Email Alert | RSS

Chinese Journal of Antituberculosis ›› 2025, Vol. 47 ›› Issue (4): 513-519.doi: 10.19982/j.issn.1000-6621.20240445

• Review Articles • Previous Articles     Next Articles

Research progresses on the role and mechanism of calcium-binding protein S100A12 and neutrophil extracellular trap formation in lung injury of severe pulmonary tuberculosis patients

Song Yunlin1, Buzukela Abuduaini1, Wang Guirong2, Zhang Jiyuan3, Lu Xiaobo4()   

  1. 1Department of Intensive Care Unit, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830013, China
    2Department of Laboratory Medicine, Beijing Chest Hospital, Capital Medical University, Beijing 101149, China
    3First Clinical Institute of Xinjiang Medical University, Urumqi 830013, China
    4Center of Infection, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830013, China
  • Received:2024-10-08 Online:2025-04-10 Published:2025-04-02
  • Contact: Lu Xiaobo, Email: xjykdluxiaobo@126.com
  • Supported by:
    National Natural Science Foundation of China(82360381);State Key Laboratory of Pathogenesis, Prevention, Treatment of Central Asian High Incidence Diseases Fund of China(SKL-HIDCA-2021-JH13)

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

CLC Number: