scholarly journals Enterococcus Faecium is a Risk Factor for The Outbreak of Anxiety and Depression in Patients With Inflammatory Bowel Disease

2020 ◽  
Author(s):  
Hyo-Min Jang ◽  
Jeon-Kyung Kim ◽  
Min-Kyung Joo ◽  
Yun-Jung Shin ◽  
Kyung-Eon Lee ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Cell Population ◽  
Enterococcus Faecium ◽  
Fecal Microbiota ◽  
Specific Pathogen Free ◽  
Germ Free ◽  
Specific Pathogen ◽  
Inflammatory Bowel ◽  
Anxiety Depression

Abstract BackgroundThe gut microbiota closely communicate with the brain through the microbiota-gut-brain axis. The interaction between gut microbiota may regulate the occurrence of neuropsychiatric disorders, including depression. Therefore, we transplanted the fecal microbiota of patients with inflammatory bowel disease (IBD) or their overpopulated gut bacteria into specific-pathogen-free or germ-free mice and examined their effects regarding the occurrence of colitis and anxiety/depression. ResultsFecal microbiota transplantations (FMTs) from patients with IBD with (/D+) or without depression (/D-) caused IBD-like colitis in the transplanted mice: they increased myeloperoxidase activity and NF-κB+/CD11c+ cell population in the colon. FMTs from patients with IBD/D+ caused anxiety-/depression-like behaviors and NF-κB+/Iba1+ and lipopolysaccharide (LPS)+/Iba1+ cell population and decreased the BDNF+/NeuN+ cell population in the hippocampus. FMTs from patients with IBD/D- caused anxiety-like, but not depression-like, behaviors. α-/β-diversities and composition of microbiota in the feces of patients with IBD (IBD-F) were different from those of healthy-control feces (HC-F). The Enterobacteriaceae and Enterococcaceae populations and fecal lipopolysaccharide levels were higher in IBD-F vs. HC-F. Moreover, the Enterococcaceae population was higher in IBD/D+-F vs. IBD/D--F, while the Bifidobacteria population was lower in IBD/D+-F. FMT from HC alleviated the IBD/D+-F-induced anxiety-/depression-like behaviors and colitis in the transplanted mice. Furthermore, it suppressed IBD/D+-F-induced Enterococcus sp. population in the feces. Enterobacteriaceae Klebsiella oxytoca, Klebsiella pneumoniae, Escherichia coli, and Cronobacter sakazakii abundant in IBD-F, singly or together, caused depression with colitis in germ-free and specific-pathogen-free mice, while Enterococcus faecium abundant in IBD/D+-F did not cause not anxiety/depression and colitis. However, the combination of Enterobacteriaceae with Enterococcus faecium synergistically deteriorated depression and colitis, while its combination with Bifidobacterium longum attenuated them. ConclusionThe interaction between gut microbiota Enterobacteriaceae, Enterococci, and Bifidobacteria may regulate the outbreak of anxiety/depression and IBD through the modulation of NF-κB-involved BDNF expression and gut microbiota. Enterococcus faecium, a probiotic strain, is a risk factor for the outbreak of anxiety/depression in patients with IBD.

scholarly journals Transplantation of fecal microbiota from patients with inflammatory bowel disease and depression alters immune response and behavior in recipient mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hyo-Min Jang ◽  
Jeon-Kyung Kim ◽  
Min-Kyung Joo ◽  
Yoon-Jung Shin ◽  
Chang Kyun Lee ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Cell Population ◽  
Bowel Disease ◽  
Fecal Microbiota ◽  
Cell Populations ◽  
Microbiota Composition ◽  
Gut Dysbiosis ◽  
Inflammatory Bowel ◽  
Anxiety Depression

