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. Escherichia coli K1 strain (E. coli K1) is the most common Gram-negative bacterial pathogen that causes neonatal meningitis. The mechanism of nicotine promoting E. coli 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 E. coli K1 infection could decrease the survival of intracellular bacteria, while nicotine exposure could inhibit the HBMEC autophagic response of E. coli K1 infection by activating the NF-kappa B and PI3K/Akt/mTOR pathway. We concluded that nicotine could inhibit HBMEC autophagy upon E. coli K1 infection and decrease the scavenging effect on E. coli 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，尼古丁是环境烟草烟雾的核心成分。自噬是宿主细胞消除侵入性病原体和抵抗感染的重要途径。大肠杆菌 K1株（大肠杆菌K1）是引起新生儿脑膜炎的最常见的革兰氏阴性细菌病原体。尼古丁促进机制大肠杆菌目前尚不清楚K1能否入侵人脑微血管内皮细胞（HBMEC），后者是血脑屏障的主要成分。我们的研究发现HBMEC自噬水平在大肠杆菌 K1感染可减少细胞内细菌的存活，而尼古丁暴露可抑制HBMEC自噬反应。 大肠杆菌通过激活NF-κB和PI3K / Akt / mTOR途径来感染K1。我们得出的结论是尼古丁可以抑制HBMEC自噬大肠杆菌 感染K1并降低对K1的清除作用 大肠杆菌 K1，从而促进新生儿脑膜炎的发生和发展。