Clinical significance of serum transforming growth factor‑β1 and procollagen type I N‑propeptide in post‑tuberculosis tracheobronchial stenosis

Abstract

Non-invasive strategies for monitoring posttuberculosis (TB) tracheobronchial stenosis (PTTS) are clinically important but currently lacking. Transforming growth factor-β1 (TGF-β1) and procollagen type I N-propeptide (PINP) have been identified as markers of fibrosis. The present study aimed to investigate the clinical significance of serum TGF-β1 and PINP in PTTS. Serum samples were collected from 119 patients with tracheobronchial TB after the condition was treated for at least 6 months (59 patients with airway stenosis and 60 patients with no stenosis). Serum TGF-β1 and PINP levels were measured using ELISA and compared between the groups. Relationships between serum TGF-β1 and PINP levels and clinical characteristics, interventional bronchoscopy and outcomes of airway stenosis were analysed. The correlation between TGF-β1 and PINP, and their diagnostic efficacy for airway stenosis were also analysed. The TGF-β1 and PINP levels in the airway stenosis group were higher than those in the non-stenosis group. Furthermore, airway stenosis with atelectasis or mucus plugging was associated with higher TGF-β1 levels, and airway stenosis with atelectasis, mucus plugging, right main bronchus stenosis or severe airway tracheal stenosis was associated with higher PINP levels. In addition, TGF-β1 and PINP levels increased after interventional bronchoscopy therapy and airway stenosis with recurrent stenosis was associated with higher baseline levels of both markers. Finally, TGF-β1 levels were positively correlated with PINP levels in patients with airway stenosis. The area under the receiver operating characteristic curve of TGF-β1 and PINP for distinguishing airway stenosis from non-stenosis cases was 0.824 (95% CI: 0.748-0.900) and 0.863 (95% CI: 0.796-0.930), respectively. Therefore, TGF-β1 and PINP are potential biomarkers that may be useful for diagnosing and monitoring PTTS.

miR-34c-5p inhibited fibroblast proliferation, differentiation and epithelial-mesenchymal transition in benign airway stenosis via MDMX/p53 pathway

“…Given that brosis plays an important part in the genesis and development of BAS, the inhibition of brosis can alleviate traumatic tracheal stenosis (Enyuan, et al,2018;Xiao, et al,2020;Wu, et al,2021). Fibrosis is hallmarked by the aggregation of myo broblasts, the proliferation of collagen and the deposition of extracellular matrices.…”

“…Previous studies have suggested that the genesis and progression of BAS are caused by airway mucosal in ammation, mucosal abnormal hyperplasia, epithelial-mesenchymal transition (EMT) and brous scar formation under the in uence of various factors such as infection, trauma and hypoxia, which leads to stenosis (Shi, et al,2021;Wu, et al,2021;Wei, et al,2023). Owing to the action of cytokines like transforming growth factor-β1 (TGF-β1) following BAS, tracheobronchial broblasts aberrantly aggregate and proliferate, which results in the proliferation of granulation tissues and brosis (Wu, et al,2021;Xu, et al,2021). Given that the treatment of BAS is challenging due to a paucity of speci c drugs and treatments, taking effective measures during the early stage of tracheal injury is warranted to alleviate airway injury and the pathological repair process (Enyuan, et al,2018).…”

The upregulation and SNP of Transforming growth factor-β1 in COPD patients with or without pulmonary fibrosis

“…For example, the Pulmonary hypertension (PH), as a common complication for COPD, has been reported that "TC" genotype of TRPV1 SNP rs3744683 was a protective factor for PH in COPD patients compared with the genotype of "TT" [41,42]. SNP at + 869 site of TGF-β1 has been reported in various diseases such as hepatocellular carcinoma and tracheobronchial stenosis, but no consistent conclusion in COPD [43,44]. Here, we detected SNPs of TGF-β1 in 98 COPD patients and 90 healthy volunteers, and no differences in age, gender, BMI and smoking index was found between the COPD group and the control group in our study.…”

miR-34c-5p inhibited fibroblast proliferation, differentiation and epithelial-mesenchymal transition in benign airway stenosis via MDMX/p53 pathway

“…Previous studies have suggested that the genesis and progression of BAS are caused by airway mucosal inflammation, mucosal abnormal hyperplasia, epithelial-mesenchymal transition (EMT) and fibrous scar formation under the influence of various factors, such as infection, trauma and hypoxia, which leads to stenosis (Shi, et al 2021 ; Wu, et al 2021 ; Wei, et al 2023 ). Owing to the action of cytokines like transforming growth factor-β1 (TGF-β1) following BAS, tracheobronchial fibroblasts aberrantly aggregate and proliferate, which results in the proliferation of granulation tissues and fibrosis (Wu, et al 2021 ; Xu, et al 2021 ). Given that the treatment of BAS is challenging due to a paucity of specific drugs and treatments, it is warranted to take effective measures during the early stage of tracheal injury to alleviate airway injury and the pathological repair process (Enyuan, et al 2018 ).…”