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Red osier dogwood extract vs. trimethoprim-sulfadiazine (Part 2). Pharmacodynamic effects on ileal and cecal microbiota of broiler chickens challenged orally with Salmonella Enteritidis.
With the subsisting restrictions on the use of antibiotics in poultry production, the use of plant extracts has shown some promising antimicrobial capacity similar to antibiotics; however, such capacity is largely dependent on their total polyphenol concentration and profile. Given the emerging antimicrobial potential of red osier dogwood (ROD) extract, the study aimed to investigate the pharmacodynamic effect of ROD extract on the ileal and cecal microbiota of broiler chickens challenged orally with Salmonella Enteritidis (SE). A 21 d 4 × 2 factorial experiment was conducted based on 2 main factors, including diets and SE challenge. A total of 384 one-day-old mixed-sex Cobb-500 broiler chicks were randomly allotted to 4 dietary treatments; Negative control (NC), NC + 0.075 mg trimethoprim-sulfadiazine (TMP/SDZ)/kg of diet, and NC containing either 0.3 or 0.5% ROD extract. On d 1, half of the birds were orally challenged with 0.5 mL of phosphate-buffered saline (Noninfected group) and the remaining half with 0.5 mL of 3.1 × 105 CFU/mL SE (Infected group). Dietary treatments were randomly assigned to 8 replicate cages at 6 birds/cage. On d 21, 10 birds/treatment were euthanized and eviscerated to collect ileal and cecal digesta for gut microbiota analysis. The ileal and cecal microbiota was dominated by phyla Firmicutes, Proteobacteria, and Actinobacteriota. The SE infection decreased (P < 0.05) the relative abundance of Proteobacteria and Actinobacteriota in the ileum and ceca, respectively, however, it increased (P < 0.05) Proteobacteria in the ceca. Both 0.3 and 0.5% ROD extracts (P < 0.05) depressed the relative abundance of Actinobacteriota in the ileum but marginally improved (P < 0.05) it in the ceca compared to the TMP/SDZ treatment. Dietary TMP/SDZ increased (P < 0.05) genus Bifidobacterium at the ileal and cecal segments compared to other treatments. Dietary 0.3 and 0.5% marginally improved (P < 0.05) Bifidobacterium in the ceca and depressed (P < 0.05) Weissella and was comparably similar to TMP/SDZ in the ileum. Regardless of the dietary treatments and SE infection, alpha diversity differed (P < 0.05) between ileal and cecal microbiota. Beta diversity was distinct (P < 0.05) in both ileal and cecal digesta along the SE infection model. Conclusively, both ROD extract levels yielded a pharmacodynamic effect similar to antibiotics on ileal and cecal microbiota.
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Microbiota metabolites modulate the T helper 17 to regulatory T cell (Th17/Treg) imbalance promoting resilience to stress-induced anxiety- and depressive-like behaviors.
Chronic stress disrupts immune homeostasis while gut microbiota-derived metabolites attenuate inflammation, thus promoting resilience to stress-induced immune and behavioral abnormalities. There are both peripheral and brain region-specific maladaptations of the immune response to chronic stress that produce interrelated mechanistic considerations required for the design of novel therapeutic strategies for prevention of stress-induced psychological impairment. This study shows that a combination of probiotics and polyphenol-rich prebiotics, a synbiotic, attenuates the chronic-stress induced inflammatory responses in the ileum and the prefrontal cortex promoting resilience to the consequent depressive- and anxiety-like behaviors in male mice. Pharmacokinetic studies revealed that this effect may be attributed to specific synbiotic-produced metabolites including 4-hydroxyphenylpropionic, 4-hydroxyphenylacetic acid and caffeic acid. Using a model of chronic unpredictable stress, behavioral abnormalities were associated to strong immune cell activation and recruitment in the ileum while inflammasome pathways were implicated in the prefrontal cortex and hippocampus. Chronic stress also upregulated the ratio of activated proinflammatory T helper 17 (Th17) to regulatory T cells (Treg) in the liver and ileum and it was predicted with ingenuity pathway analysis that the aryl hydrocarbon receptor (AHR) could be driving the synbiotic's effect on the ileum's inflammatory response to stress. Synbiotic treatment indiscriminately attenuated the stress-induced immune and behavioral aberrations in both the ileum and the brain while in a gut-immune co-culture model, the synbiotic-specific metabolites promoted anti-inflammatory activity through the AHR. Overall, this study characterizes a novel synbiotic treatment for chronic-stress induced behavioral impairments while defining a putative mechanism of gut-microbiota host interaction for modulating the peripheral and brain immune systems.
