Increased Tertiary Lymphoid Structures are Associated with Exaggerated Lung Tissue Damage in Smokers with Pulmonary Tuberculosis.

Yue ZHANG; Liang LI; Zi Kang SHENG; Ya Fei RAO; Xiang ZHU; Yu PANG; Meng Qiu GAO; Xiao Yan GAI; Yong Chang SUN

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Increased Tertiary Lymphoid Structures are Associated with Exaggerated Lung Tissue Damage in Smokers with Pulmonary Tuberculosis.

Author: Yue ZHANG ¹ ; Liang LI ² ; Zi Kang SHENG ¹ ; Ya Fei RAO ¹ ; Xiang ZHU ³ ; Yu PANG ⁴ ; Meng Qiu GAO ² ; Xiao Yan GAI ¹ ; Yong Chang SUN ¹
Author Information

1. Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing 100191, China.
2. Department of Tuberculosis, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing 101149, China.
3. Department of Pathology, Peking University Third Hospital, Beijing 100191, China.
4. Department of Bacteriology and Immunology, Beijing Chest Hospital, Capital Medical University/Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing 101149, China.
Publication Type:Journal Article
Keywords: Cigarette smoking; Pulmonary tertiary lymphoid structures; Tuberculosis
MeSH: Humans; Male; Tuberculosis, Pulmonary/immunology*; Middle Aged; Tertiary Lymphoid Structures/pathology*; Adult; Lung/pathology*; Smoking/adverse effects*; Smokers; Aged; Tomography, X-Ray Computed
From: Biomedical and Environmental Sciences 2025;38(7):810-818
CountryChina
Language:English
Abstract: OBJECTIVE:Cigarette smoking exacerbates the progression of pulmonary tuberculosis (TB). The role of tertiary lymphoid structures (TLS) in chronic lung diseases has gained attention; however, it remains unclear whether smoking-exacerbated lung damage in TB is associated with TLS. This study aimed to analyze the characteristics of pulmonary TLS in smokers with TB and to explore the possible role of TLS in smoking-related lung injury in TB.
METHODS:Lung tissues from 36 male patients (18 smokers and 18 non-smokers) who underwent surgical resection for pulmonary TB were included in this study. Pathological and immunohistological analyses were conducted to evaluate the quantity of TLS, and chest computed tomography (CT) was used to assess the severity of lung lesions. The correlation between the TLS quantity and TB lesion severity scores was analyzed. The immune cells and chemokines involved in TLS formation were also evaluated and compared between smokers and non-smokers.
RESULTS:Smoker patients with TB had significantly higher TLS than non-smokers ( P < 0.001). The TLS quantity in both the lung parenchyma and peribronchial regions correlated with TB lesion severity on chest CT (parenchyma: r = 0.5767; peribronchial: r = 0.7373; both P < 0.001). Immunohistochemical analysis showed increased B cells, T cells, and C-X-C motif chemokine ligand 13 (CXCL13) expression in smoker patients with TB ( P < 0.001).
CONCLUSION:Smoker TB patients exhibited increased pulmonary TLS, which was associated with exacerbated lung lesions on chest CT, suggesting that cigarette smoking may exacerbate lung damage by promoting TLS formation.