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Journal of Tuberculosis and Lung Disease ›› 2022, Vol. 3 ›› Issue (2): 137-141.doi: 10.19983/j.issn.2096-8493.20210135

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Mechanism of rapamycin target protein/autophagy signaling pathway in tuberculous tracheal bronchial stenosis

ZHOU Lei, LUO Li, LU Zhi-bin, DING Yan, XIAO Yang-bao   

  1. Endoscopy Center, Hu’nan Chest Hospital, Changsha 410013, China
  • Received:2021-10-21 Online:2022-06-30 Published:2022-04-18
  • Supported by:
    Natural Science Foundation of Changsha City(kq2014187);Clinical Medical Technology Innovation Guidance Project of Hu’nan Province(2020SK50701)

Abstract: Objective: To investigate the expression and role of rapamycin target protein/autophagy (mTOR/autophagy) signaling pathway in tuberculous tracheobronchial stenosis.Methods: A total of 10 patients with pulmonary Aspergillus who needed surgical resection in Hu’nan Chest Hospital from June 2020 to June 2021 were collected as the normal control group. And 27 patients with tuberculous tracheal bronchial stenosis over the same period were collected, including 13 patients with tuberculous hyperplasia (tuberculous hyperplasia group) and 14 patients with tuberculous scar (tuberculous scar group). The tracheal bronchial tissue of each group was collected. Immunohistochemistry was used to detect mTOR, autophagy-related protein LC3, transform growth factor-β1 (TGF-β1), collagen 1 (COL-1) protein expression, Western blotting was used to detect mTOR and the expression of LC3 prote, and PCR was used to detect the expression of TGF-β1 and COL-1 mRNA.Results: (1) By immunohistochemistry and western blotting, mTOR protein expressions in tuberculous hyperplasia group and tuberculous scar group were significantly higher than those in the normal control group ((0.074±0.008) vs. (0.028±0.004), t=0.045, P<0.001; (3.397±0.312) vs. (0.028±0.004), t=2.419, P<0.001; (0.041±0.004) vs. (0.980±0.091), t=0.013, P=0.036; (2.261±0.175) vs. (0.980±0.091), t=1.283, P<0.001). (2) By immunohistochemistry and and mRNA, TGF-β1 protein expressions in tuberculous hyperplasia group,and the tuberculous scar group were (0.062±0.008) and (0.039±0.006), (6.930±0.606) and (3.350±0.582), respectively; which were significantly higher than those in the normal control group (immunohistochemistry, 0.019±0.006, t=0.043, P<0.001 and t=0.020, P=0.009, respectively; mRNA, 1.000±0.000, t=5.930, P<0.001 and t=2.353, P=0.001, respectively). (3) In tuberculous hyperplasia group and the tuberculous scar group, COL-1 protein expressions were (0.056±0.009) and (0.032±0.003) by immunohistochemistry and (6.803±1.110) and (2.730±0.547) by mRNA, which were significantly higher than those in the normal control group ((0.018±0.002) and (1.000±0.000), t=0.038, P<0.001; t=0.013, P=0.026; t=0.013, P=0.026; t=5.803, P<0.001; t=1.730, P=0.025, respectively). (4) By immunohistochemistry and Western blotting, LC3 protein expressions in the tuberculous hyperplasia group andin the tuberculous scar group were (0.023±0.007) and (0.046±0.008), (0.140±0.030) and (0.236±0.030), which were significantly lower than those in the normal control group ((0.070±0.005) and (0.320±0.049), t=0.047, P<0.001; t=0.023, P=0.009; t=0.179, P<0.001; t=0.083, P=0.034).Conclusion: Tuberculous tracheobronchial stenosis may be related to fibrosis caused by overexpression of TGF-β1 and COL-1 after activation of mTOR/autophagy signaling pathway.

Key words: Tuberculous, Bronchi, Autophagy, Fibrosis

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