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杯状细胞化生及黏液过度分泌是气道慢性炎症的重要病理改变,气管支气管树杯状细胞化生是黏蛋白的主要来源也是黏液过度分泌的结构基础。杯状细胞主要分泌黏蛋白5AC。感染因素、炎症/免疫反应介质、蛋白酶、内、外化合物等均可诱导黏蛋白5AC转录并可能参与转录后水平的分泌调控,表皮生长因子受体信号转导通路是诱导MUC5AC基因表达的主要通路。不同刺激物诱导杯状细胞增生和化生,气道上皮细胞如纤毛细胞和Clara细胞等可转分化成杯状细胞,目前认为杯状细胞化生的关键介导环节涉及白介素-13和表皮生长因子受体,而Bcl-2则与化生杯状细胞寿命的维持有关。
Goblet cell metaplasia and mucus hypersecretion are important pathological changes of chronic airway inflammation. Tracheal bronchial goblet cell metaplasia is the main source of mucin and the structural basis of mucus hypersecretion. Goblet cells mainly release mucin 5AC. Infection factors, inflammatory / immune response mediators, proteases, internal and external compounds all induced mucin 5AC transcription and may be involved in the post-transcriptional regulation of secretion. EGFR signal transduction pathway is the main pathway to induce MUC5AC gene expression . Different stimuli induce goblet cell proliferation and metaplasia. Airway epithelial cells such as ciliary cells and Clara cells can be differentiated into goblet cells. At present, the key mediators of goblet cell metaplasia are interleukin-13 and epidermal growth Factor receptor, while Bcl-2 is associated with the maintenance of metaplastic goblet cell longevity.