AbstractGut dysbiosis is closely associated with the occurrence of inflammatory bowel disease (IBD) and psychiatric disorder. Here, to understand the difference of gut microbiota composition and physiological effect between IBD patients with (IBD/D+) or without depression (IBD/D−), we analyzed the fecal microbiota composition of patients with IBD with (/D+) or without depression (/D−) and healthy volunteers (HVs) and examined the effects of these fecal microbiota transplantations (FMTs) on the occurrence of systemic inflammation and anxiety/depression in mice. FMTs from patients with IBD/D+ or IBD/D− caused IBD-like colitis in the transplanted mice: they increased the myeloperoxidase activity, IL-1β and IL-6 expression, and NF-κB+/CD11c+ cell population in the colon. Transplantation of the IBD/D+ patient feces (IBD/D+-F) caused IBD-like colitis more strongly than that of IBD/D−-F. FMTs from patients with IBD/D+ also caused anxiety-/depression-like behaviors, increased the NF-κB+/Iba1+ and lipopolysaccharide (LPS)+/Iba1+ cell populations, and decreased the BDNF+/NeuN+ cell population in the hippocampus. They increased LPS levels in the blood. FMTs from patients with IBD/D− caused anxiety-like, but not depression-like, behaviors. α-/β-diversities and composition of gut microbiota in IBD-F were different from those of HV feces (HV-F). The Enterobacteriaceae and Enterococcaceae populations and LPS levels were higher in the IBD-F than in the HV-F. The Enterococcaceae population was higher in IBD/D+-F vs. IBD/D−-F. However, the transplantation of HV-F into mice previously transplanted with IBD/D+-F significantly reduced depression-like behaviors, NF-κB+/Iba1+ and LPS+/Iba1+ cell populations in the hippocampus, LPS levels in the feces and blood, and IL-1β expression in the colon. These findings suggest that the outbreak of depression/anxiety may be dependent on the systemic inflammation with a leaky gut through the gut dysbiosis-attributable overproduction of bacterial LPS and suppression of tight junction protein expression in patients with IBD.

scholarly journals Microbiota Facilitates the Formation of the Aminated Metabolite of Tea Polyphenols Which Trap Deleterious Reactive Endogenous Metabolites (P06-022-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Shuwei Zhang ◽  
Yantao Zhao ◽  
Christina Ohland ◽  
Christian Jobin ◽  
Shengmin Sang
Keyword(s):  
Gut Microbiota ◽  
Chronic Diseases ◽  
Green Tea ◽  
Tea Polyphenols ◽  
Specific Pathogen Free ◽  
Tea Polyphenol ◽  
Germ Free ◽  
Specific Pathogen ◽  
Conjugated Metabolites

Abstract Objectives The in vivo mechanism of tea polyphenol-mediated prevention of many chronic diseases is still largely unknown. Studies have shown that accumulation of toxic reactive cellular metabolites, such as ammonia and reactive carbonyl species (RCS), is one of the causing factors to the development of many chronic diseases. The objective of this study is to investigated the in vivo interaction between tea polyphenols and ammonia and RCS. Methods In mice, we gave 200 mg/kg tea polyphenol ((-)-epigallocatechin-3-gallate (EGCG) or theaflavin) to CD-1 mice, 129/SvEv specific-pathogen-free (SPF) mice, or germ-free (GF) mice. Urinary and fecal samples were collected in metabolic cages for 24 h. In humans, two healthy volunteers drank 4 cups of Lipton green tea every day for four days. On the fourth day, 24 h urinary and fecal samples were collected after consuming the first cup of tea. Using LC tandem mass, we searched the formation of the aminated and RCS conjugated metabolites of tea polyphenols. Chemical standards were synthesized to confirm the structures of these metabolites. In order to study the impact of gut microbiota on the formation of these metabolites, we also quantified the concentrations of these metabolites in SPF and GF mice. Results We found that both EGCG and theaflavin could rapidly react with ammonia to generate the aminated metabolites. Both tea polyphenols and their aminated metabolites could further scavenge RCS, such as methylglyoxal (MGO), malondialdehyde (MDA), and trans-4-hydroxy-2-nonenal (4-HNE), to produce the RCS conjugates of tea polyphenols and the aminated tea polyphenols. Both the aminated and the RCS conjugated metabolites of EGCG were detected in human after drinking four cups of green tea per day. By comparing the levels of the aminated and the RCS conjugated metabolites in EGCG or theaflavin exposed germ-free (GF) mice and specific-pathogen-free (SPF) mice, we demonstrated that gut microbiota facilitate the formation of the aminated metabolites of tea polyphenols, the RCS conjugates of tea polyphenols, and the RCS conjugates of the aminated tea polyphenols. Conclusions Altogether, this study provides in vivo evidences that tea polyphenols have the capacity to scavenge toxic reactive metabolic wastes. This finding opens a new window to understand the underlying mechanisms by which drinking tea could prevent the development of chronic diseases. Funding Sources We gratefully acknowledge financial support from NIH R01 grant AT008623 to this work.

