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Zinc Deficiency During Pregnancy Leads to Altered Microbiome and Elevated Inflammatory Markers in Mice.
Zinc is an essential trace metal for bacteria of the intestinal flora. Approximately 20% of dietary zinc - intake is used by intestinal bacteria. The microbiome has recently been described as an important factor for healthy brain function via so-called gut-brain interactions. Similarly, zinc deficiency has been associated with neurological problems such as depression, mental lethargy and cognitive impairments in humans and animal models. However, the underlying pathomechanisms are currently not well understood and a link between zinc deficiency and altered microbiota composition has not been studied. Especially during pregnancy, women may be prone to low zinc status. Thus, here, we investigate whether zinc deficiency alters gut-brain interaction in pregnant mice by triggering changes in the microbiome. To that end, pregnant mice were fed different diets being zinc-adequate, deficient in zinc, or adequate in zinc but high in zinc uptake antagonists for 8 weeks. Our results show that acute zinc-deficient pregnant mice and pregnant mice on a diet high in zinc uptake antagonists have an altered composition of gastro-intestinal (GI) microbiota. These changes were accompanied by alterations in markers for GI permeability. Within the brain, we found signs of neuroinflammation. Interestingly, microbiota composition, gut pathology, and inflammatory cytokine levels were partially rescued upon supplementation of mice with zinc amino-acid conjugates (ZnAA). We conclude that zinc deficiency may contribute to abnormal gut-brain signaling by altering gut physiology, microbiota composition and triggering an increase of inflammatory markers.
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Lacticaseibacillus paracasei NCU-04 relieves constipation and the depressive-like behaviors induced by loperamide in mice through the microbiome-gut-brain axis.
Constipation is a prevalent gastrointestinal condition that significantly affects patients' physical and mental well-being, yet current treatments often lack safety and efficacy. Emerging evidence highlights the critical role of the microbiota-gut-brain axis (MBGA) in managing constipation, paving the way for probiotics as an adjuvant treatment to improve constipation symptoms. In this study, we isolated a gut probiotic strain, Lacticaseibacillus paracasei NCU-04, and investigated its improvement effects on loperamide-induced constipation in mice. We demonstrated that L. paracasei NCU-04 exhibited excellent probiotic properties, including robust growth, strong antibacterial and antioxidant capacities, and a lack of hemolytic activity in vitro. The administration of L. paracasei NCU-04 effectively improved the defecation-related indicators such as the fecal water content, time to the first black stool defecation, and intestine transit rate, suggesting enhanced gut immobility in constipated mice. Additionally, L. paracasei NCU-04 significantly reduced colon inflammation induced by loperamide. Further, L. paracasei NCU-04 increased levels of colonic motilin, 5-hydroxytryptamine (5-HT), and c-kit, while decreased that of aquaporin 3, vasoactive intestinal peptide, and peptide YY. Notably, L. paracasei NCU-04 effectively upregulated the expression of 5-HT and its receptor (i.e., 5-HT4R) in the brains of constipated mice. High-throughput sequencing revealed that L. paracasei NCU-04 restored the diversity and composition of the gut microbiota disturbed by loperamide, and significantly increased the relative abundance of Prevotella and Lactobacillus genera in the stool, while decreased that of Odoribacter, Rikenella, and Parabacteroides. Importantly, L. paracasei NCU-04 also effectively improved the depression-like behaviors associated with constipation, possibly through 5-HT mediated MGBA. These results suggest that L. paracasei NCU-04 may offer a promising approach for treating constipation and its related depressive symptoms, supporting its potential as a functional food or adjuvant therapy for human health.
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Improvements in sleep indices during exam stress due to consumption of a Bifidobacterium longum.
