 patients included in the study, 377 hospitalized patients were longitudinally monitored, and 2001 serum samples were analyzed. Significant alterations in IgG N-glycome composition were observed in patients with severe disease and those who died. The most prominent changes included increased agalactosylation and decreased mono- and digalactosylation, features associated with a more pro-inflammatory IgG glycosylation profile. Nosocomial infections were associated with a more pro-inflammatory IgG glycosylation profile. No statistically significant differences in IgG N-glycome composition were observed between vaccinated and unvaccinated patients, although the small number of vaccinated patients limited this analysis. The observed glycomic profiles likely reflect immune responses characteristic of the early phase of the COVID-19 pandemic. Whether similar glycosylation changes occur in other infectious or inflammatory diseases remains to be established. IgG glycosylation analysis holds promise for personalized risk stratification and early therapeutic intervention in COVID-19 and other severe infectious diseases. Full article

Background: The “hygiene hypothesis” and “farm effect” suggest that early-life microbial exposure protects against allergic diseases. Maternal low-dose lipopolysaccharide (LPS) exposure during pregnancy attenuates allergic airway inflammation in offspring, yet the underlying mechanisms remain incompletely understood. Immunoglobulin G (IgG) N-glycosylation critically regulates antibody effector functions and maternal–fetal immune transfer, but its role in transgenerational allergy protection is unknown. Objective: To investigate whether maternal low-dose LPS exposure modulates serum IgG N-glycan profiles in offspring and whether these glycomic changes are associated with protection against house dust mite (HDM)-induced allergic airway inflammation. Methods: Pregnant C57BL/6J mice received intraperitoneal LPS (7 µg/kg) or phosphate-buffered saline (PBS) on gestational day 15. Offspring were sensitized with HDM extract or PBS at 6 weeks of age. Serum IgG was purified using Protein G affinity chromatography, and N-glycans were released with PNGase F, labeled with 2-aminobenzamide, and analyzed by ultra-performance liquid chromatography (UPLC) with fluorescence detection. Twelve glycan peaks (GP1-GP12) and five derived traits (galactosylation, sialylation, monogalactosylation, digalactosylation, and bisecting glycans) were quantified. Results: HDM challenge significantly altered offspring IgG glycosylation, characterized by decreased digalactosylation, total galactosylation, and sialylation, consistent with inflammatory glycan signatures reported in other inflammatory diseases. Maternal LPS exposure alone induced similar glycomic shifts in offspring (decreased digalactosylation, total galactosylation, and sialylation). In HDM-challenged offspring, maternal LPS pretreatment produced a trend toward reduced lung inflammation without statistical significance; however, IgG glycan differences between LPS-HDM and PBS-HDM groups were non-significant. Conclusions: Maternal low-dose LPS exposure reduced offspring IgG galactosylation and sialylation. HDM challenge produced similar glycomic changes. Despite a trend toward attenuation of HDM-induced lung inflammation, maternal LPS did not restore IgG glycosylation. These findings provide first evidence linking prenatal immune stimulation to transgenerational IgG glycomic remodeling. Full article

Background: Conformational stability has been shown to modulate the immunogenicity of structural class 1 viral fusion glycoproteins, yet the relationship between influenza A hemagglutinin (HA) stability and antigenicity remains poorly understood. Methods: Here, we screened a panel of 21 A/Hawaii/70/2019 (H1N1) HA mutants for expression, cleavage, and acid and conformational stability in cells. Twelve mutant HA proteins expressed from transfected plasmid constructs that showed relatively robust expression compared to WT also exhibited either altered stability or glycosylation deletion. mRNA-LNPs were generated containing these 12 HAs, along with the wild-type (WT) HA, to investigate the mutational effects on mRNA-LNP vaccine immunogenicity and protection in mice. Hemagglutination inhibition, microneutralization, and total serum IgG ELISAs were performed using a panel of H1N1 antigens to evaluate humoral immune responses at 28 days post vaccination. The vaccinated mice were then subjected to lethal challenge with a forward-drifted H1N1 virus. Results: Most mutant HA candidates elicited WT-like serological responses and provided protection against challenge, although noticeable decreases in serological responses and, to a lesser extent, protection were observed, especially among G72K- and R109E-vaccinated mice. Of note, substitutions at position E107 enhanced total IgG responses against the HA stalk. Modest, but detectable, increases in antibody-dependent cellular cytotoxicity (ADCC) were also observed, particularly with E107R. Although substitution-specific differences in weight loss were found in E107-vaccinated mice challenged with a mouse-adapted Cal/09 virus, these differences were minor, and protection against the forward-drifted challenge virus and a heterologous PR8 challenge virus was no different from that in mice vaccinated with WT HA. Conclusions: These findings demonstrate the ability of specific substitutions to alter components of humoral immunity by shifting HA domain-specific antibody responses, which could prove useful in the design and development of HA vaccine antigens possessing optimized immunogenicity. Full article

