Egg masses of Aplysia depilans consist of long and intertwined strings containing numerous capsules with eggs. Light microscopy stains and transmission electron microscopy revealed four layers in the gelatinous sheath that encircled and aggregated the chain of egg capsules. The outermost layer has a fluffy structure. The second, third, and fourth layers consisted of reticulated matrices with different densities. The second and third layers were divided into 5‒6 strata each. The fourth and innermost layer of the gelatinous sheath has a higher density and no visible stratification. This layer glues the tightly packed capsules to one another and to the outer layers of the gelatinous sheath. The thin wall of the capsules is formed by a homogeneous and highly electron-dense material. Inside the capsules, the eggs or embryos were bathed in an electron-lucent aqueous medium. Bacteria and diatoms were the most abundant microorganisms on the surface of egg strings. Bacteria penetrate the gelatinous sheath and appear to be involved in the degradation of the upper strata, but were never found inside the egg capsules. Metagenomic analysis revealed a large taxonomic diversity of bacteria associated with egg masses of A. depilans. Although 15 phyla could be recognized, the families Flavobacteriaceae (Bacteroidota), Lentisphaeraceae (Lentisphaerota), and Rhodobacteraceae (Pseudomonadota) represented 67.9% ± 11.6% of the relative abundance in the microbiome of the egg string samples. The presence of genera capable of decomposing polysaccharides, such as Tenacibaculum and Cellulophaga, supports the idea that bacteria are responsible for the degradation of the gelatinous layers of the egg strings.

Current efforts to reduce the incidence of non-communicable disease (NCD) are slow, but increasing evidence highlights the microbiome as a potential target for prevention. The majority of microbial development occurs in the first 1,000 days of life, presenting opportunities for strategic intervention to reduce the prevalence of future NCDs. In this review, we explore the social, structural, and political barriers that may hinder physiological gut microbial development in the first 1,000 days in the context of current scientific knowledge, focusing on nutritional factors in pregnancy, and during the exclusive breastfeeding and complementary feeding periods. We summarise emerging evidence and explore obstacles to nutritional choices affecting microbial development, and unpack the rhetoric that healthy eating to develop a microbiome that supports optimum health is an individual choice. As evidence on the role of the microbiome in health and disease grows, specific attention must be applied to existing social, structural, and political barriers that may hinder optimal microbial development. Addressing the role of corporate actors and social determinants influencing dietary choices and barriers surrounding breastfeeding must be prioritised, alongside efforts to advance basic scientific research. Until a wider public health perspective is taken, the success of interventions and recommendations will be limited.

Microbial dysbiosis has been linked to environmental enteropathy (EE) and alterations in nutrient absorption; however, compositional modifications following exposure to supplementary nutrients are poorly understood. Here, we report the effect of amino acid and micronutrient supplementation on the gut microbiome of adults with EE.

In the AMAZE trial, adults with EE were randomized to amino acids (AA) and/or micronutrients (MM) for 16 weeks in a 2 × 2 factorial design against placebo. Endoscopy was performed before and after intervention, during which duodenal aspirates were collected as well as fecal samples. 16S rRNA amplicon sequencing was performed on both these samples, and differences in bacterial community composition before and after interventions were investigated using differential abundance analysis, corrected using false discovery rate, plus alpha and beta diversity measurements.

HIV seropositive participants exhibited lower alpha and beta diversity at baseline. AA and/or MM supplementation did not show significant changes in abundance or diversity of genera post-intervention compared to placebo. Micronutrient supplementation resulted in an increase in the pyruvate fermentation to acetone MetaCyc pathways compared to the placebo arm.

This study provides insights into the responsiveness of the gut microbiome to micronutrient and amino acid supplementation in adults with EE.

Decreased gut microbial diversity is associated with greater depression symptoms in adults. Findings on the relationship between the gut microbiome and depression or anxiety in children and adolescents are mixed, and evidence syntheses are needed. Seven databases were searched for peer-reviewed studies on the gut microbiome and internalizing symptoms, depression, or anxiety, in children and adolescents (<19 years). Random-effects meta-analyses of alpha diversity indices were performed. Youth advisors validated the research findings’ relevance to their experiences and contributed to dissemination planning. Eight studies were included, representing 2,865 participants (mean age = 11.4 years, SD = 4.3). Study designs were cross-sectional (n = 5), longitudinal (n = 2), and interventional (n = 1). No association was found between alpha or beta diversity and internalizing problems, depression, or anxiety. Increased abundance of genera within phyla Bacillota (e.g., Fusicatenibacter) and Pseudomonadota (e.g., Escherichia), along with decreased abundance of other Bacillota genera (e.g., Faecalibacterium), were associated with depression and anxiety symptoms. This review identified preliminary associations between specific bacterial taxa and depression and anxiety in children and adolescents. Larger studies using comprehensive analytical approaches are needed to explore the role of the gut microbiome in the genesis and treatment of internalizing disorders.