Targeting the gut microbiome as an effective therapeutic strategy for psychological disorders has shown promise in recent years. Variation in the composition of the microbiota and restoration of a stable microbiome using targeted interventions (psychobiotics) including Bifidobacteria have shown promise in pre-clinical studies, but more human data is required on the potential health benefits of these live microorganisms. Bifidobacterium including Bif. longum 1714 has been shown to dampen the effects of acute stress in humans. However, its effects over a period of prolonged stress have not been examined. A randomised, placebo-controlled, repeated measures, cross-over intervention study was conducted to examine the effects of a probiotic intervention on measures of stress, cognitive performance, and mood in healthy human volunteers. Twenty male students participated in this crossover study. Post-intervention assessments took place during the university exam period, which was used as a naturalistic chronic stressor. Self-reported measures of stress, depression, sleep quality, physical activity, gastrointestinal symptoms, cognition, and mood were assessed by questionnaire. In addition, tests from the Cambridge Neuropsychological Test Automated Battery (CANTAB) were administered to all participants. Stress and depression scores increased in both placebo and probiotic treated groups during the exam period. While overall sleep quality and duration of sleep improved significantly in the probiotic treated group during exam stress compared with the placebo treated group, B. longum 1714, similar to placebo treatment, showed no efficacy in improving measures of working memory, visual memory, sustained attention or perception. Overall, while B. longum 1714 shows promise in improving sleep quality and duration, it did not alleviate symptoms of chronic stress, depression, or any measure of cognitive assessment. Thus, further mechanistic studies into the ability of B. longum 1714 to modulate sleep during prolonged periods of stress are now warranted.
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Psychobiotics for Patients with Chronic Gastrointestinal Disorders Having Anxiety or Depression Symptoms.
PURPOSE: Using psychobiotics to modify the gut microbiome has been shown to improve the anxiety and depression situation of patients with chronic gastrointestinal (GI) symptoms. This study evaluated changes in depression, anxiety, GI symptomss and side effects when patients used a multispecies probiotics product. PATIENTS AND METHODS: A single-center uncontrolled trial was conducted in patients with chronic GI symptoms, anxiety and depression who used a multispecies probiotics product. The patients were screened for anxiety and depression symptoms using the Hospital Anxiety and Depression Scale (HADS). Those who had a component score of 8 or higher were given the multispecies probiotics product for 2 months and followed up after 1 and 2 months. All data are collected and managed in a case report form. RESULTS: Eighty-three patients were enrolled, with a mean age (SD) of 43.9 (12.3) years; 73.5% of the patients were female. Of these patients, 8 met the Rome IV criteria for irritable bowel syndrome. The HADS scores displayed significant improvement at follow-up. The mean (SD) total HADS scores were 20.0 (6.3), 7.2 (5.4), and 4.9 (5.1) at baseline, 1 month, and 2 months, respectively. Quality of life also improved significantly. A small proportion (<5%) of patients developed mild symptoms, including fullness, diarrhea, and sleep complaints. CONCLUSION: After 2 months using the probiotic product, the symptoms of anxiety and depression improved significantly. Mild gastrointestinal or constitutional symptoms developed in some patients.
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Modulation of gut microbiota composition due to early weaning stress induces depressive behavior during the juvenile period in mice.
BACKGROUND: The gut microbiota plays an important role in the development of behavior and immunity in infants and juveniles. Early weaning (EW), a form of social stress in mice, leads to increased anxiety and an enhanced stress response in the hypothalamic-pituitary-adrenal axis during adulthood. Early life stress also modulates the immune system and increases vulnerability to infection. However, studies investigating the causal relationships among juvenile stress, microbiota changes, and immune and behavioral deficits are limited. Therefore, we hypothesized that EW alters gut microbiota composition and impairs the development of the nervous and immune systems. RESULTS: EW mice moved longer distances in the marble-burying test and had longer immobility times in the tail suspension test than normal weaning (NW) mice. In parallel, the gut microbiome composition differed between NW and EW mice, and the abundance of Erysipelotrichacea in EW mice at 8 weeks of age was lower than that in NW mice. In an empirical study, germ-free mice colonized with the gut microbiota of EW mice (GF-EW mice) demonstrated higher depressive behavior than GF mice colonized with normal weaning microbiota (GF-NW mice). Immune cell profiles were also affected by the EW microbiota colonization; the number of CD4 + T cells in the spleen was reduced in GF-EW mice. CONCLUSION: Our results suggest that EW-induced alterations in the gut microbiota cause depressive behaviors and modulate the immune system.
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Indole Acetic Acid Exerts Anti-Depressive Effects on an Animal Model of Chronic Mild Stress.