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic metabolic disorder associated with an elevated risk of cardiovascular disease. Mac-2 binding protein glycosylation isomer (M2BPGi), a noninvasive serum biomarker of hepatic fibrosis, has also been linked to adverse metabolic and cardiovascular outcomes. However, the association between serum M2BPGi levels and subclinical coronary atherosclerosis in individuals with MASLD remains unclear. We investigated the association between serum M2BPGi levels and coronary artery calcium score (CACS), an established imaging marker of subclinical atherosclerosis, in individuals with MASLD. Methods: This retrospective cross-sectional study included 6514 adults with MASLD who underwent health screening examinations between 2020 and 2025. Participants were categorized into quartiles according to serum M2BPGi levels: Q1 (<0.48), Q2 (0.48–0.61), Q3 (0.62–0.80), and Q4 (≥0.81). Coronary artery calcification (CAC) was defined as CACS > 0. Multivariable logistic regression analysis was performed after adjustment for age, sex, smoking status, liver enzymes, adiposity, dysglycemia, blood pressure, and lipid profile. Multivariable ordinal logistic regression analysis was additionally performed to evaluate the association between M2BPGi levels and CAC severity. Results: The prevalence of CAC increased progressively across M2BPGi quartiles (39.4%, 45.3%, 48.5%, and 57.4% for Q1–Q4, respectively; p < 0.001). In multivariable logistic regression analysis, participants in the highest M2BPGi quartile had significantly higher odds of CAC presence than those in the lowest quartile (OR, 1.32; 95% CI, 1.10–1.58; p = 0.0035). Higher M2BPGi quartiles were also independently associated with greater CAC severity in multivariable ordinal logistic regression analysis (OR, 1.33; 95% CI, 1.13–1.57; p = 0.0007 for Q4 vs. Q1). Conclusions: Higher serum M2BPGi levels were independently associated with both the presence and severity of CAC in individuals with MASLD. These findings suggest that M2BPGi may serve as a potential biomarker for identifying individuals with MASLD at increased risk of subclinical atherosclerosis and may complement conventional cardiovascular risk assessment. Full article

Outbreaks of avian infectious bronchitis virus (IBV) often occur in vaccinated flocks. The antibody-dependent enhancement (ADE) has been proposed as a potential mechanism underlying coronavirus vaccine failure. However, this hypothesis has yet to be substantiated in flocks. This study demonstrates ADE occurrence in IBV (gamacoronavirus) in vitro and in vivo. Using the SPF chicken host model, primary infection with an O-glycosylation-modified attenuated strain enhanced pathogenesis upon secondary homologous/heterologous virulent challenge, increasing morbidity/mortality (≥30%), pathological lesions, and viral loads. Notably, sequentially attenuated infections also induced ADE, suggesting live attenuated vaccine risks. The immune serum raised against the O-glycosylation-modified attenuated strain was also pre-mixed with the challenge strain, and the mixtures were then inoculated into target cells, non-susceptible macrophage cells, or a co-culture of both cell types. The serum-virus complexes replicated poorly in macrophages, yet immune cells amplified the expression of inflammatory factors and ADE-mediated viral replication in target cells, indicating a significant promoting role of immune cells in this process. The concentrations of complement component C3 and neutralizing antibodies in the immune serum were also measured, and results showed that the induction of this ADE is associated with high complement component C3 and low neutralizing antibody titers. These findings highlight risks for vaccines and antibody-based therapeutic strategies of coronavirus infection. Full article

