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Gut Microbiota and Psychological Distress in Fibromyalgia: A Systematic Review.
OBJECTIVE: This systematic review aimed to summarize the recent evidence of the relationship between gut microbiota and psychological distress in patients with fibromyalgia (FM). METHODS: According to PRISMA guidelines, we conducted a systematic search of the literature on PubMed, Scopus, EBSCO, Web of Science, and Cochrane. The records were selected using multiple combinations of relevant search terms involving microbiota, psychological distress, and FM. Articles in English with human participants were reviewed. RESULTS: The initial search identified 135 records, excluding duplicates, of which 10 research reports met the predefined inclusion criteria and were analyzed. Most studies ( n = 7) were case-control, 2 were randomized controlled trials, and 1 was observational. Most studies found an imbalance in the gut microbial communities of FM patients and a significant difference between FM patients and HC in microbiome composition/diversity or gut permeability. Intestinal dysbiosis and gut permeability were also associated with high psychological distress (emotional, cognitive, and somatic symptoms). CONCLUSIONS: Alterations in the gut microbiota of FM patients seem to support the hypothesis that gut-brain axis regulation is impaired in stress-related pain conditions. Although the results are promising, further studies are needed to clarify the role of the microbiota-gut-brain axis in the pathophysiological mechanisms underlying FM.
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Loss of eating control and cognitive flexibility: Involvement of gut microbiota.
Loss of eating control is a crucial factor in developing obesity, which has become a global health concern, causing important cardiovascular, metabolic, emotional, and cognitive co-morbidities. A major cognitive alteration associated with loss of eating control and obesity is the impairment of cognitive flexibility and inhibitory control. An increasing number of studies confirm that gut microbiota is a significant contributor to loss of eating control, obesity, and cognitive function. Therefore, we have investigated whether gut microbiota transfer from humans with impaired/not impaired cognitive flexibility could substantially affect this behavioral response in mice in the context of obesogenic versus standard diet. Mice were pretreated with an antibiotic cocktail and later received a gut microbiota transplant from human subjects. The transferred microbiota was maintained in mice for seven weeks. Afterward, behavioral tests were performed to evaluate different cognitive responses, locomotor activity, anxiety-like, and depression-like behaviors. Antibiotic treatment significantly impaired short-term memory in mice, as previously reported. Furthermore, mice that received microbiota from high and low cognitive flexibility subjects modified their short-term and long-term memory performance depending on the diet exposure. Slight changes were observed in the locomotor activity, primarily in the high-fat diet-fed antibiotic-treated mice, and no significant alterations were observed in anxiety-like or depressive-like behaviors. In summary, this study shows that gut microbiota is a major contributor to cognitive flexibility, which may open novel therapeutic strategies for combating loss of eating control and related metabolic co-morbidities.
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Polysaccharide Engineered Nanozymes Target Inflammation for Alleviating Colitis-Associated Mental Disorders via Microbiome-Gut-Brain Axis.
Molecular therapies for colitis-associated mental disorders show limited efficacy because they usually focus on a single pathway and exhibit substantial off-target toxicity toward healthy tissues. To tackle this limitation, bioinformatic approaches are employed to predict that inflammation and metabolism may be potential targets for Fucoidan. Guided by this prediction, we develop oral polysaccharide engineered nanozymes, Fucoidan-cerium nanocomplexes (FucCeNCs), which are capable of targeting the inflamed colon through electrostatic interactions, exerting anti-inflammatory effects, and concurrently regulating gut microbiota-derived metabolism. In a murine model of ulcerative colitis-associated mental disorders, FucCeNCs show anti-inflammatory and gut barrier-protective effects, thereby suppressing microglial/astrocytic overactivation and preserving neuronal integrity through the transmission of anti-inflammatory cytokines via gut-brain axis. Importantly, FucCeNCs restore gut microbial homeostasis through increasing the relative abundance of probiotics and reducing proportions of pathogens. This shift results in a marked attenuation of abnormal amino acid biosynthesis and metabolism in fecal metabolites, which in turn leads to elevated levels of bioactive metabolites such as homovanillic acid and γ-aminobutyric acid. These metabolites ultimately attenuate neuroinflammation via the microbiome-gut-brain axis, ameliorating depression- and anxiety-like behaviors. These results identify microbiome-gut-brain axis as pivotal therapeutic target for colitis-associated mental disorders therapy, which can be addressed by polysaccharide engineered nanozymes.
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Influence of Tryptophan and Serotonin on Mood and Cognition with a Possible Role of the Gut-Brain Axis.
