如PGE2和NO［10］. 通过这些因子的作用来募集、激活炎症性细胞从而调节机体的炎症过程，尤其是PAR2的激活可多方面参与肺部炎症的发生和发展. 我们也曾经用胰蛋白酶和PAR2激动肽激活肺上皮细胞，诱导其产生了趋化性细胞因子MCP1［11］， 但其释放的机制及肺上皮细胞表达PARs的生理和病理生理意义还有待进一步的探讨.

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