College of Animal Science and Technology, Shihezi University, Shihezi, 832003, China.
Cell Mol Biol Lett. 2012 Jun;17(2):249-57. doi: 10.2478/s11658-012-0009-4. Epub 2012 Feb 24.
This study investigated the role of autophagy in the survival of the invasive bacterium Brucella melitensis strain 16M in murine macrophages. Here, Brucella melitensis 16M was found to trigger autophagosome formation, enhance autophagy flux and increase the expression level of the autophagy marker protein LC3-II. When autophagy was pharmacologically inhibited by 3-methyladenine (3-MA), Brucella replication efficiency was significantly decreased (p < 0.05). These results suggest that autophagy favors Brucella melitensis 16M survival in murine macrophages.
本研究探讨了自噬在侵袭性细菌布鲁氏菌 16M 在鼠巨噬细胞中存活中的作用。在这里,发现布鲁氏菌 16M 触发自噬体形成,增强自噬流并增加自噬标记蛋白 LC3-II 的表达水平。当自噬通过 3-甲基腺嘌呤(3-MA)被药理学抑制时,布鲁氏菌的复制效率显著降低(p < 0.05)。这些结果表明自噬有利于布鲁氏菌 16M 在鼠巨噬细胞中的存活。