scholarly journals Inflammatory Bowel Disease–Associated Changes in the Gut: Focus on Kazan Patients

2020 ◽  
Author(s):  
Giuseppe Lo Sasso ◽  
Lusine Khachatryan ◽  
Athanasios Kondylis ◽  
James N D Battey ◽  
Nicolas Sierro ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Redox Status ◽  
Fecal Microbiota ◽  
Whole Genome ◽  
Industrialized Countries ◽  
Newly Industrialized Countries ◽  
Inflammatory Bowel

Abstract Background Several studies have highlighted the role of host–microbiome interactions in the pathogenesis of inflammatory bowel disease (IBD), resulting in an increasing amount of data mainly focusing on Western patients. Because of the increasing prevalence of IBD in newly industrialized countries such as those in Asia, the Middle East, and South America, there is mounting interest in elucidating the gut microbiota of these populations. We present a comprehensive analysis of several IBD-related biomarkers and gut microbiota profiles and functions of a unique population of patients with IBD and healthy patients from Kazan (Republic of Tatarstan, Russia). Methods Blood and fecal IBD biomarkers, serum cytokines, and fecal short-chain fatty acid (SCFA) content were profiled. Finally, fecal microbiota composition was analyzed by 16S and whole-genome shotgun sequencing. Results Fecal microbiota whole-genome sequencing confirmed the presence of classic IBD dysbiotic features at the phylum level, with increased abundance of Proteobacteria, Actinobacteria, and Fusobacteria and decreased abundance of Firmicutes, Bacteroidetes, and Verrucomicrobia. At the genus level, the abundance of both fermentative (SCFA-producing and hydrogen (H2)-releasing) and hydrogenotrophic (H2-consuming) microbes was affected in patients with IBD. This imbalance was confirmed by the decreased abundance of SCFA species in the feces of patients with IBD and the change in anaerobic index, which mirrors the redox status of the intestine. Conclusions Our analyses highlighted how IBD-related dysbiotic microbiota—which are generally mainly linked to SCFA imbalance—may affect other important metabolic pathways, such as H2 metabolism, that are critical for host physiology and disease development.

scholarly journals Mice, Models, Microbiota: How Can We More Accurately Reflect Human Disease?

2021 ◽  
Vol 15 (1) ◽  
pp. 8
Author(s):  
Rahman Ladak ◽  
Dana Philpott
Keyword(s):  
Gut Microbiota ◽  
Translational Research ◽  
Mouse Models ◽  
Human Disease ◽  
Specific Pathogen Free ◽  
Germ Free ◽  
Stage Of Development ◽  
Specific Pathogen

With growing evidence that human disease is affected by the microbiota, many researchers have sought to modulate the microbiomes of mice to improve translational research. Altering their microbiomes, which are usually germ-free or specific pathogen-free, might allow mice to more accurately model human disease and hence produce more applicable findings. However, this has been difficult to apply to individual projects due to the disparity of explained methods and results. In this review, we first describe the immunological functions of the gut microbiota and the methods of altering mice microbiota, from transplantation route to age of transplantation to microbiota source. We then present an approach for how the gut microbiota might be considered when modelling human disease in mice. By organizing findings by type of disease - neurological, immunological, chronic inflammatory, and cancer - we propose that mouse models can be improved by considering the source of the microbiota, the presence or absence of certain microbial phyla, and by timing the transplantation during a physiologically relevant stage of development, such as the first five weeks of life.

scholarly journals Defined microbiota transplant restores Th17/RORγt+regulatory T cell balance in mice colonized with inflammatory bowel disease microbiotas