Background: Steatotic liver disease (SLD) and sarcopenia are lifestyle-related conditions for which prevention is critical. The phase angle, which is derived from impedance, reactance, and resistance values obtained via bioelectrical impedance analysis, has emerged as a potential marker of sarcopenia. Additionally, amino acids have been implicated in the pathogenesis of both SLD and sarcopenia. This epidemiological study investigated the association between SLD and sarcopenia in a general population cohort. Methods: This cross-sectional study included 281 participants with metabolic dysfunction-associated steatotic liver disease (MASLD), 72 with metabolic alcohol-associated liver disease (MetALD), and 54 with alcohol-associated liver disease (ALD). Associations between phase angle, Mac-2-binding protein glycosylation isomer (M2BPGi) as a marker of liver fibrosis, and serum amino acid levels were analyzed. Results: The phase angle was significantly higher in the MetALD group than in the MASLD and ALD groups. Multivariate analysis identified MASLD as an independent risk factor for a low phase angle compared with MetALD. M2BPGi levels were lower in MetALD than in MASLD, and M2BPGi showed a negative correlation with the phase angle. Furthermore, MetALD was characterized by lower serine and glutamine levels than MASLD, with serine demonstrating a negative correlation with the phase angle. Conclusions: Although the possibility of residual confounding factors cannot be excluded, the present study suggests that phase angle may serve as a sensitive marker for the early decline in muscle mass in patients with SLD, comparable to grip strength and skeletal muscle mass index. Full article

Ring chromosome 14 (RC14) syndrome is an ultra-rare disorder characterized by drug-resistant epilepsy, intellectual disabilities, autism, and recurrent infections, suggesting a possible underlying immune dysregulation. We analyzed immunoglobulin G (IgG) N-glycosylation profiles in six RC14 patients and compared them with age-matched healthy controls using ultra-high-performance liquid chromatography (UHPLC) coupled with fluorescence detection (FLR) and high-resolution electrospray ionization mass spectrometry (ESI-MS). Patients showed decreased galactosylation and sialylation, resembling pro-inflammatory patterns observed in autoimmune diseases. These alterations were not observed in total serum glycoproteins, indicating a selective effect on IgG. One patient treated with intravenous immunoglobulin (IVIG) showed clinical improvement, which led us to investigate causality. Full article

Introduction: Intermittent fasting (IF) is becoming increasingly popular as a method of weight management, but it is unknown whether it affects plasticiser intake with resultant changes in glycaemic control in diabetes and vitamin D (VitD) levels; therefore, this study was undertaken in a cohort of control and type-2 diabetic (T2D) subjects during Ramadan time-restricted feeding (TRF). Methods: In T2D subjects (n = 19) and controls (n = 31) undertaking TRF, 24 h urinary levels of phthalate metabolites, bisphenols and serum VitD were determined pre- and post-TRF by liquid chromatography–tandem mass spectrometry (LC-MS/MS). Anthropometric data and glycosylated haemoglobin (HbA1c) were measured. Results: T2D subjects were older (52 versus 36.73 years, p < 0.001), and had higher BMI (36.54 versus 27.67 kg/m², p < 0.001), body weight (101.77 versus 80.36 kg, p < 0.001), and HbA1c (8.38 versus 5.46%, p < 0.001) compared to controls, while VitD levels did not differ (60.43 versus 63.95 nmol/L, p > 0.05). Post-TRF, HbA1c was unchanged in T2D subjects and there was no difference in weight, BMI or VitD. Increased mono-iso-butyl phthalate (MiBP) in T2D subjects (10 versus 6.1 ng/mL, p = 0.001) and mono-n-butyl phthalate (MnBP) in T2D subjects (37 versus 13 ng/mL, p = 0.018) and controls (8.3 versus 5.4 ng/mL, p = 0.007) were observed post-TRF; however, significance was lost after adjusting for baseline differences in age, BMI, and HbA1c using a general linear model (GLM) repeated-measures ANOVA. Despite having no median differences in DEHP (di-2-ethylhexyl phthalate) metabolites pre- and post-TRF, analyses revealed a significant time × HbA1c interaction for [mono(2-ethyl-5-carboxypentyl) phthalate, MECPP: F(1,42) = 4.79, p = 0.03, mono(2-ethyl-5-hydroxyhexyl) phthalate, MEHHP: F(1,42) = 8.56, p = 0.006, mono(2-ethylhexyl) phthalate, MEHP: F(1,42) = 4.64, p = 0.03 and mono(2-ethyl-5-oxohexyl) phthalate, MEOHP: F(1,42) = 8.19, p = 0.007] and time × group interactions [MEHHP: F(1,42) = 14.27, p < 0.001, MEHP: F(1,42) = 6.35, p = 0.01 and MEOHP: F(1,42) = 10.30, p = 0.003]. Estimated marginal means (adjusted for age, BMI, HbA1c, and VitD) further confirmed higher concentrations of DEHP metabolites [MECPP, MEHHP, MEHP, and MEOHP] in T2D participants over time compared with controls. Additionally, monomethyl phthalate (MMP) trajectories were significantly influenced by the time × group interaction (F(1,42) = 4.28, p = 0.04), with post-TRF elevations observed in T2D subjects. Vitamin D status was observed to modify mono(3-carboxypropyl) phthalate (MCPP) and MEP trajectories over time. Conclusion: Ramadan TRF is associated with changes in plasticiser metabolite levels, with estimated increased levels in T2D subjects versus healthy controls. Metabolite levels were influenced by HbA1c and vitamin D, though BMI was not observed to be a contributing factor. Full article

