<i>Lactobacillus plantarum</i> C29‐Fermented Soybean (DW2009) Alleviates Memory Impairment in 5XFAD Transgenic Mice by Regulating Microglia Activation and Gut Microbiota Composition

Lee, Hae-Ji; Hwang, Yun-Ha; Kim, Dong-Hyun

doi:10.1002/mnfr.201800359

Cited by 59 publications

(77 citation statements)

References 29 publications

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“…However, OK67 or PK16 treatment suppressed the gut microbiota LPS production and Proteobacteria population and reduced blood LPS levels. We also found that HFD induced TNF‐α expression and NF‐κB activation and the infiltration of CD11b + /CD11c + cells, which are immune cells including macrophages and dendritic cells, in the colon of mice. However, oral administration of OK67 or PK16 alleviated colitis in HFD‐induced obese mice: they inhibited HFD‐induced NF‐κB activation, TNF‐α expression, and colon shortening and increased IL‐10 expression.…”

Section: Discussionmentioning

confidence: 51%

“…Immunostaining analysis of brain and colon slices was performed according to the method of Lee et al . Briefly, the colons were cryosectioned through the coronal plane at a thickness of 30 µm, stored at 4 °C in the storing solution (30% glycerol, 30% ethylene glycol in PBS), permeabilized in 0.5% Triton X‐100, and blocked in 10% bovine serum with Tween 20.…”

Section: Methodsmentioning

confidence: 99%

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Lactobacillus sakei Alleviates High‐Fat‐Diet‐Induced Obesity and Anxiety in Mice by Inducing AMPK Activation and SIRT1 Expression and Inhibiting Gut Microbiota‐Mediated NF‐κB Activation

Jang

Han

Kim

et al. 2019

Molecular Nutrition Food Res

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Scope Long‐term feeding of a high‐fat diet (HFD) causes gastrointestinal inflammation and gut microbiota disturbance, leading to the increased occurrence of obesity and anxiety. In the present study, the effects of heat‐labile Lactobacillus sakei OK67, tyndallized OK67 (tOK67), and heat‐stable Lactobacillus sakei PK16 on HFD‐induced obesity and anxiety in mice are examined. Methods and results Obesity is induced in mice by feeding with HFD. Oral administration of live OK67, tOK67, or PK16 reduces HFD‐induced body and liver weights and blood triglyceride, total cholesterol, corticosterone, and lipopolysaccharide levels. These treatments also suppress HFD‐induced NF‐κB activation and increased HFD‐suppressed AMP‐activated protein kinase (AMPK) activation and SIRT‐1 expression in the liver. OK67 or PK16 treatment alleviates HFD‐induced anxiety‐like behaviors and increases BDNF expression and NF‐κB activation in the hippocampus. Moreover, OK67 or PK16 treatment suppresses HFD‐induced colitis and suppresses the Proteobacteria population and fecal lipopolysaccharide levels in mice. OK67 or PK16 treatment inhibits NF‐κB activation and induced AMPK activation and SIRT‐1 expression in lipopolysaccharide‐stimulated Caco‐2 cells. Overall, the antiobesity and anxiolytic effects of live OK67 are more potent than those of tOK67. Conclusion Lactobacillus sakei can alleviate HFD‐induced obesity, colitis, and anxiety by regulating gut microbiota‐mediated AMPK and NF‐κB activation and SIRT‐1 expression.

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Section: Discussionmentioning

confidence: 51%

Section: Methodsmentioning

confidence: 99%

Lactobacillus sakei Alleviates High‐Fat‐Diet‐Induced Obesity and Anxiety in Mice by Inducing AMPK Activation and SIRT1 Expression and Inhibiting Gut Microbiota‐Mediated NF‐κB Activation

Jang

Han

Kim

et al. 2019

Molecular Nutrition Food Res

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“…An imbalance in the GM can also directly cause neuroinflammation through the "brain-gut axis" (Daulatzai, 2014). Moreover, alteration of the GM by probiotics inhibits the activation of NF-κB and neuroinflammation and significantly improves cognitive activity (Lee, Hwang, & Kim, 2018). Given that gastrointestinal bacteria secrete inflammatory substances in the hippocampus and neocortex of AD patients (Y.…”

Section: Discussionmentioning

confidence: 99%

Outer membrane vesicles enhance tau phosphorylation and contribute to cognitive impairment

