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This study evaluated the effect of commercial Bacillus spp. probiotics on growth performance, immunity, gut microbiota composition, and disease resistance to Vibrio parahaemolyticus in Pacific white shrimp Litopenaeus vannamei that were reared under biofloc conditions. A 56-d feeding trial was conducted in a static biofloc system with postlarval shrimp (1.00 &#xb1; 0.03&#x2005;g). A total of 1,080 shrimp were randomly assigned to three groups: two treatment levels (recommended dose [PRO &#xd7; 1] and a doubled dose [PRO &#xd7; 2]) of a commercial probiotic blend, PRO4000X, alongside a control group (CTL; no probiotics). At the trial end point, hepatopancreas and gut samples were collected for gene expression. Gut samples were also obtained for gut microbiota analysis via 16S ribosomal RNA sequencing, and hemolymph samples were withdrawn to measure the total hemocyte count. Probiotic applications did not significantly affect growth performance, including final biomass, mean weight, survival, and feed conversion ratio under the experimental conditions. The probiotic-treated shrimp exhibited enhanced survival during a V. parahaemolyticus (strain A3) challenge, with significantly lower mortality rates (P < 0.001; 42.5 &#xb1; 4.3% for PRO &#xd7; 1 and 60 &#xb1; 6.5% for PRO &#xd7; 2) relative to the CTL (100 &#xb1; 0.00%). Immune parameters, such as total hemocyte count, did not differ. Interestingly, the expression of the antioxidant gene sod (superoxide dismutase) in the shrimp gut was significantly downregulated in the PRO &#xd7; 1 group relative to the control (P = 0.030), which suggests reduced oxidative stress under probiotic supplementation. The analysis of the gut microbiota revealed differences in alpha diversity, specifically in evenness and Shannon index, which were significantly higher in the PRO &#xd7; 1 group. The analysis of the bacterial composition also revealed minor shifts in the dominant genera. Notably, Lysobacter was more abundant in the PRO &#xd7; 1 group, which potentially reflects positive modulation of gut microbial communities in response to probiotic supplementation. Overall, the application of PRO4000X probiotics significantly reduced the V. parahaemolyticus infection in the shrimp that were reared in biofloc water and supported the regulation of immunity and microbial communities in the gut. These findings indicate that probiotics potentially help to improve shrimp health when shrimp are cultured in biofloc systems. With the growing demand for shrimp, shrimp farming has been expanding rapidly. However, the risk of disease outbreaks, especially Vibrio parahaemolyticus infections, remains a major concern. This study demonstrated that after 56 d, the commercial probiotic PRO4000X enhanced immune responses, improved gut microbiota, and contributed to better disease resistance in shrimp.

Recent studies suggest that gut microbiota play important roles in individuals with autism spectrum disorder (ASD), potentially influencing the development and severity of the condition. Oral bacteria may be directly or indirectly involved in the biological and symptomatic aspects of ASD through their effect on gut microbiota. This pilot study aimed to characterise compositional alterations in the oral and gut microbiota of individuals with ASD and to identify bacterial taxa in saliva and faeces that may serve as potential microbial indicators of ASD. Salivary and faecal samples were collected from 10 individuals with ASD and 10 typically developing controls. The oral and gut microbiota were evaluated using 16S ribosomal RNA marker-gene sequencing. Distinct features of the oral and gut microbiota were identified that differed between individuals with ASD and typically developing controls. Based on linear discriminant analysis effect size, the relative abundances of the genera Neisseria were higher in the oral microbiota of the ASD groups, whereas the genera Faecalibacterium were enriched in the gut microbiota. These findings highlight the potential relevance of the oral-gut-brain axis in ASD. Additionally, non-invasive sampling of saliva and faeces may be utilised for early ASD screening.