Wilson’s disease (WD) is an autosomal recessive disorder of copper metabolism caused by ATP7B mutations, characterized by hepatic copper accumulation and multisystem involvement. Several rare inherited and acquired conditions can closely mimic WD, posing diagnostic challenges and the risk of inappropriate therapy. By examining neuroimaging patterns and distinguishing between diagnostic criteria, this narrative review provides a comprehensive synthesis of WD-mimicking disorders, emphasizing their molecular mechanisms, clinical phenotypes, and biochemical features. WD-mimicking disorders encompass ATP7A-related neurodegenerations (Menkes disease, occipital horn syndrome, X-linked distal hereditary motor neuropathy), MEDNIK syndrome, Huppke–Brendel syndrome, aceruloplasminemia, congenital disorders of glycosylation, primary familial intrahepatic cholestasis type 3, and acquired copper deficiency syndromes. Mechanisms include systemic copper deficiency, impaired intracellular trafficking, defective ceruloplasmin biosynthesis, secondary hepatic copper accumulation, and abnormal glycosylation. Clinical features range from neurodevelopmental delay, movement disorders, and hepatic dysfunction to dermatologic, hematologic, and connective-tissue abnormalities. Biochemical profiles may overlap with WD, particularly low serum ceruloplasmin and total copper, altered urinary copper excretion, and elevated hepatic copper in some disorders. Neuroimaging and genetic testing provide critical discriminative value. Management is largely supportive, with disease-specific therapies available in selected conditions, such as subcutaneous copper in Menkes disease or monosaccharide supplementation in certain congenital disorders of glycosylation subtypes. Accurate differentiation between WD and WD-mimicking disorders requires careful integration of clinical, biochemical, imaging, and molecular data. Recognition of distinctive features and understanding underlying pathophysiology are essential to avoid misdiagnosis and inappropriate anti-copper therapy, optimize management, and improve patient outcomes. Full article

Protein glycosylation plays a pivotal role in breast cancer biology, influencing cell proliferation, adhesion, migration, and immune evasion. Aberrant N- and O-glycosylation are hallmarks of neoplastic transformation and serve as sensitive indicators of disease progression. This review aims to characterize glycoprotein biomarkers in breast cancer identified using Matrix-Assisted Laser Desorption/Ionization (MALDI) Mass Spectrometry. We examine specific glycosylation alterations—including hypersialylation, fucosylation, and truncated O-glycans—across different molecular subtypes (Luminal A/B, HER2-positive, TNBC) and assess their diagnostic and prognostic potential. Methodologically, the review contrasts MALDI-based profiling and Imaging Mass Spectrometry (MALDI-IMS) with other proteomic techniques, highlighting MALDI’s advantages in throughput and spatial resolution alongside its technical limitations. Furthermore, we discuss emerging frontiers in the field, such as the shift from whole-serum analysis to “liquid biopsy” components (e.g., extracellular vesicles). Ultimately, we argue that implementing quantitative glycoproteomics is essential for advancing personalized oncology. Full article

