Wu Chao, Yang Mengzhen, Liu Rui, Hu Hanyang, Ji Lulu, Zhang Xiaoli, Huang Shenghe, Wang Lin
Department of Histology and Embryology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.
Department of Human Anatomy, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, China.
Front Cell Infect Microbiol. 2020 Sep 15;10:484. doi: 10.3389/fcimb.2020.00484. eCollection 2020.
Studies have shown that exposure to environmental tobacco smoke can increase the risk of bacterial meningitis, and nicotine is the core component of environmental tobacco smoke. Autophagy is an important way for host cells to eliminate invasive pathogens and resist infection. K1 strain ( K1) is the most common Gram-negative bacterial pathogen that causes neonatal meningitis. The mechanism of nicotine promoting K1 to invade human brain microvascular endothelial cells (HBMECs), the main component of the blood-brain barrier, is not clear yet. Our study found that the increase of HBMEC autophagy level during K1 infection could decrease the survival of intracellular bacteria, while nicotine exposure could inhibit the HBMEC autophagic response of K1 infection by activating the NF-kappa B and PI3K/Akt/mTOR pathway. We concluded that nicotine could inhibit HBMEC autophagy upon K1 infection and decrease the scavenging effect on K1, thus promoting the occurrence and development of neonatal meningitis.
研究表明，接触环境烟草烟雾会增加细菌性脑膜炎的风险，而尼古丁是环境烟草烟雾的核心成分。自噬是宿主细胞清除入侵病原体并抵抗感染的重要方式。K1菌株（K1）是引起新生儿脑膜炎最常见的革兰氏阴性细菌病原体。尼古丁促进K1入侵血脑屏障主要成分人脑微血管内皮细胞（HBMECs）的机制尚不清楚。我们的研究发现，K1感染期间HBMEC自噬水平的升高可降低细胞内细菌的存活率，而尼古丁暴露可通过激活NF-κB和PI3K/Akt/mTOR途径抑制K1感染的HBMEC自噬反应。我们得出结论，尼古丁可在K1感染时抑制HBMEC自噬，并降低对K1的清除作用，从而促进新生儿脑膜炎的发生和发展。
