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Xiao-Yao-San suppresses psychological distress-related colorectal cancer metastasis and enhances antitumor immune responses through regulating gut microbiota-bile acid axis.
BACKGROUND: Psychiatric disorders are recognized as risk factors for tumor progression and metastasis in colorectal cancer (CRC). Xiao-Yao-San (XYS), a traditional Chinese herbal formula with antidepressant properties, has been reported to inhibit CRC growth and modulate gut microbiota. However, its efficacy and underlying mechanisms in preventing metastasis remain unclear. METHODS: The antimetastatic effect of XYS was assessed in a chronic restraint stress (CRS)-induced CRC model. XYS-associated gut microbiota was evaluated using 16S ribosomal RNA (rRNA) sequencing. Peripheral bile acid (BA) profiles were analyzed through targeted metabolomics. Fecal microbiota and commercial bacterial strains were anaerobically cultured to identify bile salt hydrolase (bsh)-expressing bacteria. XYS-mediated antitumor immune responses were determined via flow cytometry, immunohistochemistry, and cytotoxic T lymphocytes (CD8⁺ T cells)-murine colon adenocarcinoma cell line (MC38) co-culture assays. RESULTS: Administration of dried XYS decoction powder reduced liver metastatic nodules and prevented body weight loss in CRS-induced CRC mice, while also alleviating depressive-like behaviors and lowering serum stress hormone levels. High-dose XYS (2 g/kg/day) produced antimetastatic and antidepressant effects comparable to those of sertraline, although these effects were largely abolished in mice treated with antibiotic cocktails. XYS significantly modulated gut microbiota composition and serum BA profiles, particularly by restoring bsh-expressing bacteria in the cecum and increasing the proportion of free BAs. XYS also reshaped the immune landscape within metastatic foci, where enhanced antitumor CD8⁺ T cell responses were strongly associated with the altered BA profile. Among these, hyocholic acid (HCA), a free BA elevated by XYS, suppressed liver metastasis in vivo, alleviated exhaustion and restored effector function of CD8⁺ T cells in metastatic tumor microenvironment (TME), together with dose-dependently enhanced CD8+ T cell cytotoxicity against tumor cells in vitro. CONCLUSION: XYS prevents psychiatric disorder-associated CRC metastasis and strengthens antitumor immune responses by regulating bsh-expressing gut bacteria and their derived BA profiles. These findings thus offer a novel mechanistic rationale for the potential use of XYS in treating CRC patients with comorbid psychiatric disorders.
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Gut Microbiota is Altered in Patients with Alzheimer's Disease.
Previous studies suggest that gut microbiota is associated with neuropsychiatric disorders, such as Parkinson's disease, amyotrophic lateral sclerosis, and depression. However, whether the composition and diversity of gut microbiota is altered in patients with Alzheimer's disease (AD) remains largely unknown. In the present study, we collected fecal samples from 43 AD patients and 43 age- and gender-matched cognitively normal controls. 16S ribosomal RNA sequencing technique was used to analyze the microbiota composition in feces. The composition of gut microbiota was different between the two groups. Several bacteria taxa in AD patients were different from those in controls at taxonomic levels, such as Bacteroides, Actinobacteria, Ruminococcus, Lachnospiraceae, and Selenomonadales. Our findings suggest that gut microbiota is altered in AD patients and may be involved in the pathogenesis of AD.
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Therapeutic Implications of the Microbial Hypothesis of Mental Illness.
There is increasingly compelling evidence that microorganisms may play an etiological role in the emergence of mental illness in a subset of the population. Historically, most work has focused on the neurotrophic herpesviruses, herpes simplex virus type 1 (HSV-1), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) as well as the protozoan, Toxoplasma gondii. In this chapter, we provide an umbrella review of this literature and additionally highlight prospective studies that allow more mechanistic conclusions to be drawn. Next, we focus on clinical trials of anti-microbial medications for the treatment of psychiatric disorders. We critically evaluate six trials that tested the impact of anti-herpes medications on inflammatory outcomes in the context of a medical disorder, nine clinical trials utilizing anti-herpetic medications for the treatment of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) or schizophrenia, and four clinical trials utilizing anti-parasitic medications for the treatment of schizophrenia. We then turn our attention to evidence for a gut dysbiosis and altered microbiome in psychiatric disorders, and the potential therapeutic effects of probiotics, including an analysis of more than 10 randomized controlled trials of probiotics in the context of schizophrenia, bipolar disorder (BD), and major depressive disorder (MDD).
