Niacin alleviates cerebral microvascular endothelial cell apoptosis induced by hypervirulent Klebsiella Pneumoniae by reducing the accumulation of reactive oxygen species.
Y, Z., M, W., & X, C. (2026). Niacin alleviates cerebral microvascular endothelial cell apoptosis induced by hypervirulent Klebsiella Pneumoniae by reducing the accumulation of reactive oxygen species.. Frontiers in cellular and infection microbiology. https://doi.org/10.3389/fcimb.2026.1867024
Y Z, M W, X C. Niacin alleviates cerebral microvascular endothelial cell apoptosis induced by hypervirulent Klebsiella Pneumoniae by reducing the accumulation of reactive oxygen species.. Frontiers in cellular and infection microbiology. 2026; doi: 10.3389/fcimb.2026.1867024
Y Z, M W, X C. Niacin alleviates cerebral microvascular endothelial cell apoptosis induced by hypervirulent Klebsiella Pneumoniae by reducing the accumulation of reactive oxygen species.[J]. Frontiers in cellular and infection microbiology. 2026. DOI: 10.3389/fcimb.2026.1867024.
@article{y2026,
author = {Zhao Y and Wang M and Che X},
title = {Niacin alleviates cerebral microvascular endothelial cell apoptosis induced by hypervirulent Klebsiella Pneumoniae by reducing the accumulation of reactive oxygen species.},
journal = {Frontiers in cellular and infection microbiology},
year = {2026},
doi = {10.3389/fcimb.2026.1867024},
note = {PMID: 42499551},
}
TY - JOUR AU - Zhao Y AU - Wang M AU - Che X TI - Niacin alleviates cerebral microvascular endothelial cell apoptosis induced by hypervirulent Klebsiella Pneumoniae by reducing the accumulation of reactive oxygen species. T2 - Frontiers in cellular and infection microbiology PY - 2026 DO - 10.3389/fcimb.2026.1867024 AN - PMID:42499551 ER -
INTRODUCTION: Hypervirulent Klebsiella pneumoniae (hvKp) is an important pathogen causing central nervous system infections, including meningitis; however, the mechanisms by which it disrupts the blood-brain barrier remain unclear. Niacin, a vitamin B3 compound related to NAD+ metabolism, has the potential to regulate redox homeostasis. This study aimed to investigate the mechanism of hvKp-induced injury in human cerebral microvascular endothelial cell (HCMEC) and to evaluate the protective effects of niacin. METHODS: A GFP-labeled hvKp ATCC 43816 strain was used to establish an HCMEC infection model, and an hvKp mouse meningitis model was also constructed. Live-cell imaging was performed to monitor infection dynamics. Flow cytometry was used to assess infection rate, reactive oxygen species (ROS) levels, and Annexin V-FITC/PI-labeled apoptosis, while Western blotting was used to analyze apoptosis-related pathways. The experimental groups included a control group, an hvKp infection group, an hvKp plus niacin treatment group, and a niacin pretreatment group. RESULTS: hvKp caused time- and dose-dependent injury to HCMEC, characterized by intracellular proliferation followed by apoptosis induction. Mechanistically, hvKp promoted mitochondrial ROS accumulation and activated the p53-associated mitochondrial apoptotic pathway. Niacin reduced ROS levels, inhibited apoptosis, and alleviated HCMEC injury. In vivo, niacin preserved blood-brain barrier integrity, reduced central nervous system inflammation and hvKp colonization, and improved survival in infected mice. DISCUSSION: hvKp damages cerebral microvascular endothelial cells and disrupts the blood-brain barrier through the ROS-p53-mitochondrial apoptosis axis. Niacin exerts protective effects by regulating redox homeostasis, suggesting that it may serve as a host-directed adjunctive therapeutic strategy for hvKp-associated central nervous system infections.