This study evaluated the effects of the dietary administration of a glycosylated form of active vitamin D (calcitriol, 1,25(OH)₂D₃) combined with ursolic acid (UA) and oleanolic acid (OA) triterpenes on sow health and productivity. Twenty-four third-parity Landrace × Large White sows were allocated at day 108 of gestation into three groups: a control group receiving 1800 IU/kg of vitamin D₃, and two treatment groups receiving the control diet supplemented with either 0.64 µg/kg (ACTD1) or 0.96 µg/kg (ACTD2) of glycosylated 1,25(OH)₂D₃ plus 140 or 210 µg/kg of UA + OA (4:1 ratio), respectively. Diets were administered from late gestation through the end of lactation. Farrowing duration, sow body weight, backfat thickness, and litter growth were recorded. Blood samples collected at key physiological stages were analyzed for pro-inflammatory cytokines, mineral homeostasis, endocrine markers, and serum proteome. Farrowing time was reduced in both treatment groups compared with the control (p < 0.05). Treated sows exhibited lower backfat thickness at the end of lactation and improved litter weights at farrowing, after cross-fostering, and at weaning (p < 0.05). Plasma pro-inflammatory cytokines (TNF-α, IL-1α, and IL-1β) were reduced at the end of lactation in ACTD1 and ACTD2 sows, with TNF-α and IL-1β already decreased after farrowing (p < 0.05). Treated sows also displayed decreased plasma parathormone concentrations at the end of lactation, along with increased circulating 1,25(OH)₂D₃ and calcium concentrations after farrowing and at lactation end (p < 0.05), while plasma phosphate levels remained unchanged. Proteomic analysis supported the systemic availability of the supplemented compounds and their involvement in metabolic and inflammatory pathways rather than calcium transport or vitamin D binding mechanisms. Overall, this nutritional strategy influenced the immune modulation while maintaining mineral homeostasis via modest endocrine adaptations. Larger-scale trials are warranted to confirm these results and to evaluate their practical applicability under commercial production conditions. Full article

Background: Lupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE), characterised by unpredictable outcomes due to the absence of reliable biomarkers. This hypothesis-generating study aimed to evaluate whether changes in the N-glycosylation of IgG, C3, AGP, and the serum proteins over one year of treatment correlate with clinical and histological features of LN and predict renal outcomes. Methods: Serum samples from 19 treatment-naïve patients with LN were collected at baseline and 12 months post-treatment, in conjunction with per-protocol repeat kidney biopsy. IgG (Fc, Fab, and total), C3, AGP, and total serum glycoproteins were isolated and analysed as either released N-glycans or N-glycopeptides using high-throughput glycomic approaches. Clinical and histological data were obtained at both time points, along with assessments of clinical and histological response at 12 months and long-term renal function. Results: In total, we identified 24/243 increased N-glycosylation traits (2 total IgG, 5 IgG Fc, 7 IgG Fab, 5 serum glycoproteins, 4 AGP, and 1 C3) and 10/243 decreased N-glycosylation traits (7 total IgG, 2 IgG Fc, 1 IgG Fab) following treatment. Baseline AGP IORMIF1N5H6S2F1 showed a positive correlation with eGFR both at baseline (r = 0.64, p = 0.005) and at 12 months (r = 0.51, p = 0.032). Among AGP N-glycosylation traits, IVORMI1N7H8S3 (r = 0.66, p = 0.002; r = 0.48, p = 0.041, respectively), VORMI1N8H9S4 (r = 0.51, p = 0.029; r = 0.49, p = 0.038, respectively), and VORMI1N8H9S4F1 (r = 0.48, p = 0.039; r = 0.49, p = 0.034, respectively) significantly correlated with activity index (AI) at baseline and at 12 months. Presence of cellular crescents at baseline positively correlated with three AGP N-glycosylation traits: IORMISORMIIA1N4H5S2 (r = 0.49, p = 0.036), VORMII1N5H6S3F1 (r = 0.63, p = 0.006), and VORMII1N4H5S2 (r = 0.48, p = 0.046). Total serum N-glycan (structure) N5H4F1 at 12 months was associated with both clinical and histological response to treatment. Delta of total serum N-glycan structure N5H5S1 was independently associated with poor long-term outcome. Conclusions: This study suggests that glycosylation changes over one year of treatment are associated with specific clinical and histological features and both short- and long-term renal outcomes in LN. Given the small cohort size, results should be considered hypothesis-generating warranting further investigation in independent cohorts. Full article

