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Housing conditions and microbial environment do not affect the efficacy of vaccines for treatment of opioid use disorders in mice and rats.
Vaccines offer a promising prophylactic and therapeutic intervention to counteract opioid use disorders (OUD) and fatal overdoses. Vaccines generate opioid-specific antibodies that bind the target opioid, reducing drug distribution to the brain and preventing drug-induced behavioral and pharmacological effects. Due to their selectivity, anti-opioid vaccines can be administered in combination with FDA-approved medications. Because patients with OUD or other substance use disorders may be affected by other multifactorial co-morbidities, such as infection or depression, it is important to test whether vaccine efficacy is modified by factors that may impact individual innate or adaptive immunity. To that end, this study tested whether housing conditions would affect the efficacy of two lead vaccine formulations targeting oxycodone and fentanyl in male mice and rats, and further analyzed whether differences in the gastrointestinal (GI) microbiome would be correlated with either vaccine efficacy or housing conditions. Results showed that housing mice and rats in either conventional (non-controlled) or specific pathogen-free (SPF, sterile barrier maintained) environment did not affect vaccine-induced antibody responses against oxycodone and fentanyl, nor their efficacy against oxycodone- and fentanyl-induced antinociception, respiratory depression, and bradycardia. Differences in the GI microbiome detected via 16S rRNA gene sequencing were related to the housing environment. This study supports use of anti-opioid vaccines in clinical populations that may display deficits in microbiome function.
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Chronic Rhinosinusitis and Alzheimer's Disease-A Possible Role for the Nasal Microbiome in Causing Neurodegeneration in the Elderly.
Among millions of sufferers of chronic rhinosinusitis (CRS), the challenge is not only constantly coping with CRS-related symptoms, such as congested nose, sinus pain, and headaches, but also various complications, such as attention difficulties and possible depression. These complications suggest that neural activity in the central nervous system may be altered in those patients, leading to unexpected conditions, such as neurodegeneration in elderly patients. Recently, some studies linked the presence of CRS and cognitive impairments that could further develop into Alzheimer's disease (AD). AD is the leading cause of dementia in the elderly and is characterised by progressive memory loss, cognitive behavioural deficits, and significant personality changes. The microbiome, especially those in the gut, has been recognised as a human organ and plays an important role in the development of various conditions, including AD. However, less attention has been paid to the microbiome in the nasal cavity. Increased nasal inflammatory responses due to CRS may be an initial event that changes local microbiome homeostasis, which may further affect neuronal integrity in the central nervous system resulting in AD. Evidence suggests a potential of β-amyloid deposition starting in olfactory neurons, which is then expanded from the nasal cavity to the central nervous system. In this paper, we reviewed currently available evidence that suggests this potential mechanism to advise the need to investigate the link between these two conditions.
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Ultra-processed foods and multiple sclerosis: Evidence, pitfalls and perspectives.
Ultra-processed foods are increasingly recognised as drivers of adverse health outcomes, yet their implications for multiple sclerosis remain underexamined. Emerging evidence suggests that ultra-processed food-rich dietary patterns are associated with greater central adiposity, pro-inflammatory metabolic signatures, microbiota disruption and adverse neuroimmune profiles relevant to multiple sclerosis. Major conceptual pitfalls, including the heterogeneity of ultra-processed foods and the scarcity of longitudinal or interventional studies addressing neuroimmune outcomes, continue to limit interpretation. Ultra-processed food-driven comorbidities, such as obesity, hypertension, dyslipidaemia, insulin resistance and depression, may further accelerate disability accumulation and reduce treatment efficacy in multiple sclerosis, underscoring the need for integrated dietary-immune models. This review integrates evidence from epidemiology, mechanistic studies, microbiome research and exposome science to provide a coherent framework for interpreting ultra-processed food-multiple sclerosis interactions. Recognising ultra-processed food exposure as a potentially modifiable contributor to multiple sclerosis activity may inform future preventive and therapeutic strategies.
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Dietary exposures and risk of anxiety and depression symptoms in the Lothian Birth Cohort 1936: a cohort-level GLAD Project analysis.
