The Neuroprotective Effect of Short Chain Fatty Acids Against Sepsis-Associated Encephalopathy in Mice

Liu, Jiaming; Jin, Yangjie; Ye, Yanglie; Tang, Yahui; Dai, Shanshan; Li, Mengfang; Zhao, Guangju; Hong, Guangliang; Lu, Zhongqiu

doi:10.3389/fimmu.2021.626894

Cited by 21 publications

(19 citation statements)

References 89 publications

(92 reference statements)

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“… 9 , 10 SCFAs can improve cerebral damage by the blood-brain barrier (BBB). 11 The microbiota is a vital regulator of gut-brain function, and the importance of the microbiota-gut-brain axis is becoming more widely recognized. These findings suggest that the gut microbiota and its metabolites may perform a significant role in sepsis and related brain damage pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Gut Microbiota Mediates the Susceptibility of Mice to Sepsis-Associated Encephalopathy by Butyric Acid

Zhang¹,

Xu²,

Wu³

et al. 2022

JIR

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Purpose Neuroinflammation plays an important part in the pathophysiology of sepsis-associated encephalopathy (SAE). Gut microbiota and gut brain axis are considered as important mediators in the development of neurological diseases. The aim of this study was to investigate the role of intestinal microbiota in sepsis-related brain injury and to explore the underlying mechanisms. Methods Mouse model of SAE was established using cecal ligation and puncture (CLP). Based on the mouse mortality and the associated time of death, light SAE (LSAE) and severe SAE (SSAE) were classified. Fecal microbiota transplantation (FMT) was performed to verify the role of intestinal microbiota. Feces of mice in the two groups which collected before operation were sequenced for 16S and targeted short chain fatty acids. Results Intestinal microbiota from SSAE and LSAE mice displayed diverse functions. Interestingly, LSAE mice produced more butyric acid compared with SSAE mice. In the in vivo experiments, sodium butyrate (NaB) reduced the high oxidative stress levels in mice hippocampus and conferred a marked survival superiority to sepsis mice. In addition, NaB prevented the increase in intracellular reactive oxygen species (ROS) generation and inducible nitric-oxide synthase expression in LPS-stimulated primary microglia. The GPR109A/Nrf2/HO-1 signaling pathway was found to be involved in the activation of antioxidant response of primary microglia induced by sodium butyrate. Conclusion Our findings indicate a crucial role of gut microbiota in the susceptibility to SAE. Butyrate, a metabolite of intestinal microbiota, may have a neuroprotective effect in the process of sepsis by GPR109A/Nrf2/HO-1 pathway.

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Section: Introductionmentioning

confidence: 99%

Gut Microbiota Mediates the Susceptibility of Mice to Sepsis-Associated Encephalopathy by Butyric Acid

Zhang¹,

Xu²,

Wu³

et al. 2022

JIR

View full text Add to dashboard Cite

show abstract

“…Microbial metabolites are increasingly recognized as key mediators of the injury responses in multiple organs distant from the gut ( 10 – 13 ). For example, gut microbiota-generated granisetron mediates the susceptibility of sepsis-induced liver injury ( 14 ), and short-chain fatty acids exert neuroprotective effects against sepsis-induced behavioral impairment ( 15 ). However, few studies have examined the effects of microbial metabolites on gut microbes and the role of these effects in sepsis progression.…”

Section: Introductionmentioning

confidence: 99%

Indole-3-Propionic Acid as a Potential Therapeutic Agent for Sepsis-Induced Gut Microbiota Disturbance

Fang

Wang

et al. 2022

Microbiol Spectr

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The role of gut microbiota in the pathophysiology of sepsis is gaining increasing attention and developing effective and safe sepsis therapies targeting intestinal microorganisms is promising. Given the safety of probiotic supplementation or fecal microbiota transplantation in critically ill patients, identifying an abiotic agent to regulate the intestinal microbiota of septic patients is of clinical significance.

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“…In addition, fish oil ( 66 ) and tissue-non-specific alkaline phosphatase ( 67 ) may mediate SAE by affecting the BBB. Moreover, short chain fatty acids ( 68 ), Treg/Th2 cells ( 69 ), Takeda G protein-coupled receptor 5 ( 70 ), and artemisinin ( 71 ) can regulate neuroinflammation through immune-mediated microglia activation.…”

Section: Discussionmentioning

confidence: 99%

Emerging Trends and Hot Spots in Sepsis-Associated Encephalopathy Research From 2001 to 2021: A Bibliometric Analysis

et al. 2022

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Study ObjectivesTo evaluate sepsis-associated encephalopathy (SAE) research and to quantitatively and qualitatively predict research hot spots using bibliometric analysis.MethodsWe extracted relevant publications from the Web of Science Core Collection on July 28, 2021. We investigated the retrieved data by bibliometric analysis (e.g. co-cited and cluster analysis, keyword co-occurrence) using the software CiteSpace and VOSviewer, the Online Analysis Platform of Literature Metrology (http://bibliometric.com/) and Bibliometrix to analyse and predict the trends and hot spots in this field.Main ResultsWe identified 1,582 published articles and reviews on SAE from 2001 to 2021. During this period, the number of manuscripts on SAE increased steadily and peaked in 2021. The USA and China were the leading countries that had a critical impact on SAE research. Among all institutions, Vanderbilt University and Pittsburgh University held leading positions and became central in the collaboration network. Among all the journals, Critical Care Medicine published the maximum number of manuscripts in the field of SAE within 20 years. Dal-Pizzol Felipe was the most productive author (61 papers) and received the largest number of citations (930 citations). Co-citation cluster analysis revealed that the most popular terms on SAE in the manner of cluster labels were critical illness, sepsis-associated encephalopathy, polymicrobial sepsis, posterior reversible encephalopathy syndrome, rat brain, intensive care unit, prior sepsis, molecular hydrogen, inflammation drive, metabolic encephalopathies, delirium pathophysiology, and clinical neuroscience. Keyword burst detection indicated that neuroinflammation, blood-brain barrier (BBB) and mitochondria dysfunction were the current research hot spots.ConclusionsOur study revealed that neuroinflammation, blood-brain barrier, and mitochondria dysfunction had been the research foci of SAE over the past 20 years. These have emerged as the basis for transformation from basic research to clinical application in finding effective methods for the prevention and treatment of SAE.

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The Neuroprotective Effect of Short Chain Fatty Acids Against Sepsis-Associated Encephalopathy in Mice

Cited by 21 publications

References 89 publications

Gut Microbiota Mediates the Susceptibility of Mice to Sepsis-Associated Encephalopathy by Butyric Acid

Gut Microbiota Mediates the Susceptibility of Mice to Sepsis-Associated Encephalopathy by Butyric Acid

Indole-3-Propionic Acid as a Potential Therapeutic Agent for Sepsis-Induced Gut Microbiota Disturbance

Emerging Trends and Hot Spots in Sepsis-Associated Encephalopathy Research From 2001 to 2021: A Bibliometric Analysis

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