Nicotine Reduces Human Brain Microvascular Endothelial Cell Response to Escherichia coli K1 Infection by Inhibiting Autophagy

• Published in: Frontiers in cellular and infection microbiology 2020-09, Vol.10, p.484-484
• Main Authors: Wu, Chao, Yang, Mengzhen, Liu, Rui, Hu, Hanyang, Ji, Lulu, Zhang, Xiaoli, Huang, Shenghe, Wang, Lin
• Format: Article
• Language: English
• Subjects: autophagy; Cellular and Infection Microbiology; Escherichia coli; human brain microvascular endothelial cells; neonatal meningitis; nicotine
• ISSN: 2235-2988; 2235-2988
• DOI: 10.3389/fcimb.2020.00484

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.