Mucins are highly glycosylated proteins that form the structural basis of mucus and represent a key component of innate immunity at mucosal surfaces, particularly in the respiratory tract. Beyond their mechanical barrier function, mucins actively participate in pathogen trapping, regulation of mucociliary clearance, modulation of inflammatory responses, and maintenance of epithelial homeostasis. Dysregulation of mucin synthesis, composition, or transport contributes to mucus hypersecretion, impaired airway clearance, and chronic inflammation in respiratory diseases such as asthma, chronic obstructive pulmonary disease, and cystic fibrosis. This review summarizes current insights into mucin biology, including their biosynthesis, structure, classification, and regulation, with emphasis on the gel-forming mucins MUC5AC and MUC5B. The role of mucins in mechanical protection, host–pathogen interactions, control of inflammation, and coordination of innate immune responses is reviewed. Attention is given to the interplay between mucins, immune cells, and microbial communities in maintaining airway barrier integrity. The article further examines mucoactive therapeutic strategies aimed at restoring mucus barrier function. Expectorants, mucolytics, mucoregulators, and mucokinetic agents are reviewed with respect to their mechanisms of action and clinical relevance. Established drugs, including N-acetylcysteine, carbocysteine, dornase alfa, ambroxol, and hypertonic solutions, are considered alongside emerging molecular targets such as NF-κB-dependent regulation of mucin expression, calcium-activated chloride channels, MARCKS-mediated mucin exocytosis, purinergic signaling pathways, and NO/cGMP signaling. Non-pharmacological approaches, including airway clearance techniques and respiratory rehabilitation, are covered concisely. Conclusions: Overall, this review highlights mucins as dynamic regulators of innate immunity and underscores the need for mechanism-based, personalized mucoactive therapies to improve outcomes in chronic inflammatory airway diseases.

Background: Recurrent pregnancy loss (RPL) is frequently linked to antiphospholipid antibodies, yet many affected women are seronegative for the classical (Sydney) criteria antibodies. In a previously characterized cohort, an extended antiphospholipid antibody panel was positive in 79% of women with RPL, with the strongest associations for antibodies against prothrombin, annexin V and β₂-glycoprotein I. Whether this association reflects molecular endometrial dysfunction was unclear. Objective: To examine endometrial expression of ten decidualization- and inflammation-related genes in women with RPL, stratified by APL status, focusing on the dominant antibody specificity: anti-β₂-glycoprotein I. Methods: Thirty-nine women with RPL (≥2 losses), a subsample of a published 100-patient cohort, underwent mid-luteal Pipelle endometrial biopsy followed by RT-PCR for C4BPA, CXCL1, HAND2, HPRT1, IFNG, IL15, IL8 (CXCL8), MMP10, TNC and VEGFB. Antibodies were measured by antiphospholipid 10 Dot line immunoblot (Generic Assays, Germany). The analysis used Mann–Whitney U, Fisher’s exact test, Benjamini–Hochberg correction and ROC analysis. Results: Antibody prevalence in the subsample matched the parent cohort (Pearson r = 0.999). Of ten transcripts, only HAND2 showed a nominally significant reduction in APL+ women (median ΔCt −2.04 vs. −1.30; p = 0.037; rank-biserial r = −0.47); this signal did not survive Benjamini–Hochberg correction (q = 0.372). The signal was specific to anti-β₂GPI (p = 0.064; AUC 0.700), not to annexin V or prothrombin. A cut-off of HAND2 ΔCt ≤ −1.60 identified APL+ status with 73% sensitivity, 78% specificity and OR 9.62 (95% CI 1.64–56.4; p = 0.015). HAND2 clustered with IL15 (ρ = 0.65) and VEGFB (ρ = 0.70). Conclusions: Anti-β₂-glycoprotein I antibodies, the dominant APL specificity in RPL, are associated with reduced endometrial HAND2 expression. This exploratory data outline a candidate molecular pathway linking extended antiphospholipid serology to impaired endometrial receptivity.

Background: The Turkestan region is one of the regions with a high birth rate; therefore, analysis of the effectiveness of an early detection system for chromosomal abnormalities in this region is important for practical healthcare. Objective: To evaluate the diagnostic potential of first-trimester prenatal screening markers for identifying Down syndrome in the Turkestan region. Methods: A retrospective analytical study was conducted based on the analysis of medical records of pregnancies registered at perinatal centers in the Turkestan region between 2020 and 2025. The final analytical sample included 143 cases, comprising 71 pregnancies affected by Down syndrome and 72 randomly selected pregnancy cases included for comparative analysis. Maternal age, nuchal translucency (NT) thickness, pregnancy-associated plasma protein A (PAPP-A), free beta-human chorionic gonadotropin (free β-hCG), and fetal nasal bone hypoplasia/aplasia were assessed. Multivariable logistic regression and receiver operating characteristic (ROC) curve analysis were used. Results: In the multivariable analysis, maternal age (odds ratio [OR] = 1.16; p < 0.001) and NT (OR = 3.01; p = 0.001) showed statistically significant independent associations with Down syndrome. PAPP-A and free β-hCG did not demonstrate statistically significant independent associations in the multivariable model. The area under the ROC curve (AUC) was 0.855 for Model 1 and 0.903 for Model 2, which additionally included fetal nasal bone status. Conclusions: The exploratory models demonstrated good discriminatory performance within the present retrospective analytical sample. Maternal age and ultrasound markers showed the strongest associations with Down syndrome in the multivariable analysis. These models are not intended for direct clinical application at this stage and require external validation in independent and representative prenatal screening populations before their potential clinical utility can be assessed.