Correlation Between Gut Microbiota Shifts, Lipopolysaccharide Levels, and Neuroinflammatory Responses Following Ischemic Stroke
- 1School of Food Science and Engineering, Xinjiang Institute of Technology, No. 1 Xuefu Road West, Aksu 843100, China
- 2Gansu Key Laboratory of Biomonitoring and Bioremediation for Environmental Pollution, School of Life Sciences, Lanzhou University, No. 222 South Tianshui Road, Lanzhou 730000, China
Abstract
Background: The microbiota–gut–brain axis (MGBA) is increasingly recognized as a contributor to ischemic stroke pathophysiology, yet the relationship between gut microbial changes and neuroinflammation remains incompletely understood. This study aimed to investigate whether shifts in gut microbiota are associated with concurrent changes in lipopolysaccharide (LPS) levels and neuroinflammatory responses following ischemic stroke. Methods: Using a photothrombotic mouse model, we measured LPS in the gut, serum, and brain via ELISA and immunohistochemistry. Gentamycin was administered to deplete gut bacteria and assess its effects on LPS and stroke recovery. Upon TLR4 inhibition with TAK-242, microglial polarization and inflammatory cytokines were evaluated, and dose-dependent LPS supplementation was performed. Results: Ischemic stroke was accompanied by elevated LPS levels in the gut, circulation, and brain, paralleling Verrucomicrobiota expansion. Antibiotic treatment reduced Verrucomicrobiota and LPS in the gut and brain, and this was associated with worsened stroke outcomes. TLR4 inhibition was associated with altered microglial phenotypes and inflammatory markers. Exogenous LPS produced dose-dependent effects, whereas endogenous LPS levels remained low. Conclusions: These findings reveal a spatial correlation between gut microbial shifts, circulating LPS, and cerebral LPS immunoreactivity, suggesting LPS may serve as a correlative marker of gut–brain interactions following ischemic stroke.
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BibTeX
@article{li2026correlation,
title = {{Correlation Between Gut Microbiota Shifts, Lipopolysaccharide Levels, and Neuroinflammatory Responses Following Ischemic Stroke}},
author = {Kemin Li and Wancong Ding and Shuang Wang and Gaowei Pan and Shengxiang Zhang},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15191819},
url = {https://europepmc.org/article/PMC/PMC13664211},
note = {CC BY},
}
RIS
TY - JOUR
TI - Correlation Between Gut Microbiota Shifts, Lipopolysaccharide Levels, and Neuroinflammatory Responses Following Ischemic Stroke
AU - Kemin Li
AU - Wancong Ding
AU - Shuang Wang
AU - Gaowei Pan
AU - Shengxiang Zhang
PY - 2026
DA - 2026/10/01
JO - Cells
DO - 10.3390/cells15191819
UR - https://europepmc.org/article/PMC/PMC13664211
AB - Background: The microbiota–gut–brain axis (MGBA) is increasingly recognized as a contributor to ischemic stroke pathophysiology, yet the relationship between gut microbial changes and neuroinflammation remains incompletely understood. This study aimed to investigate whether shifts in gut microbiota are associated with concurrent changes in lipopolysaccharide (LPS) levels and neuroinflammatory responses following ischemic stroke. Methods: Using a photothrombotic mouse model, we measured LPS in the gut, serum, and brain via ELISA and immunohistochemistry. Gentamycin was administered to deplete gut bacteria and assess its effects on LPS and stroke recovery. Upon TLR4 inhibition with TAK-242, microglial polarization and inflammatory cytokines were evaluated, and dose-dependent LPS supplementation was performed. Results: Ischemic stroke was accompanied by elevated LPS levels in the gut, circulation, and brain, paralleling Verrucomicrobiota expansion. Antibiotic treatment reduced Verrucomicrobiota and LPS in the gut and brain, and this was associated with worsened stroke outcomes. TLR4 inhibition was associated with altered microglial phenotypes and inflammatory markers. Exogenous LPS produced dose-dependent effects, whereas endogenous LPS levels remained low. Conclusions: These findings reveal a spatial correlation between gut microbial shifts, circulating LPS, and cerebral LPS immunoreactivity, suggesting LPS may serve as a correlative marker of gut–brain interactions following ischemic stroke.
SN - 2073-4409
ER -