Sepsis is a life-threatening condition in which early host responses critically determine organ dysfunction, yet strategies targeting this critical window remain limited. We investigated whether pre-septic modulation of host metabolism and gut microbiota could mitigate early organ injury in severe polymicrobial sepsis. Male Sprague-Dawley rats were pretreated for 4 weeks and then subjected to cecal ligation and perforation (CLP). Outcomes were assessed within the first 24 h after sepsis induction, with survival monitored for 7 days. Gut microbiota composition was analyzed at the group level before and after CLP. Early sepsis was characterized by adrenal catecholamine depletion, ileal villus shortening, colonic inflammatory activation, rapid gut microbiota restructuring, and hepatic oxidative stress with selective inflammatory transcriptional activation. Although pretreatments altered baseline gut microbiota composition and partially preserved commensal and short-chain fatty acid-associated taxa, they did not improve survival nor prevent early intestinal and hepatic injury. Early mortality occurred exclusively in meldonium-pretreated animals, indicating a potential trade-off of metabolic preconditioning under severe septic stress. Despite pretreatment-specific modulation of selected antioxidant enzymes, hepatic redox imbalance and stress-associated protein oxidation persisted during early sepsis. Collectively, these observations indicate an apparent dissociation at the group level between gut microbiota remodeling and early gut-liver injury. The first 24 h after sepsis onset thus emerge as a period of limited pharmacological plasticity, underscoring the need for therapeutic strategies that directly target the robust, systemic, host-driven stress mechanisms predominating during this early phase in severe sepsis.

Cancer cachexia profoundly impacts patient survival and quality of life. Current treatments fail to halt this trajectory, highlighting an urgent clinical need for host-directed therapies capable of uncoupling skeletal muscle wasting from tumor progression. This study investigated the therapeutic potential of micheliolide (MCL) across distinct tumor contexts. We employed immunocompetent murine models of colon cancer (CT26) and lung cancer (LLC) cachexia, pseudo-germ-free (pseudo-GF) mice, murine C2C12 myotubes, and primary human skeletal muscle cells. We evaluated MCL's impact on muscle wasting, systemic inflammation (splenic CD4+ T cell phenotypes), gut microbiota composition, and short-chain fatty acid (SCFA) production. The direct effects of Phocaeicola vulgatus (P. vulgatus) administration were also assessed in the CT26 model. MCL functions as a potent host-directed therapy, ameliorating muscle wasting in both models-particularly CT26-completely uncoupling muscle preservation from tumor cytotoxicity. In vitro, MCL directly prevented catabolism in both C2C12 and human primary myotubes. In vivo, MCL robustly rescued muscle mass and function. This was associated with the suppression of local muscle NF-&#x3ba;B hyperactivation and a marked reduction in the absolute counts of activated (CD25+) and exhaustion marker-expressing (PD-1+, TIM-3+) splenic CD4+ and CD8+ T cells, resolving splenomegaly. Crucially, targeted microbiota depletion in pseudo-GF mice entirely abrogated these anti-cachectic benefits, establishing the gut microbiome as an indispensable mediator. MCL selectively enriched the beneficial bacterium P. vulgatus while differentially suppressing potential pathobionts like Enterococcus faecalis in CT26 and Streptococcus acidominimus in LLC. Microbial functional analysis indicated MCL increased the predicted potential for biotin biosynthesis in the CT26 model. Correlation analyses linked P. vulgatus abundance and increased SCFAs to reduced cachexia severity and modulated T cell profiles. Validating its functional significance, oral P. vulgatus administration significantly attenuated muscle wasting, increased cecal butyrate, and beneficially altered specific gut bacterial taxa in the CT26 model. By therapeutically rewiring the gut-immune-muscle axis, MCL exerts pronounced and context-dependent anti-cachectic efficacy. Through dampening of systemic inflammation via T cell modulation, beneficial remodeling of the gut microbiota, and enhancement of predicted microbial biosynthesis pathways, MCL serves as a highly translational, host-directed intervention to mitigate cancer-induced systemic catabolism independent of tumor growth inhibition. Video Abstract.

