Cell-mediated immune responses of beta-glucan on the pathogenesis of chronic tuberculosis infection

Tuberculosis (TB) has become the most common reason for contagious disease-related fatalities globally. Due to the estimated 8.6 million fresh tuberculosis infections and 1.6 million fatalities, this disease is a leading contributor to mortality globally. Tuberculosis refers to a condition in which individuals are infected with M. tuberculosis but do not exhibit clinical symptoms and are generally not capable of transmitting the disease. β-glucan, a biologically active polysaccharide known for its immunomodulatory properties, has recently gained attention for its role in regulating metabolic and immune responses. Through mechanisms such as trained immunity, macrophage activation, and cytokine modulation, β-glucan may enhance host defense against M. tuberculosis and influence susceptibility to tuberculosis disease progression. Hence, this study focuses on the underlying relationship of beta-glucan involved in Tuberculosis infection, along with their physiopathology, and, clinical implications including the immunological responses.