Peripheral Dopamine Controlled by Gut Microbes Inhibits Invariant Natural Killer T Cell-Mediated Hepatitis

Xue, Rufeng; Zhang, Huimin; Pan, Jun; Du, Zhiwei; Zhou, Wenjie; Zhang, Zhi; Tian, Zhigang; Zhou, Rongbin; Bai, Li

doi:10.3389/fimmu.2018.02398

Cited by 67 publications

(60 citation statements)

References 50 publications

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“…Concerning DA, this is further confirmed by the high levels of tyrosine hydroxylase found in the small intestine [140]. Moreover, antibiotics-induced gut microbiota depletion decreases intestinal DA synthesis in mice [141] and GF mice show unequal brain mRNA expression of DA D1 receptor (D1R), being upregulated within the hippocampus and reduced at dorsal and ventral striatum level [1]. Hence, DA metabolism is drastically affected by the alteration of microbiota ecosystem.…”

Section: N-3 Pufas Serotonin Dopamine and Npdsmentioning

confidence: 85%

Dietary Fatty Acids and Microbiota-Brain Communication in Neuropsychiatric Diseases

Marrone

Coccurello

2019

Biomolecules

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The gut-brain axis is a multimodal communication system along which immune, metabolic, autonomic, endocrine and enteric nervous signals can shape host physiology and determine liability, development and progression of a vast number of human diseases. Here, we broadly discussed the current knowledge about the either beneficial or deleterious impact of dietary fatty acids on microbiota-brain communication (MBC), and the multiple mechanisms by which different types of lipids can modify gut microbial ecosystem and contribute to the pathophysiology of major neuropsychiatric diseases (NPDs), such as schizophrenia (SCZ), depression and autism spectrum disorders (ASD).

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Section: N-3 Pufas Serotonin Dopamine and Npdsmentioning

confidence: 85%

Dietary Fatty Acids and Microbiota-Brain Communication in Neuropsychiatric Diseases

Marrone

Coccurello

2019

Biomolecules

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“…Vitamin B6 depletion in AIMD may affect the metabolism of catecholamines, including L-dopa, dopamine, noradrenaline, and adrenaline, which are major neurotransmitters associated with the regulation of arousal. About half of the total peripheral dopamine is produced in the intestinal tract, and the levels of this metabolite are reduced under the AIMD condition 31,32 . Moreover, increased amounts of the inhibitory neurotransmitters GABA and glycine were observed under the AIMD condition.…”

Section: Discussionmentioning

confidence: 99%

Gut microbiota depletion by chronic antibiotic treatment alters the sleep/wake architecture and sleep EEG power spectra in mice

Ogawa

Miyoshi

Obana

et al. 2020

Sci Rep

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Dysbiosis of the gut microbiota affects physiological processes, including brain functions, by altering the intestinal metabolism. Here we examined the effects of the gut microbiota on sleep/wake regulation. C57BL/6 male mice were treated with broad-spectrum antibiotics for 4 weeks to deplete their gut microbiota. Metabolome profiling of cecal contents in antibiotic-induced microbiota-depleted (AIMD) and control mice showed significant variations in the metabolism of amino acids and vitamins related to neurotransmission, including depletion of serotonin and vitamin B6, in the AIMD mice. Sleep analysis based on electroencephalogram and electromyogram recordings revealed that AIMD mice spent significantly less time in non-rapid eye movement sleep (NREMS) during the light phase while spending more time in NREMS and rapid eye movement sleep (REMS) during the dark phase. The number of REMS episodes seen in AIMD mice increased during both light and dark phases, and this was accompanied by frequent transitions from NREMS to REMS. In addition, the theta power density during REMS was lower in AIMD mice during the light phase compared with that in the controls. Consequently, the gut microbiota is suggested to affect the sleep/wake architecture by altering the intestinal balance of neurotransmitters.

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“…A regulatory axis from the gut microbes to neurotransmitter and then to autoimmune system was proposed in both rodents and humans (Tognini, 2017 ). Xue et al ( 2018 ) showed that depletion of dopaminergic neurons significantly promoted activation of mice hepatic iNKT cells and augmented concanavalin A-induced liver injury by D1-like receptor-PKA pathway in mice. In the present study, expression of the genes in IGF-1/DAF-16 signaling ( age-1 and daf-16 ) and innate immune signaling pathways ( pmk-1 and sek-1 ) was significantly down-regulated in the mutant defective in cat-2 , and supplementation of dopamine to mutant cat-2 restored the expression of these genes to the level in the WT.…”

Section: Discussionmentioning

confidence: 99%

The Role of Neurotransmitters in the Protection of Caenorhabditis Elegans for Salmonella Infection by Lactobacillus

Liu

Jiang

et al. 2020

Front. Cell. Infect. Microbiol.

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Salmonellosis is a common foodborne disease. We previously reported the protection of Caenorhabditis elegans from Salmonella Typhimurium DT104 infection by Lactobacillus zeae LB1. However, the mechanism is not fully understood. C. elegans exhibits behavior plasticity when presented with diverse pathogenic or commensal bacteria. Whether it can exert approach avoidance to S . Typhimurium through altering its neurological activity remains to be determined. In the current study, both the wild type and mutants defective in serotonin or dopamine production of C. elegans were used to investigate olfactory preference of the nematode to L. zeae LB1, DT104, and Escherichia coli OP50 by choice assays, and its resistance to DT104 infection and the protection offered by L. zeae LB1 using a life-span assay. The expression of target genes in C. elegans was also examined by real-time quantitative PCR. Results showed that pre-exposure to L. zeae LB1 did not elicit aversive olfactory behavior of the nematode toward DT104. Both mutants tph-1 and cat-2 succumbed faster than the wild type when infected with DT104. While pre-exposure to L. zeae LB1 significantly increased the survival of both the wild type and mutant tph-1 , it provided no protection to mutant cat-2 . Supplementation of dopamine resulted in both the resistance of mutant cat-2 to S . Typhimurium infection and the protection from L. zeae LB1 to the same mutant. Gene expression data also supported the observations in the life-span assay. These results suggest that both serotonin and dopamine play a positive role in the host defense of C. elegans to S . Typhimurium infection and that the L. zeae LB1 protection is not dependent on modifying olfactory preference of the nematode but mediated by dopamine that may have involved the regulation of p38-mitogen-activated protein kinase and insulin/insulin-like growth factor signaling pathways.

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Peripheral Dopamine Controlled by Gut Microbes Inhibits Invariant Natural Killer T Cell-Mediated Hepatitis

Cited by 67 publications

References 50 publications

Dietary Fatty Acids and Microbiota-Brain Communication in Neuropsychiatric Diseases

Dietary Fatty Acids and Microbiota-Brain Communication in Neuropsychiatric Diseases

Gut microbiota depletion by chronic antibiotic treatment alters the sleep/wake architecture and sleep EEG power spectra in mice

The Role of Neurotransmitters in the Protection of Caenorhabditis Elegans for Salmonella Infection by Lactobacillus

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