Haskap berries have great potential as a superfood due to high polyphenolic content which confers both anti-inflammatory and antioxidant activity. These health impacts are mitigated, at least in part, by the gut microbiome as most ingested polyphenols pass to the large intestine for microbial enzymatic action and conversion to secondary phenolic metabolites. These microbial actions mediate both the bioavailability and the bioefficacy of Haskap-derived phenolics. However, clinical intervention trials characterizing the impact of long-term Haskap consumption on human health and the interaction between Haskap-derived phenolics and the gut microbiome are limited. This study aims to determine the impact of Haskap consumption on gut microbiome composition, gut microbial and serum metabolites, and other health outcome metrics in a cohort of adults with both low and high risk of metabolic syndrome. This is a four-armed, randomized, triple-blind, placebo-controlled clinical trial conducted in a cohort of adults with both low and high risk of metabolic syndrome. A total of 120 participants (60 metabolically healthy, 60 metabolically unhealthy) will be randomized in a 1:1 ratio to consume a daily dose of either Haskap or placebo juice for 8 weeks. Outcome measures will be collected before and after the intervention period to determine the health impacts of Haskap in both groups. Primary outcome measures include fasting blood markers of glucose and lipid metabolism and inflammation, fat oxidation rates during submaximal exercise, 16S rRNA fecal microbial composition data, and mass spectrometry-acquired fecal and serum metabolomic data. Secondary outcome measures include anthropometric and sleep quality measures as well as acute and habitual dietary intake data. Investigating how the gut microbiome influences the health benefits of consuming Haskap berries will help elucidate potential mechanisms of Haskap-induced metabolic health benefits and help inform the development of effective strategies to decrease metabolic disease risk through Haskap consumption. ClinicalTrials.gov NCT06546020. Registered on 1 August 2024.

Bacteriophages play crucial roles in modulating the human gut microbiome, yet structural characterization of prevalent gut phages remains limited. Here, we present high-resolution cryo-EM structures of Parabacteroides phage PD491P1, which is one of the most abundant bacteriophages in the human gut. The structures reveal its mature virion organization, including the capsid, head-to-tail interface, and tail tip regions. Strikingly, PD491P1 exhibits an exceptionally extensive disulfide bond network that covalently stabilizes nearly the entire virion. Unique structural features include an elaborate portal-adaptor-terminator interface and distinctive, upward-pointing and flexible tail fibers with multiple putative host recognition domains. These structural adaptations may enable phage PD491P1 to achieve survival and robust infection in the challenging gut environment. These findings expand our understanding of gut phage structural diversity, reveal mechanistic insights into phage stability and infection, and provide a foundation for future development of phage-based microbiome therapeutics.

Fine particulate matter (PM2.5) is a major airborne pollutant in low-temperature livestock housing. Individual environmental factors have been widely studied. However, the actual growth environments of livestock and poultry usually involve the combined effects of multiple environmental factors. This study aims to investigate the fundamental mechanisms underlying energy metabolism disorders in the lung-intestine axis of finishing pigs under the combined effects of low temperature and PM2.5. This study characterized the physical, chemical, and microbial composition of the PM2.5 collected from pig houses. Inflammatory responses and energy metabolism were assessed at the tissue level. Key signaling pathways were functionally validated using in vitro cell models. Analysis of the lung-gut transcriptome elucidated the specific mechanisms by which the lung-gut axis responds to adverse environmental injuries. This study found that PM2.5 affects the energy metabolism process of lung macrophages, and low temperatures exacerbate the effects of PM2.5. Environmental factors trigger lactate production and mitochondrial dysfunction in macrophages through the HIF-PDK pathway. This dysfunction results in the release of pro-inflammatory factors that mediate systemic inflammation. Elevated levels of intestinal injury markers detected in serum indicate intestinal damage. Lung-gut transcriptomic analysis revealed impairments in immune and metabolic pathways. These findings were validated in intestinal tissues, supporting the activation of the lung-gut axis, which mediates systemic inflammation and intestinal damage following respiratory exposure. In summary, these findings elucidate the specific mechanisms through which combined cold exposure and PM2.5 exposure disrupt pulmonary and intestinal immune-metabolic homeostasis. This underscores the necessity of implementing interventions in intensive livestock production systems.