BACKGROUND: Mental disorders such as anxiety and depression are leading contributors to disability worldwide, with growing concern in older adults-particularly in Scotland-where poor diet and mental health challenges are common. While the Global Burden of Disease (GBD) study has identified dietary risk factors for physical health, their associations with mental health in later life remain underexplored. METHODS: We used data from 880 participants (mean age 70y) of the Lothian Birth Cohort 1936 in Scotland to examine cross-sectional associations between 11 GBD-defined dietary exposures (fruit, vegetables, legumes, wholegrains, milk, fibre, calcium, polyunsaturated fatty acids, red meat, processed meat, sugar-sweetened beverages) and symptoms of anxiety and depression. Analyses followed harmonised protocols from the Global burden of disease Lifestyle And mental Disorders (GLAD) project (DERR2-10.2196/65576). Dietary exposures were standardised (g/day or % kcal/day), and mental health symptoms dichotomised using the Hospital Anxiety and Depression Scale (HADS ≥8 vs <8). Logistic regression models estimated odds ratios per one standard deviation increase, unadjusted and adjusted for age, sex, and education. Sensitivity analyses used energy-adjusted dietary intakes. RESULTS: Higher milk and calcium intakes were associated with greater odds of anxiety (milk adjusted OR = 1.194, 95% CI 1.018-1.400; calcium adjusted OR = 1.210, 95% CI 1.027-1.426), and higher sugar-sweetened beverage intake with greater odds of depression (adjusted OR = 1.243, 95% CI 1.007-1.535). After energy-adjustment, higher milk intake remained associated with anxiety (adjusted OR = 1.196, 95% CI = 1.020-1.403), higher fruit intake was associated with lower odds of anxiety (adjusted OR = 0.792, 95% CI 0.640-0.981), and sugar-sweetened beverages remained associated with depression (adjusted OR = 1.249, 95% CI 1.013-1.541). No other associations were significant. CONCLUSIONS: In older Scottish adults, we observed only modest evidence that certain GBD-defined dietary exposures are associated with anxiety and depression symptoms.
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The skin microbiome and affective symptoms: neuroimmune, neuroendocrine, and sensory pathways linking inflammatory dermatoses to mood and anxiety burden.
The skin functions as a neuro-immuno-endocrine organ with an extensive microbial interface capable of bidirectional signaling with the central nervous system. While the gut-brain axis is well established, the skin-microbiota-brain (SMB) axis remains underexplored, particularly with respect to affective symptom dimensions (depression, anxiety, stress) that commonly co-occur with chronic inflammatory dermatoses. This review synthesizes evidence across clinical, translational, and experimental studies and organizes it by strength (associational findings, mechanistic plausibility, and limited interventional signals). We outline a systems-level model in which cutaneous microbial dysbiosis is associated with brain-relevant pathways via immune, neuropeptide, and metabolic routes. Candidate mediators include cytokines (IL-6, IL-17, TNF-α), neuropeptides (e.g., substance P, CGRP), and microbial-derived metabolites (e.g., SCFA-like compounds and tryptophan catabolites). These signals are hypothesized to influence neuroimmune tone and neurovascular signaling based largely on broader systemic inflammation and stress biology; direct causal evidence specifically attributing affective outcomes to skin microbiome perturbations in humans remains limited. In parallel, top-down neuroendocrine signaling via hypothalamic-pituitary-adrenal (HPA) axis activation, cortisol-related signaling, and sympathetic outflow can alter skin barrier function, antimicrobial peptide expression, and microbial ecology, potentially contributing to symptom-maintaining loops (e.g., itch-sleep disruption-stress). Importantly, we consider counterarguments (psychosocial burden, reverse causality, treatment effects, and the localized nature of lesions) and identify research priorities required to test causality (longitudinal sampling, mechanistic biomarker panels, and preregistered interventional studies with affective endpoints and mediation analyses). By integrating dermatological, microbiological, and neuroimmunological evidence within a symptom-centered framework, the SMB axis is positioned as a biologically plausible but still evolving model that may help explain affective symptom burden in subsets of patients with inflammatory skin disease and guide mechanism-informed translational research.
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The Microbiome and Mental Health: Looking Back, Moving Forward with Lessons from Allergic Diseases.
Relationships between gastrointestinal viscera and human emotions have been documented by virtually all medical traditions known to date. The focus on this relationship has waxed and waned through the centuries, with noted surges in interest driven by cultural forces. Here we explore some of this history and the emerging trends in experimental and clinical research. In particular, we pay specific attention to how the hygiene hypothesis and emerging research on traditional dietary patterns has helped re-ignite interest in the use of microbes to support mental health. At present, the application of microbes and their structural parts as a means to positively influence mental health is an area filled with promise. However, there are many limitations within this new paradigm shift in neuropsychiatry. Impediments that could block translation of encouraging experimental studies include environmental forces that work toward dysbiosis, perhaps none more important than westernized dietary patterns. On the other hand, it is likely that specific dietary choices may amplify the value of future microbial-based therapeutics. Pre-clinical and clinical research involving microbiota and allergic disorders has predated recent work in psychiatry, an early start that provides valuable lessons. The microbiome is intimately connected to diet, nutrition, and other lifestyle variables; microbial-based psychopharmacology will need to consider this contextual application, otherwise the ceiling of clinical expectations will likely need to be lowered.