Microbiomes are communities of microorganisms that form close associations with metazoan hosts and have important roles in host biological processes. With the advent of Next Generation Sequencing, the microbiomes of myriad animals and plants have been described. However, the microbiomes of parasites have received little attention, which is surprising considering their ecological and medical importance. This study characterizes, for the first time, the microbiome of Dujardinascaris helicina, a gastrointestinal nematode parasite of the American crocodile. Dujardinascaris helicina were isolated from crocodiles residing in two geographically separated habitats across Belize. Using 16S sequencing, we compare β-diversity between sampling locations using generalized linear mixed modeling. Our results show that D. helicina microbiomes differ in composition depending on location. We also show that D. helicina microbiomes show strong shifts toward consolidation of specific taxa when proximity to human modified environments increases.

Colorectal cancer (CRC) represents a relevant public health problem, with high incidence and mortality in Western countries. CRC can occur as sporadic (65%–75%), common familial (25%), or as a consequence of an inherited predisposition (up to 10%). While unravelling its genetic basis has been a long trip leading to relevant clinical implementation over more than 30 years, other contributing factors remain to be clarified. Among these, micro-organisms have emerged as critical players in the development and progression of the disease, as well as for CRC treatment response. Fusobacterium nucleatum (Fn) has been associated with CRC development in both pre-clinical models and clinical settings. Fusobacteria are core members of the human oral microbiome, while being less prevalent in the healthy gut, prompting questions about their localization in CRC and its precursor lesions. This review aims to critically discuss the evidence connecting Fn with CRC pathogenesis, its molecular subtypes and clinical outcomes.

The endocannabinoidome (eCBome) and the gut microbiota have been implicated in diet-induced obesity and impaired metabolism. While the eCBome and the gut microbiome are known to respond to diet macronutrient composition, interaction with micronutrient intake has been relatively unexplored. Iron (Fe) is an essential micronutrient for the function of enzymes involved in energy and lipid metabolism. Here, we evaluated how 28 days of Fe depletion and enrichment, in interaction with Low Fat-Low Sucrose (LFLS) or High Fat-High Sucrose (HFHS) diets, affect the host via the eCBome, and modulate intestinal gut microbial communities. Circulating levels of N-oleoyl-ethanolamine (OEA) showed an elevation associated with Fe-enriched LFLS diet, while the Fe-depleted HFHS diet showed an elevation of N-arachidonoyl-ethanolamine (anandamide, AEA) and a decrease of circulating linoleic acid. In parallel, the response of intestinal inflammatory mediators to Fe in the diet showed decreased levels of prostaglandins PGE1, PGE3, and 1a,1b-dihomo PGF2α in the caecum. Individual differences in microbial taxa were less pronounced in the ileum than in the caecum, where Eubacterium coprostanoligenes group showed an increase in relative abundance associated with Fe-depleted LFLS diets. In conclusion, our study shows that Fe intake modulates the response to the macronutrient composition of the diet in mice.

Early gut microbiome development may impact brain and behavioral development. Using a nonhuman primate model (Macaca mulatta), we investigated the association between social environments and the gut microbiome on infant neurodevelopment and cognitive function. Infant rhesus monkeys (n = 33) were either mother-peer-reared (MPR) or nursery-reared (NR). Neurodevelopmental outcomes, namely emotional responsivity, visual orientation, and motor maturity, were assessed with the Primate Neonatal Neurobehavioral Assessment (PNNA) at 14–30 days. Cognitive development was assessed through tasks evaluating infant reward association, cognitive flexibility, and impulsivity at 6–8 months. The fecal microbiome was quantified from rectal swabs via 16S rRNA sequencing. Factor analysis was used to identify “co-abundance factors” describing patterns of microbial composition. We used multiple linear regressions with AIC Model Selection and differential abundance analysis (MaAsLin2) to evaluate relationships between co-abundance factors, microbiome diversity, and neuro-/cognitive development outcomes. At 30 days of age, a gut microbiome co-abundance factor, or pattern, with high Prevotella and Lactobacillus (β = −0.88, p = 0.04, AIC Weight = 68%) and gut microbiome alpha diversity as measured by Shannon diversity (β = −1.33, p = 0.02, AIC Weight = 80%) were both negatively associated with infant emotional responsivity. At 30 days of age, being NR was also associated with lower emotional responsivity (Factor 1 model: β = −3.13, p < 0.01; Shannon diversity model: β = −3.77, p < 0.01). The infant gut microbiome, along with early-rearing environments, may shape domains of neuro-/cognitive development related to temperament.