The serotonergic system forms a diffuse network within the central nervous system and plays a significant role in the regulation of mood and cognition. Manipulation of tryptophan levels, acutely or chronically, by depletion or supplementation, is an experimental procedure for modifying peripheral and central serotonin levels. These studies have allowed us to establish the role of serotonin in higher order brain function in both preclinical and clinical situations and have precipitated the finding that low brain serotonin levels are associated with poor memory and depressed mood. The gut-brain axis is a bi-directional system between the brain and gastrointestinal tract, linking emotional and cognitive centres of the brain with peripheral functioning of the digestive tract. An influence of gut microbiota on behaviour is becoming increasingly evident, as is the extension to tryptophan and serotonin, producing a possibility that alterations in the gut may be important in the pathophysiology of human central nervous system disorders. In this review we will discuss the effect of manipulating tryptophan on mood and cognition, and discuss a possible influence of the gut-brain axis.
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Manipulation of gut microbiota blunts the ventilatory response to hypercapnia in adult rats.
BACKGROUND: It is increasingly evident that perturbations to the diversity and composition of the gut microbiota have significant consequences for the regulation of integrative physiological systems. There is growing interest in the potential contribution of microbiota-gut-brain signalling to cardiorespiratory control in health and disease. METHODS: In adult male rats, we sought to determine the cardiorespiratory effects of manipulation of the gut microbiota following a 4-week administration of a cocktail of antibiotics. We subsequently explored the effects of administration of faecal microbiota from pooled control (vehicle) rat faeces, given by gavage to vehicle- and antibiotic-treated rats. FINDINGS: Antibiotic intervention depressed the ventilatory response to hypercapnic stress in conscious animals, owing to a reduction in the respiratory frequency response to carbon dioxide. Baseline frequency, respiratory timing variability, and the expression of apnoeas and sighs were normal. Microbiota-depleted rats had decreased systolic blood pressure. Faecal microbiota transfer to vehicle- and antibiotic-treated animals also disrupted the gut microbiota composition, associated with depressed ventilatory responsiveness to hypercapnia. Chronic antibiotic intervention or faecal microbiota transfer both caused significant disruptions to brainstem monoamine neurochemistry, with increased homovanillic acid:dopamine ratio indicative of increased dopamine turnover, which correlated with the abundance of several bacteria of six different phyla. INTERPRETATION: Chronic antibiotic administration and faecal microbiota transfer disrupt gut microbiota, brainstem monoamine concentrations and the ventilatory response to hypercapnia. We suggest that aberrant microbiota-gut-brain axis signalling has a modulatory influence on respiratory behaviour during hypercapnic stress. FUND: Department of Physiology and APC Microbiome Ireland, University College Cork, Ireland.
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Gut microbial diversity analysis using Illumina sequencing for functional dyspepsia with liver depression-spleen deficiency syndrome and the interventional Xiaoyaosan in a rat model.
AIM: To investigate gut microbial diversity and the interventional effect of Xiaoyaosan (XYS) in a rat model of functional dyspepsia (FD) with liver depression-spleen deficiency syndrome. METHODS: The FD with liver depression-spleen deficiency syndrome rat model was established through classic chronic mild unpredictable stimulation every day. XYS group rats received XYS 1 h before the stimulation. The models were assessed by parameters including state of the rat, weight, sucrose test result and open-field test result. After 3 wk, the stools of rats were collected and genomic DNA was extracted. PCR products of the V4 region of 16S rDNA were sequenced using a barcoded Illumina paired-end sequencing technique. The primary composition of the microbiome in the stool samples was determined and analyzed by cluster analysis. RESULTS: Rat models were successfully established, per data from rat state, weight and open-field test. The microbiomes contained 20 phyla from all samples. Firmicutes, Bacteroidetes, Proteobacteria, Cyanobacteria and Tenericutes were the most abundant taxonomic groups. The relative abundance of Firmicutes, Proteobacteria and Cyanobacteria in the model group was higher than that in the normal group. On the contrary, the relative abundance of Bacteroidetes in the model group was lower than that in the normal group. Upon XYS treatment, the relative abundance of all dysregulated phyla was restored to levels similar to those observed in the normal group. Abundance clustering heat map of phyla corroborated the taxonomic distribution. CONCLUSION: The microbiome relative abundance of FD rats with liver depression-spleen deficiency syndrome was significantly different from the normal cohort. XYS intervention may effectively adjust the gut dysbacteriosis in FD.
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Christensenella minuta mitigates behavioral and cardiometabolic hallmarks of social defeat stress.