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Prebiotic inulin supplementation modulates the immune response and restores gut morphology in Giardia duodenalis-infected malnourished mice.
Malnutrition induces a state of growth retardation and immunologic depression, enhancing the host susceptibility to various infections. In the present study, it was observed that prebiotic supplementation either prior or simultaneously with Giardia infection in malnourished mice significantly reduced the severity of giardiasis and increased the body and small intestine mass, along with increased lactobacilli counts in faeces compared with malnourished-Giardia-infected mice. More specifically, prebiotic supplementation significantly increased the levels of anti-giardial IgG and IgA antibodies and anti-inflammatory cytokines IL-6 and IL-10 and reduced the pro-inflammatory cytokine TNF-α, along with increased levels of nitric oxide in both the serum and intestinal fluid of malnourished-prebiotic-Giardia-infected mice compared with malnourished-Giardia-infected mice. Histopathology and scanning electron microscopy of the small intestine also revealed less cellular and mucosal damage in the microvilli of prebiotic-supplemented malnourished-Giardia-infected mice compared with severely damaged mummified and blunted villi of malnourished-Giardia-infected mice. This is the first study to report that prebiotic supplementation modulated the gut morphology and improved the immune status even in malnourished-Giardia-infected mice.
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Probiotics for preventing gestational diabetes.
BACKGROUND: Gestational diabetes mellitus (GDM) is associated with a range of adverse pregnancy outcomes for mother and infant. The prevention of GDM using lifestyle interventions has proven difficult. The gut microbiome (the composite of bacteria present in the intestines) influences host inflammatory pathways, glucose and lipid metabolism and, in other settings, alteration of the gut microbiome has been shown to impact on these host responses. Probiotics are one way of altering the gut microbiome but little is known about their use in influencing the metabolic environment of pregnancy. This is an update of a review last published in 2014. OBJECTIVES: To systematically assess the effects of probiotic supplements used either alone or in combination with pharmacological and non-pharmacological interventions on the prevention of GDM. SEARCH METHODS: We searched Cochrane Pregnancy and Childbirth's Trials Register, ClinicalTrials.gov, the WHO International Clinical Trials Registry Platform (ICTRP) (20 March 2020), and reference lists of retrieved studies. SELECTION CRITERIA: Randomised and cluster-randomised trials comparing the use of probiotic supplementation with either placebo or diet for the prevention of the development of GDM. Cluster-randomised trials were eligible for inclusion but none were identified. Quasi-randomised and cross-over design studies were not eligible for inclusion in this review. Studies presented only as abstracts with no subsequent full report of study results were only included if study authors confirmed that data in the abstract came from the final analysis. Otherwise, the abstract was left awaiting classification. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed study eligibility, extracted data and assessed risk of bias of included studies. Data were checked for accuracy. MAIN RESULTS: In this update, we included seven trials with 1647 participants. Two studies were in overweight and obese women, two in obese women and three did not exclude women based on their weight. All included studies compared probiotics with placebo. The included studies were at low risk of bias overall except for one study that had an unclear risk of bias. We excluded two studies, eight studies were ongoing and three studies are awaiting classification. Six included studies with 1440 participants evaluated the risk of GDM. It is uncertain if probiotics have any effect on the risk of GDM compared to placebo (mean risk ratio (RR) 0.80, 95% confidence interval (CI) 0.54 to 1.20; 6 studies, 1440 women; low-certainty evidence). The evidence was low certainty due to substantial heterogeneity and wide CIs that included both appreciable benefit and appreciable harm. Probiotics increase the risk of pre-eclampsia compared to placebo (RR 1.85, 95% CI 1.04 to 3.29; 4 studies, 955 women; high-certainty evidence) and may increase the risk of hypertensive disorders of pregnancy (RR 1.39, 95% CI 0.96 to 2.01, 4 studies, 955 women), although the CIs for hypertensive disorders of pregnancy also indicated probiotics may have no effect. There were few differences between groups for other primary outcomes. Probiotics make little to no difference in the risk of caesarean section (RR 1.00, 95% CI 0.86 to 1.17; 6 studies, 1520 women; high-certainty evidence), and probably make little to no difference in maternal weight gain during pregnancy (MD 0.30 kg, 95% CI -0.67 to 1.26; 4 studies, 853 women; moderate-certainty evidence). Probiotics probably make little to no difference in the incidence of large-for-gestational age infants (RR 0.99, 95% CI 0.72 to 1.36; 4 studies, 919 infants; moderate-certainty evidence) and