Metabolic dietary patterns, including the Empirical Dietary Index for Hyperinsulinaemia (EDIH) and Empirical Dietary Inflammatory Pattern (EDIP), are known to impact multiple chronic diseases, but the role of the colonic microbiome in mediating such relationships is poorly understood. Among 1,610 adults with faecal 16S rRNA data in the TwinsUK cohort, we identified the microbiome profiles for EDIH and EDIP (from food frequency questionnaires) cross-sectionally using elastic net regression. We assessed the association of the dietary pattern-related microbiome profile scores with circulating biomarkers in multivariable-adjusted linear regression. In addition, we used PICRUSt2 to predict biological pathways associated with the enriched microbiome profiles, and further screened pathways for associations with the dietary scores in linear regression analyses. Microbiome profile scores developed with 32 (EDIH) and 15 (EDIP) genera were associated with higher insulin and homeostatic model assessment of insulin resistance. Six genera were associated with both dietary scores: Ruminococcaceae_UCG-008, Lachnospiraceae_UCG-008, Defluviitaleaceae_UCG-011 Anaeroplasma, inversely and Negativibacillus, Streptococcus, positively. Further, pathways in fatty acid biosynthesis, sugar acid degradation, and mevalonate metabolism were associated with insulinaemic and inflammatory diets. Dietary patterns that exert metabolic effects on insulin and inflammation may influence chronic disease risk by modulating gut microbial composition and function.

Host–bacterial communities (microbiomes) are influenced by a wide range of factors including host genotype and parasite exposure. However, few studies disentangle temporal and host-genotype-specific variation in microbiome response to infection across several host tissues. We experimentally exposed the freshwater crustacean Daphnia magna to its fungal parasite Metschnikowia bicuspidata and characterized changes in host–bacterial communities associated with the parasite's development within the host. We used 16S rRNA gene sequencing to assess bacterial communities of the host (a) 24 h (‘initial parasite exposure’) and (b) 10 days (‘successful infection’) after exposure to a standard dose of M. bicuspidata spores, in host guts, body tissue (excluding guts) and whole individuals. We also investigated whether bacterial community responses to parasite exposure varied by host genotype.

Parasite exposure did not immediately alter host gut bacterial communities, but drove host-genotype-specific changes in the bacterial community composition of whole individuals. We validated that these changes were not driven by shifts in bacterial communities of the culturing medium, due to the addition of the parasite spore solution. Successful infection (i.e. the proliferation of M. bicuspidata spores in the host body) reduced alpha diversity and shifted abundance of dominant bacterial orders in the gut. Moreover, it induced a host-genotype-specific changes in body bacterial community composition. Overall, bacterial community responses to parasite exposure and subsequent infection are complex: they occur in a host-genotype-dependent manner, differentially at distinct timepoints after parasite exposure, and in specific host tissue.

The relationship between nutrition and ageing is complex. The metabolism and synthesis of micronutrients within the gut microbiome can influence human health but is challenging to study. Furthermore, studying ageing in humans is time-consuming and difficult to control for environmental factors. Studies in model organisms can guide research efforts in this area. This review describes how the nematode Caenorhabditis elegans can be used to study how bacteria and diet influence ageing and inform follow-on studies in humans. It is known that certain bacteria accelerate ageing in C. elegans. This age-accelerating effect is prevented by inhibiting folate synthesis within the bacteria, and we propose that in the human microbiome, certain bacteria also accelerate ageing in a way that can be modulated by interfering with bacterial folate synthesis. Bacterial-derived folates do not promote ageing themselves; rather, ageing is accelerated by bacteria in some way, either through secondary metabolites or other bacterial activity, which is dependent on bacterial folate synthesis. In humans, it may be possible to inhibit bacterial folate synthesis in the human gut while maintaining healthy folate status in the body via food and supplementation. The supplement form of folic acid has a common breakdown product that can be used by bacteria to increase folate synthesis. Thus, supplementation with folic acid may not be good for health in certain circumstances such as in older people or those with an excess of proteobacteria in their microbiome. For these groups, alternative supplement strategies may be a safer way to ensure adequate folate levels.

