关键词: 中性粒细胞, 结核, 肺, 肺损伤, 作用机制

Abstract:

The incidence and mortality rates of severe pulmonary tuberculosis remain persistently high. However, the disease face significant diagnostic challenges due to the lack of specificity in clinical signs and symptoms during the early stages of the disease. Furthermore, the therapeutic of severe tuberculosis has become being complicated due to multiple factors, such as drug-drug interactions, drug-disease interactions, and adverse drug reactions, all of which together pose new challenges for tuberculosis prevention and control. The pathogenesis of severe tuberculosis involves a complex interaction between the host and Mycobacterium tuberculosis, yet the mechanism of pathogenesis remains incompletely understood. Recent studies indicate that calcium-binding protein S100A12 (hereafter “S100A12”) and neutrophil extracellular traps (NETs) are essential in developing severe tuberculosis. S100A12 drives the formation of NETs, and serve as a key protein mediating the physiopathological effects of NETs. S100A12 contributes to the mechanism of lung function injury in severe tuberculosis patients through regulation the release of immune cells, inflammatory cytokine release, and their interaction. Nevertheless, the regulatory mechanisms of S100A12 and NETs in severe tuberculosis pathogenesis has not been fully elucidated. Given this, this review aims to comprehensively summarize the research progress on S100A12 and NETs in severe tuberculosis and their potential molecular mechanisms to provide a new scientific basis and innovative insights for exploring therapeutic strategies for severe tuberculosis.

Key words: Neutrophils, Tuberculosis, pulmonary, Lung injury, Mechanism of action