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Modulatory activity of N-palmitoyl-D-glucosamine in bridging gut dysbiosis and pain mechanisms.
Gut dysbiosis, characterized by an imbalance in the composition and function of microbiota, has emerged as a critical factor in the regulation of pain transmission and behavior through the gut-brain axis. When dysbiosis occurs, these regulatory functions are disrupted, leading to systemic inflammation and altered signaling at central nervous system. In this study, we examined the therapeutic potential of palmitoyl glucosamine (PGA), a fatty acid amide with sharp anti-inflammatory properties, in a gut dysbiosis condition induced by antibiotic exposure in male mice. At the intestine level, PGA treatment reduced proinflammatory biomarkers and affects gut microbiota balance. Moreover, it reduced visceral hypersensitivity and pain transmission to the spinal cord by reducing the expression of mechanosensitive ion channel Piezo-2. Finally, PGA counteracted the affective comorbidities of dysbiosis, including depressive-like behavior and impaired cognition. This study sheds light on the function of gut microbiota in the control of pain pathways and provides new insights into the advantages of PGA treatment in managing pathological conditions linked to microbiota-related immune and sensory dysregulation.
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Neurobiological Processes Induced by Aerobic Exercise through the Endocannabinoidome.
Evidence suggesting the triangulation of the endocannabinoid system, exercise, and neurological health is emerging. In addition to the endocannabinoids N-arachidonoylethanolamine (anandamide; AEA) and 2-arachidonoylglycerol (2-AG), the expanded endocannabinoid system, known as the endocannabinoidome (eCBome), appears to be an important player in this relationship. The eCBome includes several endocannabinoid-like mediators such as N-acylethanolamines and 2-monoacylglycerols, the enzymes involved in their biosynthesis and degradation, and the receptors they affect. This review aims to relate the functional interactions between aerobic exercise, and the molecular and cellular pathways related to endocannabinoids, in the hypothalamus, hippocampus, and the periphery, with special attention given to associations with emotional state, cognition, and mental health. Given the well-documented roles of many eCBome members in regulating stress and neurological processes, we posit that the eCBome is an important effector of exercise-induced central and peripheral adaptive mechanisms that benefit mental health. Gut microbiota imbalance, affecting the gut-brain axis and metabolism, also influences certain eCBome-modulated inflammation pathways. The integrity of the gut microbiota could thus be crucial in the onset of neuroinflammation and mental conditions. Further studies on how the modulation by exercise of the peripheral eCBome affects brain functions could reveal to be key elements in the prevention and treatment of neuropsychological disorders.
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Magnoflorine alleviates colitis-induced anxiety-like behaviors by regulating gut microbiota and microglia-mediated neuroinflammation.
BACKGROUND: Inflammatory bowel disease (IBD) and anxiety are often comorbid and are interconnected through the microbiota-gut-brain axis. Therapeutic medications for anxiety are often constrained by adverse effects that limit their long-term use. Therefore, recent research has focused on identifying natural, safe drugs for anxiety, and elucidating the precise mechanisms underlying the interplay between drugs and the gut-brain axis in modulating mood. RESULTS: We revealed a significant association between active ulcerative colitis (UC) and anxiety. The results of Mendelian randomization analysis suggested that UC has a causal relationship with anxiety, but not depression. We identified Ziziphus jujuba, a natural plant, as a dual therapeutic agent for both UC and anxiety using the Batman database. Magnoflorine, the predominant compound found in Ziziphus jujuba, exhibits promising therapeutic properties for the treatment of UC and anxiety disorders. We found that magnoflorine not only alleviated colitis but also reduced colitis-induced anxiety behaviors through the gut microbiota. Mechanistically, magnoflorine increased the abundance of Odoribacteraceae and Ruminococcus and regulated bile acid metabolism, especially hyodeoxycholic acid (HDCA) in mice with colitis. HDCA supplementation alleviated both colitis and colitis-induced anxiety. HDCA inhibited the binding of lipopolysaccharide to the TLR4/MD2 complex, thereby inhibiting microglial activation and alleviating neuroinflammation. CONCLUSION: Our study revealed that magnoflorine alleviated colitis-induced anxiety-like behaviors by regulating the gut microbiota and microglia-mediated neuroinflammation, which has the potential to treat patients with IBD and anxiety disorders. Video Abstract.
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Recent advances in diagnosis and management of irritable bowel syndrome.