2020 ◽  
Vol 117 (35) ◽  
pp. 21536-21545 ◽  
Author(s):  
Graham J. Britton ◽  
Eduardo J. Contijoch ◽  
Matthew P. Spindler ◽  
Varun Aggarwala ◽  
Belgin Dogan ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Th17 Cells ◽  
Fecal Microbiota Transplantation ◽  
Cell Subset ◽  
Treg Cells ◽  
Fecal Microbiota ◽  
Inflammatory Bowel

The building evidence for the contribution of microbiota to human disease has spurred an effort to develop therapies that target the gut microbiota. This is particularly evident in inflammatory bowel diseases (IBDs), where clinical trials of fecal microbiota transplantation have shown some efficacy. To aid the development of novel microbiota-targeted therapies and to better understand the biology underpinning such treatments, we have used gnotobiotic mice to model microbiota manipulations in the context of microbiotas from humans with inflammatory bowel disease. Mice colonized with IBD donor-derived microbiotas exhibit a stereotypical set of phenotypes, characterized by abundant mucosal Th17 cells, a deficit in the tolerogenic RORγt+regulatory T (Treg) cell subset, and susceptibility to disease in colitis models. Transplanting healthy donor-derived microbiotas into mice colonized with human IBD microbiotas led to induction of RORγt+Treg cells, which was associated with an increase in the density of the microbiotas following transplant. Microbiota transplant reduced gut Th17 cells in mice colonized with a microbiota from a donor with Crohn’s disease. By culturing strains from this microbiota and screening them in vivo, we identified a specific strain that potently induces Th17 cells. Microbiota transplants reduced the relative abundance of this strain in the gut microbiota, which was correlated with a reduction in Th17 cells and protection from colitis.

scholarly journals Fecal microbiota profile in patients with inflammatory bowel disease in Taiwan

2020 ◽  
Author(s):  
Tien-En Chang ◽  
Jiing-Chyuan Luo ◽  
Ueng-Cheng Yang ◽  
Yi-Hsiang Huang ◽  
Ming-Chih Hou ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Structural Difference ◽  
Fecal Microbiota ◽  
Control Group ◽  
Sequence Variant ◽  
Healthy Controls ◽  
Significant Difference ◽  
Inflammatory Bowel

Abstract Background Inflammatory bowel disease (IBD) is a chronic inflammatory disease that associated with complicated interaction between immune, gut microbiota and environmental factors in a genetically vulnerable host. Dysbiosis is often seen in patients with IBD. Our aim is to investigate the fecal microbiota in patients with IBD and compared to healthy controls in Taiwan. Methods In this cross-sectional study, we investigated fecal microbiota in 20 patients with IBD and 48 healthy controls. Fecal samples from both IBD patients and controls were analyzed by next-generation sequencing method and relevant software. Results The IBD group showed lower bacterial richness and diversity compared to the control group. The principal coordinate analysis also revealed significant structural difference between the IBD group and the control group. These findings were consistent whether the analysis was based on operational taxonomic unit or amplicon sequence variant. However, no significant difference was found when comparing the composition of fecal microbiota between ulcerative colitis (UC) and Crohn’s disease (CD). Further analysis showed that Lactobacillus, Enterococcus, Bifidobacterium and Veillonella were dominant in the IBD group, while Faecalibacterium and Subdoligranulum were dominant in the control group at genus level. When comparing UC, CD and control group, Lactobacillus, Bifidobacterium and Enterococcus were identified as dominant genera in the UC group. Fusobacterium and Escherichia_Shigella were dominant in the CD group. Faecalibacterium and Subdoligranulum were dominant in the control group. Conclusions Compared to the healthy control, the IBD group showed dysbiosis with a significant decreased in both richness and diversity of gut microbiota.

scholarly journals Gut microbiota modification as an option in multiple sclerosis management

2020 ◽  
Author(s):  
Beata Zwiernik ◽  
Tomasz Arłukowicz ◽  
Marcin Mycko ◽  
Jacek Zwiernik
Keyword(s):  
Multiple Sclerosis ◽  
Inflammatory Bowel Disease ◽  
Immune System ◽  
Gut Microbiota ◽  
Medical Literature ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
T And B Cells ◽  
Inflammatory Bowel ◽  
Comprehensive Intervention

