A variety of benign and malignant disorders affecting the trachea can theoretically be treated by simple resection and subsequent end-to-end anastomosis of remained trachea. Unfortunately, it is feasible only when the affected tracheal length does not exceed 50% of the entire length in adults and about 30% in children. Tracheal transplantation may be a treatment option for those patients, but still has many problems to be solved, such as immunological rejection, revascularization, infection and granulation tissue hyperplasia. This review focuses on how to use different methods to inhibit immunological rejection of tracheal transplantation, and current research progress of immunological rejection in tracheal allograft.
Tissue-engineered tracheal transplantation has been reported and the technique of decellularized scaffold's preparation is mature. Regeneration of epithelium, cartilage and blood vessel is particularly important during tracheal transplantation. With the increasing improvement on cell acquisition and cell culture, as well as the factor of auxesis and cell differentiation, tissue-engineered technique provided possibility and clinical value for regeneration of epithelium, cartilage and blood vessel. This review focuses on the improvement and prospect of regeneration of epithelium, cartilage and blood vessel during tracheal transplantation.
ObjectiveTo investigate that the TGF- beta/Smad signaling pathway mediated epithelial mesenchymal transition (EMT) in trachea stenosis after transplantation. Methods180-220 g male rats (n=50) were randomly divided into a control group and an experimental group. no surgical operation rats were in the control group. tracheal transplantation rats (Wistar-SD rat) were in the experimental group. Graft specimens were obtained in rats on 3,7,10,14,35,90 days after operation. HE staining is used to explain the fibrosis degree of tracheal stenosis. The fibrosis degree of tracheal stenosis was detected by calculating the fibrosis rate. Immunohistochemical staining was used to detect transplanted tracheal, such as EMT related molecules E-cadherin, vimentin, alpha-SMA expression, p-Smad2/3 expression and transcription factor ZEB1, Snail1 expression in tracheal graft specimens. ResultsHE staining showed that the tracheal fibrosis rate of the control group was 0.171±0.020, fibrosis rate was 0.537±0.013 (P < 0.01) on the third day after transplantation. The result of immunohistochemical staining showed that vimentin positive epithelial cells increased significantly (P < 0.05). E-cadherin expression significantly reduced (P < 0.05). Compared with the control group, TGF- beta expression increased (P < 0.05) in the experiment group. Compared with the control group, the expression of p-Smad2/3, the transcription factor ZEB1 and Snail1 significantly increased (P < 0.05) in the experiment group. ConclusionMechanism of tracheal stenosis may be due to EMT. At the same time, TGF- beta/Smad signaling pathway and transcription factor ZEB1, Snail1 may regulate the EMT.