Thermal processing and storage of edible oils promote lipid oxidation, generating compounds that may affect nutritional quality and consumer safety. After ingestion, these compounds are further transformed by gut microbiota, altering their chemical fate and biological impact. The current study applied an integrated gas chromatography-mass spectrometry (GC-MS) and ultra-high-performance liquid chromatography-high-resolution mass spectrometry-tandem mass spectrometry (UPLC-HRMS/MS) workflow coupled with feature-based molecular networking (FBMN) and chemometric analysis to simultaneously track primary and secondary metabolites formed during oil oxidation and subsequent gut microbial metabolism in corn, sesame, and sunflower oils. Metabolite profiling enabled the annotation of 89 primary metabolites by GC-MS and 55 secondary metabolites by UPLC-HRMS/MS-FBMN. Gut microbiota incubation markedly reduced several oxidation-related compounds, including 2,4-decadienal (0.05-0.11%), 2,4-nonadienal (0.01-0.25%), N-nitrosodiethanolamine (0.03-0.05%), 3,5-diethyl-2-methylpyrazine (0.02-0.24%), oxalic acid (1.2-1.8%), and diethylene glycol (0.2-0.4%), compared with uninoculated controls. In contrast, microbial incubation increased phenol (39-46%) and indole (18.2-22.6%), indicating active microbial metabolism of aromatic amino acids. These findings demonstrate how oxidation-derived oil metabolites are dynamically reshaped by human gut microbiota using a unified multi-platform metabolomics strategy, providing insight into the post-ingestion chemical fate of thermally processed edible oils.

How gut microbiota alterations may contribute to host inflammation and metabolomic profiles affecting atherosclerosis is not fully elucidated, especially in the context of HIV. We examined associations between gut microbial features (measured by shotgun metagenomics) and subclinical carotid atherosclerosis, as assessed by high-resolution B-mode ultrasound, in 359 men from the MACS/WIHS Combined Cohort Study. We measured 822 plasma metabolites using LC-MS/MS, and up to 2866 circulating proteins by the Olink Explore 3072/384 platform (with a primary focus on 617 proteins related to inflammation and immune function). Carotid artery plaque was detected in 115/359 men (32%). Adlercreutzia equolifaciens and Eubacterium sp3131 were associated with lower odds of plaque (OR [95% CI] = 0.57 [0.43, 0.77], 0.84 [0.76, 0.93], respectively), while Coprococcus sp13142 was associated with higher odds of plaque (OR [95% CI] = 1.14 [1.06, 1.23]). Results were consistent in men both with and without HIV. A. equolifaciens was positively correlated with HDL cholesterol and inversely correlated with systolic blood pressure. These plaque-associated microbial species were also associated with a range of circulating metabolites and inflammatory proteins. For example, A. equolifaciens positively correlated with the metabolites palmitoyl-EA and mesobilirubinogen, and inversely correlated with the pro-inflammatory chemokine CXCL9, the immune regulator CD160, and IL-24. We identified gut microbial features associated with carotid artery atherosclerosis, consistent across HIV status; these associations were partially explained by specific microbiota-related metabolites and inflammatory markers. If validated, these findings suggest gut microbiota-related targets for CVD prevention. The study was funded by the National Heart, Lung, and Blood Institute (U01HL146204-04S1, K01HL169019).

