Dectin-1 signaling on colonic γδ T cells promotes psychosocial stress responses

Zhu, Xiaolei; Sakamoto, Shinji; Ishii, Chiharu; Smith, Matthew D.; Ito, Koki; Obayashi, Mizuho; Unger, L; Hasegawa, Yuto; Kurokawa, Shunya; Kishimoto, Toshifumi; Li, Hui; Hatano, Shoji; Wang, Tza‐Huei; Yoshikai, Yasunobu; Kano, Shin-ichi; Fukuda, Shinji; Sanada, Kenji; Calabresi, Peter A.; Kamiya, Atsushi

doi:10.1038/s41590-023-01447-8

Cited by 35 publications

(16 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A decrease in certain Lactobacilli associated with increased differentiation and accumulation of IL-17-producing γδ17 T cells in the meninges was observed in a study analyzing the microbiome characteristics of stress-sensitive mice and patients with major depression. This study demonstrates that this alteration promoted stress-induced social avoidance behaviors in mice and oral administration of the dectin-1 ligand porin glucan modulated the stress response to chronic social stress 149. Another study reported that plant-derived diosgenin might reduce inflammation-related brain injury by regulating the Firmicutes and Lactobacillus, enhancing neurotrophic functions, and suppressing inflammatory and neuroendocrine activities 150.…”

mentioning

confidence: 69%

“…Reshape the GM profile and maintain gut immune homeostasis Optimize synapse and cognition-associated genes, and improve cognitive impairment [148] Dectin-1 ligand pachyman Regulate gut immunity homeostasis and control Treg cell differentiation in the intestine Prevent stress-induced behavioral abnormalities [149] Diosgenin Upregulate the relative abundance of Lactobacillus and the expression of SCFAs, and restore the activity of the HPA axis Alleviate inflammation-related brain injury behavior [150] Abbreviations: BBB, blood-brain barrier; GM, gut microbiota; HPA, hypothalamic-pituitary-adrenal; SCFAs, short-chain fatty acids.…”

Section: Drugs Impact On Microbiota Effects Referencesmentioning

confidence: 99%

See 1 more Smart Citation

Treatment of preterm brain injury via gut‐microbiota–metabolite–brain axis

Li,

Liu,

Shi

2023

CNS Neurosci Ther

View full text Add to dashboard Cite

BackgroundBrain injury in preterm infants potentially disrupts critical structural and functional connective networks in the brain. It is a major cause of neurological sequelae and developmental deficits in preterm infants. Interesting findings suggest that the gut microbiota (GM) and their metabolites contribute to the programming of the central nervous system (CNS) during developmental stages and may exert structural and functional effects throughout the lifespan.AimTo summarize the existing knowledge of the potential mechanisms related to immune, endocrine, neural, and blood–brain barrier (BBB) mediated by GM and its metabolites in neural development and function.MethodsWe review the recent literature and included 150 articles to summarize the mechanisms through which GM and their metabolites work on the nervous system. Potential health benefits and challenges of relevant treatments are also discussed.ResultsThis review discusses the direct and indirect ways through which the GM may act on the nervous system. Treatment of preterm brain injury with GM or related derivatives, including probiotics, prebiotics, synbiotics, dietary interventions, and fecal transplants are also included.ConclusionThis review summarizes mechanisms underlying microbiota‐gut‐brain axis and novel therapeutic opportunities for neurological sequelae in preterm infants. Optimizing the initial colonization and microbiota development in preterm infants may represent a novel therapy to promote brain development and reduce long‐term sequelae.

show abstract

mentioning

confidence: 69%

Section: Drugs Impact On Microbiota Effects Referencesmentioning

confidence: 99%

Treatment of preterm brain injury via gut‐microbiota–metabolite–brain axis

Li,

Liu,

Shi

2023

CNS Neurosci Ther

View full text Add to dashboard Cite

show abstract

“… Medina-Rodriguez et al (2023) found that the microbial effect was dependent on the presence of Th17 cells in the recipient, which plays a key role in regulating behavioral changes induced by the microbiome of depressed patients. Zhu et al (2023) reported that specific Lactobacillus species affected stress-induced social-avoidance behavior by involving in T cell differentiation mediated immune response. Combined with our research and published literatures, microbiota affects behavioral changes mainly or partly involved in immune response.…”

Section: Discussionmentioning

confidence: 99%

Role of microbiota-gut-brain axis in natural aging-related alterations in behavior

Jing,

Wang,

Bai

et al. 2024

Front. Neurosci.

