Background: Stigma associated with tuberculosis (TB) continues to undermine patient well-being, treatment adherence, and public health goals and objectives. This study aims to systematically review the literature to identify and synthesize TB stigma reduction interventions published between 2015 and 2025. Methods: Following the PRISMA guidelines, we conducted a comprehensive literature search across PubMed, Scopus, Science Direct, ProQuest, and Google Scholar. Eligible studies included those with qualitative, quantitative, and mixed-methods designs that focused on interventions related to TB-related stigma. We categorized the studies into three groups: (1) intervention development studies, (2) TB treatment programs with stigma reduction outcomes, (3) stigma-specific interventions. Data extraction and quality appraisal were conducted independently by two reviewers using the Mixed Methods Appraisal Tool (MMAT). Results: A total of 15 studies met the inclusion criteria. Five studies focused on co-developing stigma interventions, which incorporated multi-level and multicomponent strategies targeting internalized, enacted, anticipated, and intersectional stigma. Two studies assessed TB treatment-related interventions (e.g., home-based care, digital adherence tools) with incidental stigma reduction effects. The remaining seven studies implemented stigma-targeted interventions, including educational programs, video-based therapy, peer-led support, and anti-self-stigma toolkits. Interventions addressed stigma across individual, interpersonal, institutional, community, and policy levels. Conclusions: This review highlights the evolution and diversification of TB stigma interventions over the past decade. While earlier interventions emphasized education and support, recent strategies increasingly integrate peer leadership, digital platforms, and socio-ecological frameworks. The findings underscore the need for comprehensive, contextually grounded interventions that reflect the lived experiences of people affected by TB.

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.