【摘要】 解析单核细胞增生李斯特菌（Listeria monocytogenes,Lm）内化素InlJ在黏附侵袭、胞内增殖及线粒体损伤中的作用特性，明确其在噬菌体抗胞内Lm感染中的潜在调控机制。结果表明，内化素基因inlJ缺失株NJ05-ΔinlJ对Caco-2细胞的黏附和侵袭能力分别降低56.37%和17.74%，细胞内增殖能力亦显著下降。内化素InlJ缺失减少了细胞线粒体活性氧的聚积且不影响膜电位，即内化素InlJ缺失可显著降低Lm对细胞的毒性。然而，缺失株对Lm噬菌体vB-LmoM-SH3-3的敏感性却显著升高，成斑效率为野生型Lm的1.37倍，体外裂解能力增强。利用噬菌体预处理Caco-2细胞可降低Lm对细胞的黏附、侵袭能力以及胞内增殖效率，同时可有效缓解Lm对细胞线粒体造成的损伤。由此可见，内化素家族新成员InlJ是影响线粒体损伤的重要因素，能够调节Lm与噬菌体间的相互作用，为噬菌体在抗胞内菌感染的应用开发奠定基础。更多还原

【Abstract】 This study aimed to elucidate the functional characteristics of internalin InlJ from Listeria monocytogenes(Lm) in adhesion, invasion, intracellular proliferation, and mitochondrial damage and to clarify its regulatory mechanism in phagemediated control of intracellular Lm infection. The results indicated that the ability of an inlJ deletion strain of Lm NJ05, NJ05-ΔinlJ, to adhere to and invade Caco-2 cells decreased by 56.37% and 17.74%, respectively, and the intracellular proliferation capacity also significantly decreased compared with the parental strain. The absence of InlJ resulted in decreased accumulation of mitochondrial reactive oxygen species(ROS) without affecting the membrane potential, thereby reducing the cytotoxicity of Lm. However, the NJ05-ΔinlJ strain displayed heightened sensitivity to phage vB-LmoMSH3-3, with its efficiency of plating(EOP) 1.37 times that of the wild-type strain, and showed substantially enhanced lytic activity in vitro. Pre-treatment of Caco-2 cells with the phage led to a significant reduction in their adhesion to and invasion by Lm and its intracellular proliferation, and effectively alleviated mitochondrial damage caused by Lm. Thus, InlJ, a newly identified member of the internalin family, acts as an important factor influencing mitochondrial damage and regulates the interaction between Lm and phages, laying the foundation for the application of phages in combating intracellular bacterial infections.更多还原