Psychological stress during early development and adolescence may increase the risk of psychiatric and cardiometabolic comorbidities in adulthood. The gut microbiota has been associated with mental health problems such as depression and anxiety and with cardiometabolic disease, but the potential role of the gut microbiota in their comorbidity is not well understood. We investigated the effects and mode of action of the intestinal bacterium Christensenella minuta DSM 32891 on stress-induced mental health and cardiometabolic disturbances in a mouse model of social defeat stress. We demonstrate that administered C. minuta alleviates chronic stress-induced depressive, anxiogenic and antisocial behavior. These effects are attributed to the bacterium's ability to modulate the hypothalamic-pituitary-adrenal axis, which mediates the stress response. This included the oversecretion of corticosterone and the overexpression of its receptors, as well as the metabolism of dopamine (DA) and the expression of its receptors (D1, D2L and D2S). Additionally, C. minuta administration reduced chronically induced inflammation in plasma, spleen and some brain areas, which likely contribute to the recovery of physical and behavioral function. Furthermore, C. minuta administration prevented chronic stress-induced cardiovascular damage by regulating key enzymes mediating liver fibrosis and oxidative stress. Finally, C. minuta increased the abundance of bacteria associated with mental health. Overall, our study highlights the potential of microbiota-directed interventions to alleviate both the physical and mental effects of chronic stress.
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Gut Microbiota and Neurologic Diseases and Injuries.
The brain-gut axis is a bidirectional communication pathway connecting the central nervous system (CNS) and the gastrointestinal tract via nerve transmission, hormone, immune system, and other molecular signals. The bacterial flora of the human gut contributes direct and indirect signals to the CNS along the brain-gut axis. Alterations in gut flora, a state known as dysbiosis, has been tied to systemic inflammation, increased bacterial translocation, and increased absorbance of microbial by-products. An increase in recent literature has highlighted the role of the gut-brain axis in CNS pathology. This chapter reviews the association between gut flora dysbiosis and disorders of the central nervous system including autoimmune disease, developmental disorders, physiologic response to traumatic injury, and neurodegenerative disease.
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Pulsatilla chinensis Saponins Ameliorate Inflammation and DSS-Induced Ulcerative Colitis in Rats by Regulating the Composition and Diversity of Intestinal Flora.
Pulsatilla chinensis (Bunge) Regel is a commonly used Chinese medicine for clearing away heat and detoxification, cooling blood, stopping dysentery, and anti-inflammatory effects. Pulsatilla chinensis saponins (PRS) have been identified to be responsible for producing these pharmacological activities. Studies have shown that Pulsatilla decoction has a good therapeutic effect on ulcerative colitis (UC), however, the therapeutic effect of PRS on UC has not been reported. Therefore, the purpose of this study was to investigate the possible anti-UC activity of PRS using a dextran sulfate sodium (DSS)-induced rat model, and further study the mechanism of PRS in the treatment of UC. The fecal and colon samples were collected from rats to monitor the changes in the composition and diversity of the intestinal flora, and pathological colon sections were also made to examine the mesenteric hemorheological characteristics. The results showed that PRS significantly reduced the mesenteric blood flow in UC rats and significantly alleviated the inflammatory response, which indicates that saponins are involved in the anti-UC effects of PRS. At the same time, it is also suggested that the regulation of intestinal flora by Pulsatilla chinensis saponins is an important pathway for its anti-UC activity, which may be ascribed to the increase in beneficial bacteria like norank_F_Muribaculaceae and norank_F_norank_O_Clostridia_UCG-014, and decrease in the harmful Bacteroides.
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Transcriptional markers of excitation-inhibition balance in germ-free mice show region-specific dysregulation and rescue after bacterial colonization.
BACKGROUND: Studies of germ-free (GF) mice demonstrate that gut microbiota can influence behaviour by modulating neurochemical pathways in the brain, and that bacterial colonization normalizes behavioural deficits in GF-mice. Since disrupted GABAergic and glutamatergic signaling are reported in mood disorders, this study investigated the effect of gut microbiota manipulations on EIB-relevant gene expression in the brain. METHODS: GF Swiss-Webster mice were colonized with E. coli JM83, complex microbiota (specific-pathogen-free; SPF), or no microbiota, and compared with controls (n = 6/group). 21 synaptic genes representing GABAergic, glutamatergic, BDNF, and astrocytic functions were measured in the hippocampus, amygdala, and prefrontal cortex using quantitative PCR. Gene co-expression analysis was used to identify gene modules related to colonization status, and compared by permutation analysis. Gene expression profiles were compared to existing post-mortem cohorts of depressed subjects (n = 28 cases vs 28 controls). RESULTS: Region-specific alterations in gene expression were observed in GF-mice compared to controls. 58% of all genes (14/24) altered in GF-mice were normalized following SPF-colonization. GF-mice displayed disorganization of gene co-expression networks in all three brain regions (hippocampus, p = 0.0003; amygdala, p = 0.0012; mPFC, p = 0.0069), which was restored by SPF colonization in hippocampus (p v.s. GF = 0.0003, p v.s. control = 0.60). The hippocampal gene expression profile in GF-mice was significantly correlated with that in human depression (ρ = 0.51, p = 0.027), and this correlation was not observed after colonization. CONCLUSION: Together, we show that the absence of gut microbiota disrupts the expression of EIB-relevant genes in mice, and colonization restores EIB-relevant expression, in ways that are relevant to human depression.