may make little to no difference in neonatal adiposity (2 studies, 320 infants; data not pooled; low-certainty evidence). One study reported adiposity as fat mass (MD -0.04 kg, 95% CI -0.12 to 0.04), and one study reported adiposity as percentage fat (MD -0.10%, 95% CI -1.19 to 0.99). We do not know the effect of probiotics on perinatal mortality (RR 0.33, 95% CI 0.01 to 8.02; 3 studies, 709 infants; low-certainty evidence), a composite measure of neonatal morbidity (RR 0.69, 95% CI 0.36 to 1.35; 2 studies, 623 infants; low-certainty evidence), or neonatal hypoglycaemia (mean RR 1.15, 95% CI 0.69 to 1.92; 2 studies, 586 infants; low-certainty evidence). No included studies reported on perineal trauma, postnatal depression, maternal and infant development of diabetes or neurosensory disability. AUTHORS' CONCLUSIONS: Low-certainty evidence from six trials has not clearly identified the effect of probiotics on the risk of GDM. However, high-certainty evidence suggests there is an increased risk of pre-eclampsia with probiotic administration. There were no other clear differences between probiotics and placebo among the other primary outcomes. The certainty of evidence for this review's primary outcomes ranged from low to high, with downgrading due to concerns about substantial heterogeneity between studies, wide CIs and low event rates. Given the risk of harm and little observed benefit, we urge caution in using probiotics during pregnancy. The apparent effect of probiotics on pre-eclampsia warrants particular consideration. Eight studies are currently ongoing, and we suggest that these studies take particular care in follow-up and examination of the effect on pre-eclampsia and hypertensive disorders of pregnancy. In addition, the underlying potential physiology of the relationship between probiotics and pre-eclampsia risk should be considered.
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cFOS expression in the prefrontal cortex correlates with altered cerebral metabolism in developing germ-free mice.
INTRODUCTION: The microbiota plays a critical role in modulating various aspects of host physiology, particularly through the microbiota-gut-brain (MGB) axis. However, the mechanisms that transduce and affect gut-to-brain communication are still not well understood. Recent studies have demonstrated that dysbiosis of the microbiome is associated with anxiety and depressive symptoms, which are common complications of metabolic syndrome. Germ-free (GF) animal models offer a valuable tool for studying the causal effects of microbiota on the host. METHODS: We employed gene expression and nuclear magnetic resonance (NMR)-based metabolomic techniques to investigate the relationships between brain plasticity and immune gene expression, peripheral immunity, and cerebral and liver metabolism in GF and specific pathogen-free (SPF) mice. RESULTS: Our principal findings revealed that brain acetate (p = 0.012) was significantly reduced in GF relative to SPF mice, whereas glutamate (p = 0.0013), glutamine (p = 0.0006), and N-acetyl aspartate (p = 0.0046) metabolites were increased. Notably, cFOS mRNA expression, which was significantly decreased in the prefrontal cortex of GF mice relative to SPF mice (p = 0.044), correlated with the abundance of a number of key brain metabolites altered by the GF phenotype, including glutamate and glutamine. DISCUSSION: These results highlight the connection between the GF phenotype, altered brain metabolism, and immediate-early gene expression. The study provides insight into potential mechanisms by which microbiota can regulate neurotransmission through modulation of the host's brain and liver metabolome, which may have implications for stress-related psychiatric disorders such as anxiety.
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Interaction of the microbiota with the human body in health and diseases.
The human body contains many microorganisms, including a large number of bacteria, viruses, fungi, and protozoa, which are referred to as the microbiota. Compared with the number of cells comprising the human body, that of the microbiota has been found to be much larger. The microbiome is defined as microorganisms and their genomes have been shown to contain about 100 times more genes than the human genome. The microbiota affects many vital functions in the human body. It contributes to regulation of the immune system, digestion of food, production of vitamins such as B12 and K, metabolization of xenobiotic materials, and many other tasks. Many factors affect the microbiota biodiversity, such as diet, medicines including antibiotics, relationships with the environment, pregnancy, and age. Studies have shown that the lack of microbiota diversity leads to many diseases like autoimmune diseases such as diabetes type I, rheumatism, muscular dystrophy, problems in blood coagulation due to lack of vitamin K, and disturbances in the transfer of nerve cells due to lack of vitamin B12, in addition to its involvement in a number of conditions such as cancer, memory disorders, depression, stress, autism, and Alzheimer's disease. The aim of this review is to summarize the latest studies discussing the relationship between the microbiota and the human body in health and diseases.