Wei

Peng

Mai

et al. 2019

Journal Cellular Physiology

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Outer membrane vesicles (OMVs) are nanosized vesicles produced by the gut microbiota (GM). The GM is well-known to be involved in the pathological process of Alzheimer's disease (AD). However, the mechanism of OMVs is not clear. In the present study, we demonstrated the involvement of OMVs in the development of cognitive (learning and memory) dysfunction induced by blood-brain barrier (BBB) disruption. More important, further study showed that OMVs induced tau phosphorylation by activating glycogen synthase kinase 3β (GSK-3β) in the hippocampus. OMVs activated astrocytes and microglia, increased secretion of inflammatory cytokines (nuclear factor κB, interleukin-1β, and tumour necrosis factor-α) in the hippocampus. Therefore, OMVs increase the permeability of the BBB and promote the activation of astrocytes and microglia, inducing an inflammatory response and tau hyperphosphorylation by activating the GSK-3β pathway and finally leading to cognitive impairment. K E Y W O R D SAlzheimer's disease, astrocytes, blood-brain barrier, glycogen synthase kinase 3β, gut microbiota, inflammatory cytokines, interleukin-1β, microglia, nuclear factor κB, outer membrane vesicles, tau, tumour necrosis factor-α

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“…A spontaneous (actual) alternation was defined as entries into all three arms on consecutive choices and was calculated as the ratio (%) of actual to possible alternations. A novel object recognition (NOR) task was performed in the apparatus consisting of a darkopen field box (45 × 45 × 50 cm) according to the method of Lee et al (47). For the first trial, a mouse was placed in the box containing two identical objects and the frequency of touching each object was recorded for 10 min.…”

Section: Cognitive and Depressive Behavioral Tasksmentioning

confidence: 99%

“…Genomic DNA was extracted from the fresh stools of five mice (not trans-cardiacally perfused with 4% paraformaldehyde for brain and colon tissue sections) using a commercial DNA isolation kit (QIAamp DNA stool mini kit), as previously reported (11,47). Briefly, genomic DNA was extracted from the fresh stools of mice using a commercial DNA isolation kit (QIAamp DNA stool mini kit).…”

Section: Microbiota Sequencingmentioning

confidence: 99%

Interplay Between Human Gut Bacteria Escherichia coli and Lactobacillus mucosae in the Occurrence of Neuropsychiatric Disorders in Mice

et al. 2020

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To understand the roles of human gut bacteria in the occurrence of neuropsychiatric disorders, we isolated inflammatory Escherichia coli K1 and anti-inflammatory Lactobacillus mucosae from healthy human feces and examined their effects on the occurrence of altered microbiota, cognitive decline, and depression in mice. Oral gavage of Escherichia coli K1 caused colitis, cognitive decline, and depression in mice in the elevated plus maze, tail suspension, and forced swimming tasks. However, NK41 treatment reduced K1-induced cognitive decline and anxiety/depression. Furthermore, NK41 treatment increased K1-suppressed brain-derived neurotrophic factor (BDNF) expression and BDNF + /NeuN + cell population and suppressed K1-induced NF-κB activation and LPS + /Iba1 + and NF-κB + /Iba1 + (microglial) cell populations in the hippocampus. NK41 treatment also suppressed K1-induced TNF-α and LPS levels in the blood and TNF-α expression, myeloperoxidase activity, NF-κB + /CD11c + and CD11b + /CD11c + cell populations in the colon. Furthermore, NK41 treatment decreased K1-induced colonic MUC2 expression, gut Proteobacteria population, and fecal LPS levels and modified the bacterial abundance related to polysaccharide breaking and biosynthesis. In conclusion, the overgrowth of inflammatory bacteria such as Escherichia coli in the gastrointestinal tract can cause neuropsychiatric disorders with gut microbiota alteration and the superiority of anti-inflammatory bacteria such as Lactobacillus mucosae can alleviate neuropsychiatric disorders with the attenuation of altered microbiota.

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Lactobacillus plantarum C29‐Fermented Soybean (DW2009) Alleviates Memory Impairment in 5XFAD Transgenic Mice by Regulating Microglia Activation and Gut Microbiota Composition

Abstract: FDS and C29 alleviates the decrease in cognitive function and inhibited amyloid-β expression in Tg mice by regulating microglia activation and gut microbiota composition.

Cited by 59 publications

References 29 publications

Lactobacillus sakei Alleviates High‐Fat‐Diet‐Induced Obesity and Anxiety in Mice by Inducing AMPK Activation and SIRT1 Expression and Inhibiting Gut Microbiota‐Mediated NF‐κB Activation

Lactobacillus sakei Alleviates High‐Fat‐Diet‐Induced Obesity and Anxiety in Mice by Inducing AMPK Activation and SIRT1 Expression and Inhibiting Gut Microbiota‐Mediated NF‐κB Activation

Outer membrane vesicles enhance tau phosphorylation and contribute to cognitive impairment

Interplay Between Human Gut Bacteria Escherichia coli and Lactobacillus mucosae in the Occurrence of Neuropsychiatric Disorders in Mice

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