View full text Add to dashboard Cite

IntroductionAging is a complex, time-dependent biological process that involves a decline of overall function. Over the past decade, the field of intestinal microbiota associated with aging has received considerable attention. However, there is limited information surrounding microbiota-gut-brain axis (MGBA) to further reveal the mechanism of aging.MethodsIn this study, locomotory function and sensory function were evaluated through a series of behavioral tests.Metabolic profiling were determined by using indirect calorimetry.16s rRNA sequence and targeted metabolomics analyses were performed to investigate alterations in the gut microbiota and fecal short-chain fatty acids (SCFAs). The serum cytokines were detected by a multiplex cytokine assay.The expression of proinflammatory factors were detected by western blotting.ResultsDecreased locomotor activity, decreased pain sensitivity, and reduced respiratory metabolic profiling were observed in aged mice. High-throughput sequencing revealed that the levels of genus Lactobacillus and Dubosiella were reduced, and the levels of genus Alistipes and Bacteroides were increased in aged mice. Certain bacterial genus were directly associated with the decline of physiological behaviors in aged mice. Furthermore, the amount of fecal SCFAs in aged mice was decreased, accompanied by an upregulation in the circulating pro-inflammatory cytokines and increased expression of inflammatory factors in the brain.DiscussionAging-induced microbial dysbiosis was closely related with the overall decline in behavior, which may attribute to the changes in metabolic products, e.g., SCFAs, caused by an alteration in the gut microbiota, leading to inflammaging and contributing to neurological deficits. Investigating the MGBA might provide a novel viewpoint to exploring the pathogenesis of aging and expanding appropriate therapeutic targets.

show abstract

“… 214 The commensal bacteria, Segmented filamentous bacterium , for example, is sufficient to promote Th17 cell- induced depressive-like behaviors in mice and Segmented filamentous bacterium -specific Th17 cells have been shown to migrate to the hippocampus after stress. 107 Recently, Lactobacillus - dependent colonic IL-17A-producing T cells were shown to promote chronic social defeat 215 and IL-17A-producing T cells also promote anxiety-like behaviors, 216 pointing to the importance of IL-17A in promoting microbial-dependent stress-related behaviors. The importance of Th17 cells in mediating the effect of the microbiota after stress was further demonstrated using fecal transfer.…”

Section: Gut-brain Axis Immunity and Stressmentioning

confidence: 99%

Stress in the microbiome-immune crosstalk

Beurel

2024

Gut Microbes

View full text Add to dashboard Cite

The gut microbiota exerts a mutualistic interaction with the host in a fragile ecosystem and the host intestinal, neural, and immune cells. Perturbations of the gastrointestinal track composition after stress have profound consequences on the central nervous system and the immune system. Reciprocally, brain signals after stress affect the gut microbiota highlighting the bidirectional communication between the brain and the gut. Here, we focus on the potential role of inflammation in mediating stress-induced gut-brain changes and discuss the impact of several immune cells and inflammatory molecules of the gut-brain dialogue after stress. Understanding the impact of microbial changes on the immune system after stress might provide new avenues for therapy.

show abstract

Dectin-1 signaling on colonic γδ T cells promotes psychosocial stress responses

Cited by 35 publications

References 71 publications

Treatment of preterm brain injury via gut‐microbiota–metabolite–brain axis

Treatment of preterm brain injury via gut‐microbiota–metabolite–brain axis

Role of microbiota-gut-brain axis in natural aging-related alterations in behavior

Stress in the microbiome-immune crosstalk

Contact Info

Product

Resources

About