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Meningitic Escherichia coli Induction of ANGPTL4 in Brain Microvascular Endothelial Cells Contributes to Blood–Brain Barrier Disruption via ARHGAP5/RhoA/MYL5 Signaling Cascade
Open AccessArticle

Decrease of miR-19b-3p in Brain Microvascular Endothelial Cells Attenuates Meningitic Escherichia coli-Induced Neuroinflammation via TNFAIP3-Mediated NF-κB Inhibition

by Nouman Amjad 1,2, Ruicheng Yang 1,2, Liang Li 1,2, Jiyang Fu 1,2, Bo Yang 1,2, Bojie Xu 1,2, Chen Tan 1,2,3, Huanchun Chen 1,2,3 and Xiangru Wang 1,2,3,*
1
State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, China
2
Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan 430070, China
3
Key Laboratory of Development of Veterinary Diagnostic Products, Ministry of Agriculture of the People’s Republic of China, Wuhan 430070, China
*
Author to whom correspondence should be addressed.
Pathogens 2019, 8(4), 268; https://doi.org/10.3390/pathogens8040268
Received: 8 November 2019 / Revised: 22 November 2019 / Accepted: 26 November 2019 / Published: 27 November 2019
(This article belongs to the Special Issue Pathogenesis of Fungal and Bacterial Microbes)
Meningitic Escherichia coli can traverse the host’s blood–brain barrier (BBB) and induce severe neuroinflammatory damage to the central nervous system (CNS). During this process, the host needs to reasonably balance the battle between bacteria and brain microvascular endothelial cells (BMECs) to minimize inflammatory damage, but this quenching of neuroinflammatory responses at the BBB is unclear. MicroRNAs (miRNAs) are widely recognized as key negative regulators in many pathophysiological processes, including inflammatory responses. Our previous transcriptome sequencing revealed numbers of differential miRNAs in BMECs upon meningitic E. coli infection; we next sought to explore whether and how these miRNAs worked to modulate neuroinflammatory responses at meningitic E. coli entry of the BBB. Here, we demonstrated in vivo and in vitro that meningitic E. coli infection of BMECs significantly downregulated miR-19b-3p, which led to attenuated production of proinflammatory cytokines and chemokines via increasing the expression of TNFAIP3, a negative regulator of NF-κB signaling. Moreover, in vivo injection of miR-19b-3p mimics during meningitic E. coli challenge further aggravated the inflammatory damage to mice brains. These in vivo and in vitro findings indicate a novel quenching mechanism of the host by attenuating miR-19b-3p/TNFAIP3/NF-κB signaling in BMECs in response to meningitic E. coli, thus preventing CNS from further neuroinflammatory damage. View Full-Text
Keywords: meningitic Escherichia coli; brain microvascular endothelial cells; miR-19b-3p; TNFAIP3; NF-κB; neuroinflammation meningitic Escherichia coli; brain microvascular endothelial cells; miR-19b-3p; TNFAIP3; NF-κB; neuroinflammation
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Amjad, N.; Yang, R.; Li, L.; Fu, J.; Yang, B.; Xu, B.; Tan, C.; Chen, H.; Wang, X. Decrease of miR-19b-3p in Brain Microvascular Endothelial Cells Attenuates Meningitic Escherichia coli-Induced Neuroinflammation via TNFAIP3-Mediated NF-κB Inhibition. Pathogens 2019, 8, 268.

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