The sharp increase in prevalence of atopic disease suggests a role for environmental factors, such as the microbiome. Here, we study the impact of immunoglobulin A (IgA) coating of gut bacteria in infancy on allergic outcomes in two distinct populations: (1) an urbanized cohort of Rochester infants (ROC) enriched for allergies (prevalence of 40%) and (2) infants from a traditional, agrarian Old Order Mennonite (OOM) community with a low prevalence of allergies (less than 2%). We performed immunoglobulin A sequencing (IgA-SEQ) on stool samples collected at an average of 6 months of life to assess gut microbiome IgA coating levels in 9 OOM and 21 ROC infants. Atopic outcomes were diagnosed throughout the first 2 years; 10 of the ROC infants were diagnosed with atopic dermatitis and/or food allergy, while none of the OOM infants were allergic. We also assessed human milk IgA-binding of taxa-derived protein antigens, as well as IgA binding to live bacterial cell cultures. Gut microbiome composition was dominated by Bifidobacterium, followed by Ruminococcus, Enterobacteriaceae, and Blautia. Higher IgA coating of P. melaninogenica and Pasteurellaceae were associated with allergic outcomes and higher coating of R. gnavus was observed in non-allergic infants. IgA coating levels of Atopobium, Bifidobacterium, and Coprococcus were positively associated with infant age, and coating levels of Corynebacterium associated negatively with infant age. In non-allergic infants, IgA coating of Clostridium was decreased, while in allergic infants, IgA coating of Corynebacterium was decreased. Furthermore, breastfeeding was associated with higher levels of fecal IgA in infancy, and IgA-binding capacity to B. infantis, a keystone infant commensal, was subsequently assessed using in vitro experiments. Compared to the ROC cohort, milk from OOM mothers exhibited a higher level of IgA response to B. infantis and several other commensals. Surprisingly, IgA-binding to B. infantis was partially mediated by Fab-independent interactions through binding to glycosylated regions of immunoglobulins. Differential gut microbial IgA coating may play a role in development of allergic diseases in infancy. Human milk from communities with low rates of allergic diseases exhibit higher IgA responses to infant commensals, including B. infantis.

Microplastics (MP) pollution is widespread in livestock farming environments. Exposure to MP can impair the gastrointestinal barrier, alter the structure and metabolism of the microbiota, and subsequently lead to organ damage. MP not only hinder cattle farming but also enter the food chain, posing a potential risk. Polyethylene (PE), a type of MP commonly detected in ruminant feed, has not yet been studied for its specific effects on cattle. Using calves as an animal model, this study investigates how exposure to MP induces toxicity via the rumen microbiota-gut-liver axis. Exposure to MP impaired weight gain and liver development in cattle, altered liver tissue pathology, increased blood lipopolysaccharide (LPS) levels, and triggered a systemic inflammatory response, identifying the liver as the primary target organ. Inflammation was closely associated with the dysbiosis of rumen microbiota and metabolites. MP exposure also damages the barrier integrity of the rumen, jejunum, and colon. The underlying mechanism involves MP altering the rumen microbial composition, which in turn triggers metabolic disorders, activates LPS synthesis pathways, and inhibits tight junction protein expression in the jejunum and colon. Although MP do not cause significant architectural damage to muscle tissue, they disrupt lipid homeostasis and nutrient composition, thereby promoting the deposition of pro-inflammatory LPS within muscle tissue. Rumen fluid metabolomics analysis revealed that differential metabolites were mainly enriched in the ATP-binding cassette transporter (ABC) pathway, with 4-fluoro-3-phenoxybenzoic acid and isovalerylglutamic acid being significantly correlated with levels of LPS, IL-6, TNF-&#x3b1;, and IL-1&#x3b2;. Notably, the concurrent increase in TNF-&#x3b1; and LPS in both the bloodstream and liver, alongside altered blood metabolomics, indicates that MP induce hepatic damage by disrupting the rumen microbiota-gut-liver axis. Transcriptomic analysis revealed that liver inflammatory injury was closely associated with NF-&#x3ba;B activation. Further mechanistic analysis supported the central role of the TLR4/MyD88/NF-&#x3ba;B signaling pathway. MP impair liver function in cattle by disrupting the rumen microbiota-gut-liver axis. This process involves the perturbation of rumen flora and intestinal barriers, triggering LPS translocation into the bloodstream, and ultimately causing liver damage. Video Abstract.