Introduction: Multiple sclerosis (MS) is caused by the abnormal activity of the immune system. It is believed that the pathological immune response may be initiated in the intestines, the area of the largest antigen presentation. This is where autoreactive T and B cells are activated, which constitutes the pathomechanism of this disease. In a healthy organism, normal gut microbiota mediates the balance between pro- and anti-inflammatory activity of the immune system. Aim: This paper aims at describing the healthy gut microbiota, its changes in MS patients, factors that influence its composition and therapeutic corrective possibilities. Material and methods: The paper is based on available medical literature. Results and discussion: It has been evidenced that in MS patients the gut microbiota is dominated by pro-inflammatory species. This may be caused by environmental factors, for instance, the diet, antibiotics or stimulants. Methods of the microbiota correction involve dietary change, prebiotics and probiotics as well as fecal microbiota transplantation (FMT). FMT is a particularly safe and promising method that has proven its efficiency on an animal model of MS. Conclusions: Experimental research has revealed that the correction of the gut microbiota may lead to MS remission or alleviation. FMT utilized in inflammatory bowel disease seems to be presently the most comprehensive intervention. Since only incidental reports of its efficiency in humans are presently available, further clinical studies are necessary.

scholarly journals Buspirone alleviates anxiety, depression, and colitis; and modulates gut microbiota in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jeon-Kyung Kim ◽  
Sang-Kap Han ◽  
Min-Kyung Joo ◽  
Dong-Hyun Kim
Keyword(s):  
Gut Microbiota ◽  
Normal Control ◽  
Cell Population ◽  
Intraperitoneal Administration ◽  
Fecal Microbiota ◽  
Myeloperoxidase Activity ◽  
Brain Functions ◽  
Β Diversity ◽  
Tnf Α ◽  
Anxiety Depression

AbstractGut microbiota regulate the neurodevelopmental processes and brain functions through the regulation of the microbiota–gut interaction and gut–brain communication. Buspirone, an agonist for serotonin 5-HT1A receptors, is used for the treatment of anxiety/depression. Therefore, to understand the gut microbiota-mediated mechanism of buspirone on anxiety/depression, we examined its effect on the immobilization stress (IS) or Escherichia coli K1 (EC)-induced anxiety/depression in mice. Oral or intraperitoneal administration of buspirone significantly suppressed stressor-induced anxiety/depression-like behaviors in the elevated plus maze, light/dark transition, tail suspension, and forced swimming tasks. Their treatments also reduced TNF-α expression and NF-κB+/Iba1+ cell population in the hippocampus and myeloperoxidase activity and NF-κB+/CD11c+ cell population in the colon. Buspirone treatments partially restored IS- or EC-induced gut microbiota perturbation such as β-diversity to those of normal control mice: they reduced the IS- or EC-induced gut Proteobacteria population. In particular, the anxiolytic activity of buspirone was positively correlated with the populations of Bacteroides and PAC001066_g in EC- or IS-exposed mice, while the populations of Lachnospiraceae, KE159660_g, LLKB_g, Helicobacter, and PAC001228_g were negatively correlated. The anti-depressant effect of buspirone was positively correlated with the Roseburia population. The fecal microbiota transplantations from buspirone-treated mice with IS-induced anxiety/depression or normal control mice suppressed IS-induced anxiety/depression-like behaviors and reduced hippocampal NF-κB+/Iba1+ and colonic NF-κB+/CD11c+ cell populations in the transplanted mice. Furthermore, they modified IS-induced perturbation of gut microbiota composition, particularly Proteobacteria, in the transplanted mice. In conclusion, buspirone alleviates IS as well as EC-induced anxiety/depression and colitis. It also suppresses associated neuroinflammation and modulates gut microbiota. Future studies can help to explain the relationship, if any, in the central and peripheral effects of buspirone.

scholarly journals Antibiotic use differentially affects the risk of anti-drug antibody formation during anti-TNFα therapy in inflammatory bowel disease patients: a report from the epi-IIRN

Gut ◽  
2021 ◽  
pp. gutjnl-2021-325185
Author(s):  
Yuri Gorelik ◽  
Shay Freilich ◽  
Shiran Gerassy-Vainberg ◽  
Sigal Pressman ◽  
Chagit Friss ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Antibiotic Use ◽  
Microbial Composition ◽  
Germ Free ◽  
Increased Risk ◽  
C57bl Mice ◽  
Specific Pathogen ◽  
Inflammatory Bowel ◽  
Time Varying Covariates

