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观察哮喘豚鼠模型嗜酸细胞和淋巴细胞与肺微血管内皮细胞的粘附率 ;探讨肺微血管内皮细胞在哮喘豚鼠模型血清孵育下的功能变化及炎症细胞与其粘附的分子基础。设豚鼠哮喘模型及对照组观察分离的外周血淋巴细胞和嗜酸细胞与内皮细胞的粘附率。RT PCR法测定内皮细胞VCAM 1及eotaxinmRNA的表达强度 ;EMSA法测定NF κB和AP 1的DNA结合活性。与对照组血清孵育相比 ,肺微血管内皮细胞在模型组血清刺激下 :①与两组外周血淋巴细胞及仅与模型组嗜酸细胞的粘附率显著升高 (P <0 0 1) ;②VCAM 1和eotaxinmRNA表达量显著增多 (P <0 0 1或P <0 0 5 ) ,NF κB和AP 1的DNA结合活性也显著升高 (P <0 0 1)。肺微血管内皮细胞可被哮喘模型血清激活 ,使粘附分子、趋化因子及核转录因子的合成和分泌显著增多 ,从而显著提高其与炎症细胞的粘附率。嗜酸细胞的粘附需其自身及内皮细胞两者激活。肺微血管内皮细胞活化及NF kB和AP 1的DNA结合活性增高在哮喘发病中可能起重要作用。
The adhesion rate of eosinophils and lymphocytes to pulmonary microvascular endothelial cells in asthmatic guinea pig models was observed. The functional changes of pulmonary microvascular endothelial cells incubated with serum of guinea pigs with asthma and the molecular basis of adhesion of inflammatory cells to them were investigated. Set guinea pig asthma model and control group observed peripheral blood lymphocytes and eosinophils and endothelial cell adhesion rate. The expression of VCAM 1 and eotaxin mRNA in endothelial cells was determined by RT-PCR. The DNA-binding activity of NF κB and AP 1 was determined by EMSA. Compared with the control group, the level of adhesion of pulmonary microvascular endothelial cells to the model group was significantly increased (P <0.01) with that of the two groups of peripheral blood lymphocytes and the model group alone. ② The expressions of VCAM 1 and eotaxin mRNA were significantly increased (P <0.01 or P <0.05), and the DNA binding activities of NF κB and AP 1 were also significantly increased (P <0.01). Pulmonary microvascular endothelial cells can be activated by the serum of asthmatic model, resulting in a significant increase in the synthesis and secretion of adhesion molecules, chemokines and nuclear transcription factors, thereby significantly improving their adherence to inflammatory cells. Eosinophil adhesion requires activation by both itself and endothelial cells. The activation of pulmonary microvascular endothelial cells and the increased DNA binding activity of NF kB and AP 1 may play an important role in the pathogenesis of asthma.