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The liver-gut-brain axis in metabolic dysfunction-associated steatotic liver disease: bidirectional communication, clinical implications, and future perspectives.
BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects approximately one-third of adults worldwide and is increasingly recognized as a multisystem disorder. In addition to hepatic and cardiometabolic complications, many patients report fatigue, depression, anxiety, sleep disturbance, and subjective cognitive complaints. These manifestations are clinically important but correlate inconsistently with liver histology and may arise from several interacting mechanisms. AIM: To critically synthesize evidence on the liver-gut-brain axis in MASLD, distinguish established pathways from indirect or preclinical hypotheses, and evaluate implications for biomarkers, patient assessment, and treatment. METHODS: PubMed was searched through July 15, 2026 using combinations of terms related to MASLD/MASH, intestinal barrier function, gut microbiota, autonomic and stress signaling, hepatic inflammation and fibrosis, neuroinflammation, cognition, biomarkers, and treatment. Guidelines, randomized trials, prospective human studies, systematic reviews, and mechanistically informative experimental studies were prioritized. Evidence derived from cirrhosis, hepatic encephalopathy, other diseases, or animal models is explicitly identified. RESULTS: The axis comprises neural, endocrine, immune, and metabolic communication. Stress-related hypothalamic-pituitary-adrenal and sympathetic activation may influence behavior, adipose tissue, intestinal motility, mucosal immunity, and epithelial integrity. Barrier dysfunction can increase portal exposure to microbial products that activate hepatic inflammatory pathways and aggravate insulin resistance. Conversely, hepatic and intestinal cytokines, bile acids, hepatokines, and microbial metabolites may signal at vascular and neural interfaces, although direct causal evidence for brain effects in noncirrhotic MASLD remains limited. Lifestyle and cardiometabolic risk management remain foundational. Resmetirom and semaglutide have regulatory indications for selected adults with noncirrhotic MASH and moderate-to-advanced fibrosis, whereas microbiota-directed therapies and neuromodulation remain investigational. CONCLUSION: The liver-gut-brain axis is a useful integrative framework, but its component pathways have unequal evidentiary support. Longitudinal human studies using standardized hepatic, microbial, inflammatory, autonomic, and neurobehavioral outcomes are required before axis-based biomarkers or endotypes can guide routine care.
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The Gut Microbiota's Role in Neurological, Psychiatric, and Neurodevelopmental Disorders.
AIM: This article aims to explore the role of the human gut microbiota (GM) in the pathogenesis of neurological, psychiatric, and neurodevelopmental disorders, highlighting its influence on health and disease, and investigating potential therapeutic strategies targeting GM modulation. MATERIALS AND METHODS: A comprehensive analysis of the gut microbiota's composition and its interaction with the human body, particularly, its role in neurological and psychiatric conditions, is provided. The review discusses factors influencing GM composition, including birth mode, breastfeeding, diet, medications, and geography. Additionally, it examines the GM's functions, such as nutrient absorption, immune regulation, and pathogen defense, alongside its interactions with the nervous system through the gut-brain axis, neurotransmitters, and short-chain fatty acids (SCFAs). RESULTS: Alterations in the GM are linked to various disorders, including Parkinson's disease, multiple sclerosis, depression, schizophrenia, ADHD, and autism. The GM influences cognitive functions, stress responses, and mood regulation. Antibiotic use disrupts GM diversity, increasing the risk of metabolic disorders, obesity, and allergic diseases. Emerging therapies such as probiotics, prebiotics, and microbiota transplantation show promise in modulating the GM and alleviating symptoms of neurological and psychiatric conditions. CONCLUSIONS: The modulation of the GM represents a promising approach for personalized treatment strategies. Further research is needed to better understand the underlying mechanisms and to develop targeted therapies aimed at restoring GM balance for improved clinical outcomes.
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Microbe-Immune Crosstalk: Evidence That T Cells Influence the Development of the Brain Metabolome.