ObjectiveAnti-drug antibodies (ADA) to anti-tumour necrosis factor (anti-TNF) therapy drive treatment loss of response. An association between intestinal microbial composition and response to anti-TNF therapy was noted. We therefore aimed to assess the implications of antibiotic treatments on ADA formation in patients with inflammatory bowel disease (IBD).DesignWe analysed data from the epi-IIRN (epidemiology group of the Israeli IBD research nucleus), a nationwide registry of all patients with IBD in Israel. We included all patients treated with anti-TNF who had available ADA levels. Survival analysis with drug use as time varying covariates were used to assess the association between antibiotic use and ADA development. Next, specific pathogen and germ-free C57BL mice were treated with respective antibiotics and challenged with infliximab. ADA were assessed after 14 days.ResultsAmong 1946 eligible patients, with a median follow-up of 651 days from initiation of therapy, 363 had positive ADA. Cox proportional hazard model demonstrated an increased risk of ADA development in patients who used cephalosporins (HR=1.97, 95% CI 1.58 to 2.44), or penicillins with β-lactamase inhibitors (penicillin-BLI, HR=1.4, 95% CI 1.13 to 1.74), whereas a reduced risk was noted in patients treated with macrolides (HR=0.38, 95% CI 0.16 to 0.86) or fluoroquinolones (HR=0.20, 95% CI 0.12 to 0.35). In mice exposed to infliximab, significantly increased ADA production was observed in cephalosporin as compared with macrolide pretreated mice. Germ-free mice produced no ADA.ConclusionADA production is associated with the microbial composition. The risk of ADA development during anti-TNF therapy can possibly be reduced by avoidance of cephalosporins and penicillin-BLIs, or by treatment with fluoroquinolones or macrolides.

The gut microbiome modulates nitroglycerin-induced migraine-related hyperalgesia in mice

Cephalalgia ◽  
2021 ◽  
pp. 033310242110500
Author(s):  
Li Kang ◽  
Wenjing Tang ◽  
Yaofen Zhang ◽  
Mingjie Zhang ◽  
Jing Liu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Gut Microbiome ◽  
Expression Level ◽  
Specific Pathogen Free ◽  
Trigeminal Nucleus ◽  
Germ Free ◽  
Microbial Profile ◽  
Matched Healthy Control ◽  
Specific Pathogen ◽  
Healthy Control

Background Gut microbiota disturbance is increasingly suggested to be involved in the pathogenesis of migraine but this connection remains unsubstantiated. This study aimed to investigate whether the gut microbiome influences migraine-related hyperalgesia. Methods Nitroglycerin-induced hyperalgesia was evaluated in mice with different gut microbiota statuses as follows: Specific pathogen-free mice; germ-free mice; specific pathogen-free mice treated with antibiotics to deplete the gut microbiome (ABX mice); and germ-free mice transplanted with the gut microbial profile from specific pathogen-free mice (GFC mice). Moreover, nitroglycerin-induced hyperalgesia was compared between recipient mice transplanted with gut microbiota from a patient with migraine and those that received gut microbiota from a sex- and age-matched healthy control. Results In specific pathogen-free mice, a decreased mechanical threshold in the hind paw, increased grooming time, increased c-Fos expression level and decreased calcitonin gene-related peptide expression level as well as increased tumor necrosis factor-α concentration in the trigeminal nucleus caudalis were observed after nitroglycerin administration compared with saline treatment. However, increased basal sensitivity and higher basal concentrations of TNF-α in the trigeminal nucleus caudalis were observed in germ-free and ABX mice, while no significant difference in hyperalgesia was observed between the nitroglycerin group and saline group in germ-free and ABX mice. Moreover, significant hyperalgesia was induced by nitroglycerin administration in GFC mice. The mice transplanted with the gut microbial profile from a patient with migraine had more severe nitroglycerin-induced hyperalgesia than the mice receiving microbiota from a matched healthy control. Conclusion Our findings highlight the involvement of the gut microbiome in normal mechanical pain sensation and pathogenesis of migraine.

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