Maternal diet may modulate human milk microbiota, but the effects of nutritional supplements are unknown. We examined the associations of prenatal diet and supplement use with milk microbiota composition. Mothers reported prenatal diet intake and supplement use using self-administered food frequency and standardised questionnaires, respectively. The milk microbiota was profiled using 16S rRNA gene sequencing. Associations of prenatal diet quality, dietary patterns, and supplement use with milk microbiota diversity and taxonomic structure were examined using Wilcoxon signed-rank tests and multivariable models adjusting for relevant confounders. A subset of 645 mothers participating in the CHILD Cohort Study (originally known as the Canadian Healthy Infant Longitudinal Development Study) provided one milk sample between 2 and 6 months postpartum and used prenatal multivitamin supplements ≥4 times a week. After adjusting for confounders, vitamin C supplement use was positively associated with milk bacterial Shannon diversity (β = 0.18, 95% CI = 0.05, 0.31) and Veillonella and Granulicatella relative abundance (β = 0.54; 95% CI = 0.05, 1.03 and β = 0.44; 95% CI = 0.04, 0.84, respectively), and negatively associated with Finegoldia relative abundance (β = –0.31; 95% CI = –0.63, –0.01). Fish oil supplement use was positively associated with Streptococcus relative abundance (β = 0.26; 95% CI = 0.03, 0.50). Prenatal diet quality and dietary patterns were not associated with milk microbiota composition. Prenatal vitamin C and fish oil supplement use were associated with differences in the milk microbiota composition. Future studies are needed to confirm our findings and elucidate mechanisms linking maternal supplement use to milk microbiota and child health.

Cocoa-derived flavanols (CDF) may act as prebiotics. However, evidence is inconsistent, and the duration and dose of CDF intake needed to elicit any prebiotic effect are undefined. This randomized, double-blind, crossover study determined the effects of short-term, high-dose dietary supplementation with CDF versus matched placebo on gut microbiota composition in 8 healthy adults. A single faecal sample was collected 8 d after supplementation with 900 mg/d CDF or placebo. Gut microbiota composition and Bifidobacterium spp. and Lactobacillus spp. abundance were measured as secondary outcomes by 16S ribosomal ribonucleic acid (rRNA) amplicon sequencing and quantitative polymerase chain reaction, respectively. No between-treatment differences in the relative or absolute abundance of Bifidobacterium spp. (Cohen’s d = 0.89, P = 0.22) or Lactobacillus spp. (Cohen’s d = 0.42, P = 0.65) were detected. Shannon diversity (Cohen’s d = 0.38, P = 0.04) and overall community richness (Cohen’s d = 0.34, P = 0.06) were lower following CDF supplementation versus placebo, but no between-treatment differences in β-diversity or taxa relative abundances were observed. Findings are not consistent with a clear prebiotic effect of this short-term, high-dose CDF supplementation strategy relative to placebo.

The effect of single dietary fibre (DF) on lowering uric acid (UA) level has been reported in the literature. However, the potential protective mechanism of DF against potassium oxybate-induced hyperuricaemia (HUA), as modelled by prophylactic administration, remains unclear. The data demonstrate that DF significantly decreased serum and cerebral tissue UA concentrations, inhibited xanthine oxidase expression and activity in the liver and reduced levels of creatinine and urea nitrogen in the serum. Additionally, it mitigated the deposition of amyloid-β in cerebral tissue. Correlation analysis showed that DF modulated the Toll-like receptor 4/NF-κB signalling pathway, attenuating oxidative stress and inflammatory responses in HUA mice. Additionally, DF helps to maintain the composition of the gut microbiota, reducing harmful Desulfovibrio and enriching beneficial Akkermansia and Ruminococcus populations. The results of the faecal metabolomics analysis indicate that DF facilitates the regulation of metabolic pathways involved in oxidative stress and inflammation. These pathways include pyrimidine metabolism, tryptophan metabolism, nucleotide metabolism and vitamin B6 metabolism. Additionally, the study found that DF has a preventive effect on anxiety-like behaviour induced by HUA. In summary, DF shows promise in mitigating HUA and cognitive deficits, primarily by modulating gut microbiota and metabolites.