The main objective of this study was to preliminarily analyze the major flavonoid and phenolic acid components of the ethanolic extract of Gerbera delavayi Franch (E-GDF), and to evaluate its anti-inflammatory and antioxidant properties in lipopolysaccharide (LPS)-stimulated murine macrophage RAW264.7 cells and systemic inflammation mouse models. Results indicated that E-GDF was rich in flavonoids (16.35 ± 0.19 mg RT/g d.w. Plant Material) and polyphenolic compounds (36.15 ± 0.20 mg GAE/g d.w. Plant Material). LC-MS analysis of E-GDF revealed that its major flavonoid components included kaempferol glycosides, luteolin, and their glycosylated derivatives, while its phenolic acids were predominantly chlorogenic acid, caffeic acid, ferulic acid, and their corresponding glycosides. E-GDF exhibited good antioxidant activities, including the scavenging of DPPH, ABTS, ^•OH, and O₂^•− radicals. E-GDF treatment significantly inhibited the production of ROS and inflammatory mediators (NO, IL-6, TNF-α) in LPS-stimulated macrophages (RAW 264.7), while concurrently down-regulating the mRNA expression of COX-2, IL-1β, Casp1, and GSDMD-1. In addition, in vivo experiments revealed that E-GDF treatment effectively reduced the serum LPS, AST levels, as well as hepatic TNF-α, IL-6 levels in mice with LPS-induced acute liver injury. Furthermore, E-GDF significantly ameliorated LPS-induced liver pathological damage. These results provide a basis for G. delavayi as a potential antioxidant, anti-inflammatory, and hepatoprotective herbal medicine. Full article

Endometriosis (EM) is a chronic inflammatory disease characterized by the growth of endometrial-like tissue outside the uterus, yet its molecular mechanisms remain poorly understood. This study investigated the expression of mucins (MUC1, MUC2, MUC5AC, MUC6, MUC16) and their O-glycans in endometriotic lesions, given their roles in epithelial protection, adhesion, and immune modulation. Using immunohistochemistry, Western blotting, lectin profiling, histochemical staining, and transcriptomic analysis, we compared mucin levels and glycosylation patterns in eutopic and ectopic tissues from women with and without endometriosis and measured mucin-derived tumor markers in serum (CA 125/MUC16 and CA 15-3/MUC1) and peritoneal fluid (CA 125/MUC16). The results showed significant upregulation of all mucins in EM biopsies, with increased MUC1 transcript levels, while MUC6 and MUC16 protein levels did not always align with transcripts. Yet, tumor markers CA 125 and CA 15-3 showed no significant differences between groups. Looking at mucin distribution in biopsies of peritoneal (pEM), deep infiltrating and ovarian EM, MUC1 was significantly overexpressed in lesions of all EM forms, while MUC5AC was significantly elevated in pEM. Lectin analysis revealed specific glycan changes, including elevated core-1 O-glycans and α(1-2)-linked fucosylation, while sialylation remained unchanged. These findings demonstrate consistent mucin dysregulation and glycan alterations, implicating their roles in epithelial adhesion, immune evasion, and lesion persistence. Mucin biology thus emerges as a promising target for diagnostic and therapeutic strategies in endometriosis. Full article