Mechanisms underlying the promotion of 5‐hydroxytryptamine secretion in enterochromaffin cells of constipation mice by <i>Bifidobacterium</i> and <i>Lactobacillus</i>

Lu, Youyou; Zhang, Zhe; Tong, Lingjun; Zhou, Xin; Liu, Xi; Yi, Huaxi; Gong, Pimin; Liu, Tongjie; Zhang, Lanwei; Yang, Liuqing; Shi, Hanping

doi:10.1111/nmo.14082

Cited by 19 publications

(17 citation statements)

References 30 publications

(44 reference statements)

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“…A. mucinophilia and Parabacteroides colonization could alter the level of amino acids in the serum and gut lumen to modulate the levels of seizure-associated neurotransmitters, such as GABA and glutamate, in the hippocampus, thus providing protective anti-seizure effects in mice ( 20 , 112 ). Enterochromaffin cells (ECs) produce approximately 90% of 5-hydroxytryptamine (5-HT) ( 113 ). In GF mice, certain intestinal microbiota, such as spore-forming clostridia taxa, can promote 5-HT biosynthesis in the gut by upregulating colonic tryptophan hydroxylase 1, a rate-limiting enzyme for 5-HT production ( 114 , 115 ).…”

Section: Mechanism Of the Correlation Of Microbiota–gut–brain Axis And Epilepsymentioning

confidence: 99%

Microbiota–Gut–Brain Axis and Epilepsy: A Review on Mechanisms and Potential Therapeutics

et al. 2021

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The gut–brain axis refers to the bidirectional communication between the gut and brain, and regulates intestinal homeostasis and the central nervous system via neural networks and neuroendocrine, immune, and inflammatory pathways. The development of sequencing technology has evidenced the key regulatory role of the gut microbiota in several neurological disorders, including Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis. Epilepsy is a complex disease with multiple risk factors that affect more than 50 million people worldwide; nearly 30% of patients with epilepsy cannot be controlled with drugs. Interestingly, patients with inflammatory bowel disease are more susceptible to epilepsy, and a ketogenic diet is an effective treatment for patients with intractable epilepsy. Based on these clinical facts, the role of the microbiome and the gut–brain axis in epilepsy cannot be ignored. In this review, we discuss the relationship between the gut microbiota and epilepsy, summarize the possible pathogenic mechanisms of epilepsy from the perspective of the microbiota gut–brain axis, and discuss novel therapies targeting the gut microbiota. A better understanding of the role of the microbiota in the gut–brain axis, especially the intestinal one, would help investigate the mechanism, diagnosis, prognosis evaluation, and treatment of intractable epilepsy.

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Section: Mechanism Of the Correlation Of Microbiota–gut–brain Axis And Epilepsymentioning

confidence: 99%

Microbiota–Gut–Brain Axis and Epilepsy: A Review on Mechanisms and Potential Therapeutics

et al. 2021

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“…In previous studies, we found that Bif. animalis F1-7 had high hydrophobicity and self-aggregation [43] and had ability to colonize in the intestine through fluorescence colonization experiments [44]. This suggests that F1-7 has a direct probiotic effect in the gut.…”

Section: Discussionmentioning

confidence: 97%

Krill Oil Combined with Bifidobacterium animalis subsp. lactis F1-7 Alleviates the Atherosclerosis of ApoE−/− Mice

Liu

Zhang

et al. 2021

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There has been an increasing number of studies on the interaction between active substances and probiotics to improve disease. Both krill oil (KO) and probiotics have the effect of improving atherosclerotic cardiovascular disease, but the combined effect has not been explored. Therefore, the purpose of this study was to explore the improvement effect of KO combined with probiotics on atherosclerosis. The atherosclerotic plaque area of ApoE−/− mice was detected after the intervention of KO, Bifidobacterium animalis subsp. lactis F1-7 (Bif. Animalis F1-7), and KO combined with Bif. Animalis F1-7. The results showed that Bif. Animalis F1-7, KO, and KO combined with Bif. Animalis F1-7 could significantly reduce the area of atherosclerotic plaque and improve the levels of serum lipids and inflammatory factors. They could regulate the farnesoid X receptor (FXR)/cholesterol 7-alpha hydroxylase (CYP7A1) pathway to reduce lipid accumulation. The intervention groups could also improve the inflammatory response by downregulating the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) pathway. The anti-inflammatory effect of the interaction group was significantly better than that of KO. It proved that Bif. Animalis F1-7 might play a synergistic effect in the improvement of inflammation by KO to the alleviation of atherosclerosis.

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“…(2) Neurotransmitters probably mediate the in uences of intestinal microbiome on smoking. For instance, Bi dobacterium was reported to promote 5-hydroxytryptamine (5-HT) biosynthesis in colonic enterochroma n cells by activating the CGA/ADRα2A cascade signal and regulating the TRP/TPH-OR pathways [41,42]. 5-HT has been the therapeutic target for addiction to alcohol, cocaine, or drug, so it may also be for smoking [43].…”

Section: Discussionmentioning

confidence: 99%

Cross-talks Between Gut Microbiota and Tobacco Smoking: A Two-Sample Mendelian Randomization Study

Zhou

Fan²,

Zhou³

et al. 2022

Preprint

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Considerable evidence has been reported that tobacco use could cause alterations in gut microbiota composition. The microbiota-gut-brain axis also in turn hinted at a possible contribution of gut microbiota to smoking. However, population-level studies with a higher evidence level for causality are lacking. This study deployed two-sample bidirectional Mendelian randomization (MR) design to reveal the causal association between gut microbiota and tobacco smoking. The summary-level data of genome-wide association studies (GWAS) for 211 gut microbial taxa and five smoking phenotypes were acquired from meta-analyzed datasets with totally 1.7 million European ancestry-dominated samples. Our MR results confirmed the effects of smoking on three taxa (Intestinimonas, Catenibacterium, and Ruminococcaceae, observed from previous studies) with boosted evidence level and identified another thirteen taxa which may be causally affected by tobacco smoking. As for the other direction, we revealed that smoking behaviors could be potential consequence of taxa abundance. Combining with existing observational evidence, we provided novel insights regarding a positive feedback loop of smoking addiction through Actinobacteria and indicated a potential mechanism for the link between parental smoking and early smoking initiation of their children driven by Bifidobacterium. In summary, the current study suggested a substantial role of the intestinal microbes on the risk for cigarette smoking, and in turn smoking on intestinal microbes. Our findings highlighted the hazards of tobacco use for gut flora dysbiosis and shed light on the potential role of gut microbiota for tobacco control.

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Mechanisms underlying the promotion of 5‐hydroxytryptamine secretion in enterochromaffin cells of constipation mice by Bifidobacterium and Lactobacillus

Cited by 19 publications

References 30 publications

Microbiota–Gut–Brain Axis and Epilepsy: A Review on Mechanisms and Potential Therapeutics

Microbiota–Gut–Brain Axis and Epilepsy: A Review on Mechanisms and Potential Therapeutics

Krill Oil Combined with Bifidobacterium animalis subsp. lactis F1-7 Alleviates the Atherosclerosis of ApoE−/− Mice

Cross-talks Between Gut Microbiota and Tobacco Smoking: A Two-Sample Mendelian Randomization Study

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