Cross-talk between the immune system and the brain is essential to neuronal development, neuronal excitability, neuroplasticity, and neurotransmission. Gut microbiota are essential to immune system development and immune function; hence, it is essential to consider more broadly the microbiota-immune-brain axis in neurodevelopment. The gut, brain, and microbial metabolomes obtained from C57Bl/6 and T-cell-deficient mice across four developmental timepoints (postnatal day 17, 24, 28, and 84) were studied by 1H NMR spectroscopy. 16S rRNA gene sequencing was performed on cecal and fecal samples. In the absence of T-cells, the developmental trajectory of the gut microbiota and of the host's metabolic profile was altered. The novel insights from this work include (1) the requirement of functional T-cells for the normal trajectory of microbiotal development and the metabolic maturation of the supra-organism, (2) the potential role for Muribaculaceae taxa in modulating the cecal availability of metabolites previously implicated with a role in the gut-brain axis in T-cell deficient mice, and (3) the impact of T-cell-deficiency on central levels of neuroactive metabolites.
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Experience-dependent grooming microstructure alterations and gastrointestinal dysfunction in the SAPAP3 knockout mouse model of compulsive behaviour.
BACKGROUND: Compulsive- and anxiety-like behaviour can be efficiently modelled in SAPAP3 knockout (KO) mice, a preclinical model of relevance to obsessive-compulsive disorder (OCD). Although there is emerging evidence in the clinical literature of gastrointestinal dysfunction in OCD, no previous studies have investigated gut function in preclinical models of relevance to OCD. Similarly, the effects of voluntary exercise (EX) or environmental enrichment (EE) have not yet been explored in this context. METHOD: We comprehensively phenotyped the SAPAP3 KO mouse model, including the assessment of grooming microstructure, anxiety- and depressive-like behaviour, and gastrointestinal function. Mice were exposed to either standard housing (SH), exercise (EX, provided by giving mice access to running wheels), or environmental enrichment (EE) for 4 weeks to investigate the effects of enriched housing conditions in this animal model relevant to OCD. FINDINGS: Our study is the first to assess grooming microstructure, perseverative locomotor activity, and gastrointestinal function in SAPAP3 KO mice. We are also the first to report a sexually dimorphic effect of grooming in young-adult SAPAP3 KO mice; along with changes to grooming patterning and indicators of gut dysfunction, which occurred in the absence of gut dysbiosis in this model. Overall, we found no beneficial effects of voluntary exercise or environmental enrichment interventions in this mouse model; and unexpectedly, we revealed a deleterious effect of wheel-running exercise on grooming behaviour. We suspect that the detrimental effects of experimental housing in our study may be indicative of off-target effects of stress-a conclusion that warrants further investigation into the effects of chronic stress in this preclinical model of compulsive behaviour.
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Can We Modulate Our Second Brain and Its Metabolites to Change Our Mood? A Systematic Review on Efficacy, Mechanisms, and Future Directions of "Psychobiotics".
Psychobiotics, live microorganisms that provide mental health by interacting with the gut microbiota, are emerging as a promising therapeutic option for psychiatric and neurodevelopmental disorders. Their effectiveness in addressing conditions such as depression, anxiety, insomnia, stress, autism spectrum disorder (ASD), and eating disorders were examined through a comprehensive analysis of existing studies up to the first half of 2024, based on data from reliable electronic databases. We found that psychobiotics can significantly reduce symptoms of various psychiatric disorders by influencing neurotransmitter levels, regulating the hypothalamic-pituitary-adrenal (HPA) axis, and improving gut barrier function through short-chain fatty acids (SCFAs) and other metabolites. However, several limitations were identified, including inconsistent study methodologies, small sample sizes, and a lack of data on long-term safety. Addressing these limitations through rigorous research is essential for establishing standardized protocols and fully confirming the therapeutic potential of psychobiotics. In conclusion, psychobiotics show great promise as complementary treatments for mental health conditions, but continued research is necessary to refine their application and integrate them into clinical practice effectively.
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Psychobiotic Properties of Lactiplantibacillus plantarum in Neurodegenerative Diseases.