PURPOSE OF REVIEW: This review summarizes recent progress in the diagnosis and management of irritable bowel syndrome, with a focus on dietary and microbiota aspects. RECENT FINDINGS: From a pathophysiological point of view, IBS is a multifactorial condition with both peripheral (transit) as central (visceral hypersensitivity, anxiety, depression) contribution in a cumulative fashion to the symptom pattern and severity. More recently, the focus has shifted to diet and microbiota. The number of dietary options that can be used for IBS and the understanding of determinants of their efficacy is rapidly increasing. Several studies have confirmed the efficacy of the low fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) diet. Sucrose-isomaltase deficiency has emerged as pathogenetic mechanisms in a subset of patients, who do not respond to low FODMAP diet but may respond to starch and sucrose elimination. Herbal remedies, probiotics and secretagogues have been the topic of additional treatment trials. The efficacy of fecal microbiota transplantation in IBS is variable across studies, but donor selection is emerging as a critical factor. SUMMARY: Irritable bowel syndrome has evolved into a disorder of interaction between dietary factors and gut microbiota, with impact on bowel symptoms as well as extra-intestinal, central, symptoms. Dietary adjustments and treatments targeting the gut microbiota are areas of active research and clinical progress.
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Interactions Between Antidepressants and Intestinal Microbiota.
The microbiota-gut-brain axis has been shown to influence human health and diseases, including depression. The interactions between drugs and intestinal microbiota are complex and highly relevant to treat diseases. Studies have shown an interaction between antidepressants and intestinal microbiota. Antidepressants may alter the abundance and composition of intestinal microbiota, which are closely related to the treatment outcomes of depression. Intestinal microbiota can influence the metabolism of antidepressants to change their availability (e.g., tryptophan can be metabolized to kynurenine by intestinal microbiota) and regulate their absorption by affecting intestinal permeability. In addition, the permeability of the blood-brain barrier can be altered by intestinal microbiota, influencing antidepressants to reach the central nervous system. Bioaccumulation is also a type of drug-microbiota interaction, which means bacteria accumulate drugs without biotransformation. These findings imply that it is important to consider intestinal microbiota when evaluating antidepressant therapy regimens and that intestinal microbiota can be a potential target for depression treatment.
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Dietary phytic acid prevents fatty liver by reducing expression of hepatic lipogenic enzymes and modulates gut microflora in rats fed a high-sucrose diet.
OBJECTIVES: The aim of this study was to investigate the effect of phytic acid (PA) on fatty liver and gut microflora in rats fed a high-sucrose (HSC) diet. METHODS: Three groups of rats were fed a high-starch (HSR) diet or an HSC diet with or without 1.02% sodium PA for 12 d. We evaluated hepatic weight, total lipids, and triacylglycerol (TG) levels, the activities and expression of hepatic lipogenic enzymes (glucose-6-phosphate dehydrogenase, malic enzyme 1, and fatty acid synthetase), and fecal microflora. RESULTS: The HSC diet significantly increased hepatic total lipids and TG levels, and the activities and expression of the hepatic lipogenic enzymes compared with the HSR diet. These upregulations were clearly suppressed by dietary PA. Consumption of PA elevated the fecal ratio of Lactobacillus spp. and depressed the ratio of Clostridium cocoides, and suppressed the elevation in the ratio of C. leptum induced by the HSC diet. CONCLUSION: This work showed that dietary PA ameliorates sucrose-induced fatty liver through reducing the expression of hepatic lipogenesis genes and modulates gut microflora in rats.
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Beyond the gut: decoding the gut-immune-brain axis in health and disease.
Emerging research underscores the pivotal role of the gut-immune-brain axis, a dynamic bidirectional communication system involving intricate interactions between the gut microbiota, immune responses, and the central nervous system. Gut microbes and their metabolites have profound effects on immune and neurological homeostasis, influencing the development and function of multiple physiological systems. Disruption of the composition of the gut microbiota and barrier integrity has been implicated in various neurological and psychiatric disorders, including autism spectrum disorder, Alzheimer's disease, Parkinson's disease, depression, and anxiety. Most insights into these host-microbiota interactions come from preclinical models, revealing both the complexity and potential therapeutic opportunities of the gut-brain communication pathways. This review synthesizes the current understanding of these intricate interactions, exploring how microbiota-driven modulation of the gut and brain barriers, immune signaling, and neuronal pathways, such as those through the vagus nerve, contributes to health and disease. We further explore therapeutic implications, including personalized precision microbiota interventions, microbiome-derived biomarkers, and barrier-strengthening strategies. Advancing this field offers transformative potential for developing innovative, personalized therapies tailored to individual microbiomes and immune profiles, ultimately redefining clinical approaches to neurological and immune-mediated diseases.