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<p>Understanding the molecular changes that occur during the development of tracheal stenosis (TS) may enable the establishment of pharmacological treatments based on its pathophysiology. This study evaluated the expression of TNFα, IL-4, IL-10, TGF-β1, and type I collagen (Coll-I) during each phase of wound healing in an experimental model of TS. Twenty rabbits were divided into three groups: Group I (control), Group II (Sham), and Group III (TS). Tracheoscopy was performed weekly for 30 days, and tracheal biopsies were obtained for histological evaluation and analysis of mRNA and protein expression of IL-4, TNFα, IL-10, TGF-β1, and Coll-I during TS development. Group II not develop TS or molecular alterations. Group III developed TS, inflammation and fibrosis at both the macroscopic and microscopic compared with Groups I and II (<i>p</i> &lt; 0.001, Friedman test). Gene and protein expression of TNFα, TGF-β1, and IL-10 increased from day 2 to day 30, while Coll-I expression increased from day 14 onward (<i>p</i> &lt; 0.001, RM-ANOVA). IL-4 expression was not detected during TS development. We conclude that development of TS is associated with increased gene and protein expression of TNFα, TGF-β1, and IL-10 from the inflammatory phase, promoting Coll-I expression from the proliferative phase through to TS formation.</p>

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Cytokine and profibrotic gene expression during tracheal stenosis development in an experimental model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月3日

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  • Mariana Silva-Martínez,
  • J. Raúl Olmos-Zuñiga,
  • José S. López-González,
  • Miriam Galicia-Velasco,
  • Miguel Gaxiola-Gaxiola,
  • Elizabeth Morales-Salinas,
  • Dolores Aguilar-Cazares,
  • Pablo Gomes-da Silva de Rosenzweig,
  • Teresa Aguirre-Pérez

摘要

Understanding the molecular changes that occur during the development of tracheal stenosis (TS) may enable the establishment of pharmacological treatments based on its pathophysiology. This study evaluated the expression of TNFα, IL-4, IL-10, TGF-β1, and type I collagen (Coll-I) during each phase of wound healing in an experimental model of TS. Twenty rabbits were divided into three groups: Group I (control), Group II (Sham), and Group III (TS). Tracheoscopy was performed weekly for 30 days, and tracheal biopsies were obtained for histological evaluation and analysis of mRNA and protein expression of IL-4, TNFα, IL-10, TGF-β1, and Coll-I during TS development. Group II not develop TS or molecular alterations. Group III developed TS, inflammation and fibrosis at both the macroscopic and microscopic compared with Groups I and II (p < 0.001, Friedman test). Gene and protein expression of TNFα, TGF-β1, and IL-10 increased from day 2 to day 30, while Coll-I expression increased from day 14 onward (p < 0.001, RM-ANOVA). IL-4 expression was not detected during TS development. We conclude that development of TS is associated with increased gene and protein expression of TNFα, TGF-β1, and IL-10 from the inflammatory phase, promoting Coll-I expression from the proliferative phase through to TS formation.