摘要
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。
The metaplasia of goblet cells and mucous hypersecretion are the major pathologic changes of chronic airway inflammation. The metaplasia of goblet cells in tracheales-bronchial trees is the primary resource of mucous proteins and form the structural bases for mucous hypersecretion. Goblet cells usually secrete mucinSAC. Infection, inflammation, immunoreactive meditors, proteinase intrinsic or extrinsic compounds etc can induce the transcription and participate the posttranscriptional regulation of mucin5AC , moreover epidemical growth factor receptor signalling is the main pathway inducing the MUC5AC gene expression. Different stimulations can induce the goblet cells hyperp Airway epithelium such as ciliated cells and Clara cells can trans-differentiated into sumed that IL-13 and epidemical growth factor receptor are involved in goblet cells lasia and metaplasia. goblet cells. It is asmetaplasia, whereas Bcl-2 is concerned with maintaining the survival of metaplastic goblet cell.
出处
《国际病理科学与临床杂志》
CAS
2008年第1期59-63,共5页
Journal of International Pathology and Clinical Medicine