Neurodegenerative disorders are the main cause of cognitive and physical disabilities, affect millions of people worldwide, and their incidence is on the rise. Emerging evidence pinpoints a disturbance of the communication of the gut-brain axis, and in particular to gut microbial dysbiosis, as one of the contributors to the pathogenesis of these diseases. In fact, dysbiosis has been associated with neuro-inflammatory processes, hyperactivation of the neuronal immune system, impaired cognitive functions, aging, depression, sleeping disorders, and anxiety. With the rapid advance in metagenomics, metabolomics, and big data analysis, together with a multidisciplinary approach, a new horizon has just emerged in the fields of translational neurodegenerative disease. In fact, recent studies focusing on taxonomic profiling and leaky gut in the pathogenesis of neurodegenerative disorders are not only shedding light on an overlooked field but are also creating opportunities for biomarker discovery and development of new therapeutic and adjuvant strategies to treat these disorders. Lactiplantibacillus plantarum (LBP) strains are emerging as promising psychobiotics for the treatment of these diseases. In fact, LBP strains are able to promote eubiosis, increase the enrichment of bacteria producing beneficial metabolites such as short-chain fatty acids, boost the production of neurotransmitters, and support the homeostasis of the gut-brain axis. In this review, we summarize the current knowledge on the role of the gut microbiota in the pathogenesis of neurodegenerative disorders with a particular focus on the benefits of LBP strains in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, autism, anxiety, and depression.
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The effect of COVID-19 lockdown on mental health, gut microbiota composition and serum cortisol levels.
The aim of this study was to assess changes in mental health, gut microbiota composition, and stress marker serum cortisol due to COVID-19 lockdown in asymptomatic individuals. Healthy adults participated in anthropometric measurements, blood and stool sample collection pre-lockdown and post-lockdown (n = 38, 63.2% females), lifestyle and psychological questionnaires were included in pre-lockdown measurement and lockdown survey (n = 46, 67.4% females). Subjects reported significantly higher body dissatisfaction (p = 0.007) and anxiety (p = 0.002), and significantly lower positive affect (p = 0.001) during lockdown compared with pre-lockdown. According to perceived stress, 51.6% of females and 20% of males experienced moderate to high stress. This was reflected in serum cortisol levels that significantly increased only in females (p = 0.006) post-lockdown and correlated with perceived stress (p = 0.037) and anxiety (p = 0.031). In addition to psychological measures, changes in gut microbiota composition were observed. Gut microbial alpha diversity significantly decreased (p = 0.033), whereas relative abundance of Proteobacteria significantly increased (p = 0.043) post-lockdown. Depression during lockdown was moderately positively correlated with changes in Bacteroidetes abundance (p = 0.015) and negatively with changes in Firmicutes abundance (p = 0.008). Alistipes abundance post-lockdown was moderately positively correlated with anxiety (p = 0.004) and negative affect (p = 0.005) during lockdown. Despite a small sample size and not being able to perform objective measurements during lockdown, the results confirm the effect of lockdown on mental health and gut microbiota composition that could have a great impact on our health (ClinicalTrials identifier: NCT04347213).
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Lactobacillus acidophilus LA3 Suppresses Neuroinflammation via the Gut-Brain Axis.
The gut-brain axis represents a pivotal pathway through which gut microbiota influence neuroinflammation and neurological health. This study identifies Lactobacillus acidophilus LA3 as a potent probiotic strain capable of mitigating neuroinflammation. LA3 demonstrated superior efficacy in suppressing LPS-induced proinflammatory cytokines in BV-2 microglia. In an LPS-induced murine model, LA3 alleviated systemic and neuroinflammation, depressive-like behaviors, and cognitive impairment, while restoring blood-brain and gut-vascular barrier integrity. LA3 reversed gut microbiota dysbiosis, enriched short-chain fatty acid-producing bacteria, and promoted indole-3-acetic acid (IAA) levels in colonic contents and brain. The anti-inflammatory effect of LA3 was AHR-dependent, as confirmed by an AHR inhibitor in BV-2 cells. Notably, both LA3 fermentation supernatant and exogenous IAA (at the same dose as detected in the supernatant) recapitulated key aspects of LA3's effects. Collectively, L. acidophilus LA3 represents a promising next-generation probiotic targeting the gut-brain axis, with IAA serving as an important effector in neuroinflammation resolution.