铜绿假单胞菌(PA)极易在呼吸道定植与感染，巨噬细胞(Mφ)自噬在抵抗PA感染的过程中发挥着重要作用。Pec1蛋白是PA分泌的毒力因子，有关其影响宿主Mφ自噬作用的相关研究未见文献报道。我们前期研究发现：Pec1蛋白刺激Mφ后，自噬水平显著下降，胞内细菌数显著增多；且Pec1刺激Mφ后p38 MAPK 磷酸化显著增高，miR-155及miR-199a-5p 显著下调；此外，刺激后Mφ的PI3K p85表达、Akt及mTOR磷酸化皆显著上升；生物信息学预测显示，PI3K p85亚基是miR-155及miR-199a-5p的可能靶标。据此，我们拟通过体内外实验证实如下机制：PA感染Mφ，其分泌的Pec1通过激活p38 MAPK信号分子，下调miR-155和miR-199a-5p表达，抑制对PI3K p85亚基的靶向降解，进而激活PI3K/Akt/mTOR通路抑制Mφ自噬，最终有利于PA的存活。

Pseudomonas aeruginosa (PA) is prone to colonize and cause infection in the respiratory tract. Autophagy of macrophage (Mφ) plays an important role in the process of fighting infections. Pec1 protein is one of the virulence factors secreted by PA, however, its effect on the autophagy of Mφ has not been reported. Our previous studies have shown that the autophagy level decreased significantly, and intracellular bacterial count increased obviously after Pec1 stimulated Mφ. Furthermore, the phosphorylation of p38 MAPK was increased and the expressions of miR-155 and miR-199a-5p were significantly decreased after the stimulation of Mφ. In addition, expression of PI3K p85, Akt and mTOR phosphorylation of Mφ were remarkably increased after stimulation. Bioinformatics prediction shows that PI3K p85 is a possible target for these two miRNA. On this ground, we attempt to confirm the following mechanism via experiments in vivo and in vitro that Pec1 protein secreted by PA would activate the signal molecule p38 MAPK after Mφ infected by PA, thus down-regulating expression of miR-155 and miR-199a-5p, which would targeting-inhibit the subunit of degradation PI3K p85 and then activates PI3K/Akt/mTOR signaling pathway to inhibit Mφ autophagy, ultimately contributing to the survival of PA.