Indole acetic acid (IAA), an intestinal bacteria-derived tryptophan metabolite, has been detected at abnormal concentrations in the cerebrospinal fluid and urine of depressed individuals. The effects of such altered IAA concentrations on mood regulation are not known. A mouse model of unpredictable chronic mild stress (UCMS) was used to assess the effects of IAA administration (50 mg/kg). Treatment with IAA for 5 weeks attenuated depression and anxiety-like behaviours, improved hypothalamus-pituitary-adrenal axis dysfunction and increased brain-derived neurotrophic factor expression. IAA supplementation also enhanced the serotonin pathway in the brain and gut. UCMS caused an imbalance of microbial indole metabolites in the colon, whereas IAA treatment reversed this. However, IAA intake did not affect the concentrations of indoles in the brain. Intestinal bacteria in different sections of the gut were altered by IAA treatment, with the colon showing more changes than other segments. The gut microbiome in the colon had increased proportions of Ruminococcaceae UCG013, Ruminiclostridium 6, Prevotella, Alloprevotella and Bacteroides species, which can produce short-chain fatty acids and indole derivatives. Cumulatively, our study highlights the potential of IAA treatment to alleviate mood disorders and offers a theoretical basis for understanding the antidepressant effects of IAA.
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Gut microbiome, surgical complications and probiotics.
The trigger for infectious complications in patients following major abdominal operations is classically attributed to endogenous enteral bacterial translocation, due to the critical condition of the gut. Today, extensive gut microbiome analysis has enabled us to understand that almost all "evidence-based" surgical or medical intervention (antibiotics, bowel preparation, opioids, deprivation of nutrition), in addition to stress-released hormones, could affect the relative abundance and diversity of the enteral microbiome, allowing harmful bacteria to proliferate in the place of depressed beneficial species. Furthermore, these bacteria, after tight sensing of host stress and its consequent humoral alterations, can and do switch their virulence accordingly, towards invasion of the host. Probiotics are the exogenously given, beneficial clusters of live bacteria that, upon digestion, seem to succeed in partially restoring the distorted microbial diversity, thus reducing the infectious complications occurring in surgical and critically ill patients. This review presents the latest data on the interrelationship between the gut microbiome and the occurrence of complications after colon surgery, and the efficacy of probiotics as therapeutic instruments for changing the bacterial imbalance.
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Novel Multi-Strain E3 Probiotic Formulation Improved Mental Health Symptoms and Sleep Quality in Hong Kong Chinese.
Mental health issues have emerged as a significant concern in public health, given their association with physical and psychological comorbidities and the resultant socioeconomic burdens. Recent studies have highlighted the interplay between gut microbes and brain functions through the gut-brain axis. To investigate this further, we conducted a targeted 16S rRNA sequencing and comprehensive bioinformatic analysis among Southern Chinese individuals to explore the role of the gut microbiome in depression, anxiety, and sleep disturbance. We analyzed the differences in the gut microbiome profile of 68 participants with sleep disturbance and mood symptoms before and after an 8-week course of a novel oral E3 multi-strain probiotics formula. The results revealed a significant improvement in subjective sleep quality (PSQI: mean 8.79 at baseline vs. 7.10 at week 8, p < 0.001), depressive symptoms (PHQ9: mean 6.17 at baseline vs. 4.76 at week 8, p < 0.001), and anxious symptoms (GAD7: mean 4.90 at baseline vs. 3.76 at week 8, p < 0.001). Additionally, there were notable differences in beta diversity (weighted UniFrac; p = 0.045) and increased Firmicutes/Bacteroidetes (F/B) ratio (p = 4 × 10-4) were observed in the gut microbiome analysis. Furthermore, the relative abundance of Bifidobacterium bifidum (p < 0.001), Lactobacillus acidophilus (p < 0.001), Lactobacillus helveticus (p < 0.001) and Lactobacillus plantarum (p < 0.001) were significantly increased after the 8-week probiotic supplementation. Our study suggests that the gut microbial landscape varies between responders and non-responders at multiple levels, including genera, species, functional, and network interaction. Notably, the use of probiotics in populations with depressive or anxious symptoms and poor sleeping quality remodeled the gut microbiome and demonstrated improved mood and sleep quality.
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The effects of a semen cuscutae flavonoids-based antidepressant treatment on microbiome and metabolome in mice.
BACKGROUND: Depression is a prevalent psychiatric disorder and one of the leading causes of disability worldwide. Previous studies have shown that Semen Cuscutae flavonoids (SCFs) exert antidepressant effects by modulating the microbiota-neuroinflammation axis and ameliorating hippocampal metabolic disturbances. However, the impact of SCFs on gut microbiota and related metabolomics remains largely undefined. Given that the gut microbiota has been proven to play a significant role in the etiology of depression and serves as a promising target for its treatment in humans, this study aims to elucidate the antidepressant effects of SCFs and to investigate how they modulate microbial and metabolic pathways to alleviate depressive symptoms. MATERIALS AND METHODS: Chronic unpredictable mild stress (CUMS)-induced mice were used as a depression model. The normal mice and CUMS-induced mice were treated with either vehicle or with SCFs. A range of standardized behavioral assays and physiological indicators were employed to evaluate the antidepressant effects of SCFs. Upon the confirmation of the effectiveness of the SCFs treatment, the composition, richness, and diversity of the fecal microbiota were assessed using 16S rRNA gene sequencing. Additionally, fecal metabolic profiling was analyzed using UHPLC-MS/MS-based metabolomics. Multivariate data analysis was subsequently performed to identify differential metabolites and characterize alterations in fecal metabolites. Furthermore, a correlation analysis between differential metabolites and key microbiota was conducted. RESULTS: SCFs significantly ameliorated depressive behaviors and the dysregulated diversity of fecal microbiota induced by CUMS. SCFs enhanced the gut microbiota structure in the CUMS group by increasing the Firmicutes/Bacteroidota ratio, significantly elevating the abundance of Firmicutes, Lactobacillus, Limosilactobacillus, and Actinobacteria while reducing the abundance of Bacteroidota and Bacteroides in CUMS-treated mice. Fecal metabolomics analyses revealed that SCFs could modulate metabolic pathways, including aldosterone synthesis and secretion, arachidonic acid metabolism, and primary bile acid biosynthesis. CONCLUSIONS: Mice with depression induced by CUMS exhibited disturbances in both their gut microbiota and fecal metabolism. However, SCFs restored the balance of the microbial community and corrected metabolic disturbances in feces, exerting antidepressant effects through a multifaceted mechanism.
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Efficacy and Safety of Limosilactobacillus reuteri DSM 17938 in Infantile Colic: A Narrative Review From Pathogenesis to Clinical Practice.
Infantile colic is one of the most common functional gastrointestinal disorders, affecting approximately 20% of infants worldwide. Characterized by paroxysmal episodes of inconsolable crying and fussing without an obvious cause, the condition imposes a significant psychosocial burden on the family unit, acting as a primary trigger for maternal postpartum depression, parental exhaustion, and premature cessation of breastfeeding. Despite its prevalence, traditional management in primary care remains heterogeneous and often ineffective, leaving a substantial therapeutic gap. Emerging research has identified gut dysbiosis as a cornerstone of its pathogenesis, where an imbalance in early microbial colonization, characterized by reduced diversity and a higher prevalence of gas-producing coliforms, triggers intestinal inflammation and visceral hypersensitivity through the gut-brain axis. This narrative review synthesizes the current clinical evidence regarding the efficacy and safety of Limosilactobacillus reuteri DSM 17938 in the management of infantile colic. This specific probiotic strain exerts its therapeutic effects through multifaceted mechanisms, including the production of the antimicrobial metabolite reuterin, the modulation of gastrointestinal motility via microvesicles, and the reduction of low-grade gut inflammation. Clinical evidence from large-scale meta-analyses confirms that L. reuteri DSM 17938 is significantly superior to placebo, particularly in breastfed infants, where it is twice as likely to achieve a 50% reduction in crying time within 14-21 days of treatment. However, its efficacy appears less predictable in formula-fed populations, potentially due to the absence of synergistic factors found in human milk. Clinical management in primary care should prioritize a rigorous diagnostic approach to rule out organic causes through a detailed physical examination and the application of the Rome IV criteria. The cornerstone of non-pharmacological management remains empathetic parental reassurance and education to mitigate the risk of infant abuse and support family well-being. When probiotic intervention is indicated, L. reuteri DSM 17938 represents a robust, evidence-based first-line therapy for healthy, full-term infants. Regarding safety, this strain maintains an excellent profile supported by its generally recognized as safe (GRAS) status, with no significant adverse effects reported in healthy populations. Nevertheless, recent clinical scrutiny emphasizes the need for caution and the use of pharmaceutical-grade products in vulnerable groups. Ultimately, L. reuteri DSM 17938 addresses both the biological triggers of colic and the psychosocial stability of the family unit.