Foods fortified with probiotics are a fast-emerging field at the crossroads of food technology, nutritional biochemistry and microbiome science. The increased interest in the gut microbiota as a key controller of host metabolism, immunity and overall homeostasis has led to the creation of diets that provide key nutrients with live and beneficial microbes. Compared to the conventional dietary supplementation, there are improved microbe stability, bioavailability, and microbe-nutrient interactions of probiotic fortification of food matrices. This review is a summary of the literature on the impact of probiotics on the host immunological and metabolic signalling pathways, intestinal barrier functioning, and gut microbiota composition. The biological mechanisms of interaction of probiotics with the intestinal microenvironment are specifically focused on the production of short-chain fatty acids, expulsion of pathogens, the regulation of immune cells, and the communication of the gut-brain axis. New information that can be used to correlate the administration of probiotics with the improvement of gastrointestinal health, systemic inflammation, metabolic maintenance and neurobehavioral phenotypes is narratively synthesized based on available preclinical and clinical evidence. The opportunities of probiotic-enriched functional foods have been highlighted in this review as a strategic tool of disease prevention and health promotion in the context of the mechanistic knowledge in combination with translational health outcomes. The complexity in the interactions between microbial delivery systems and host physiology is the clue to the best efficacy, safety and the future innovation in the development of functional foods.

The gut microbiota plays a fundamental role in maintaining host health by regulating immune function, epithelial barrier integrity, and metabolic homeostasis. Disruption of microbial community structure (also known as dysbiosis) and altered host-microbiota interactions can shift microbial composition and metabolite production, promote immune dysregulation, and contribute to the initiation and persistence of chronic inflammation. Eicosanoids, a class of signaling lipid mediators derived from arachidonic acid , are essential modulators of acute and chronic inflammatory responses. Emerging evidence highlights a bidirectional interplay between the microbiota and eicosanoid pathways as a hallmark of chronic inflammation. Microbial taxa and their metabolites regulate arachidonic acid availability, eicosanoid biosynthesis, and receptor signaling in host cells. In turn, host-derived eicosanoids shape the gut environment, influencing the gut microbiota and host health state. This self-reinforcing loop drives key features of chronic inflammatory diseases, including a shift toward pro-inflammatory eicosanoid profiles, a relative deficiency of anti-inflammatory or pro-resolving lipid mediators, and microbiota dysbiosis. In this review, we summarize recent advances in the mechanisms underpinning microbiota-eicosanoid crosstalk, outline its contribution to chronic inflammatory diseases, and discuss the therapeutic potential of targeting this bidirectional axis.

Dysbiosis of the gut microbiota is a key driver in the onset and persistence of inflammatory bowel disease (IBD). However, the mechanisms by which microbes influence mucosal immunity via specific epithelial routes remain incompletely elucidated. Microfold (M) cells within follicle-associated epithelium serve as a critical "gateway" for luminal antigens and microbes to access the mucosal immune system. While essential for surveillance of commensal microbes, M&#xa0;cells could also be exploited by adherent-invasive strains and adverse environmental factors to amplify inflammation. Recent studies suggest that both in Crohn's disease and ulcerative colitis, M&#xa0;cell abundance and function are aberrantly regulated, linking microbial imbalance with heterogeneous mucosal inflammatory phenotypes. Traditional animal models and two-dimensional culture systems retain limited capacity to selectively manipulate M&#xa0;cells without perturbing systemic immunity, thereby constraining systematic studies of microbiota-M cell co-cultures. Advances in intestinal organoid technology now enable controlled induction of functionally mature M&#xa0;cells within three-dimensional epithelial structures, and have started to shed light on the roles of RANKL signaling, negative regulators, and microbe-associated factors in M&#xa0;cell differentiation and homeostasis. In this review, we focused on key evidence supporting microbiota-M cell interactions in IBD, discussed how M&#xa0;cell-enriched intestinal organoid models could be leveraged to dissect the impact of pathogenic microbes, candidate probiotics, dietary components, and existing therapies on these interactions as well as to evaluate the related potential and limitations for microbiome interventions and drug screening. Integrating gut microbial plasticity with M&#xa0;cell epithelial entry and organoid platforms promises to provide new experimental foundations and theoretical support for individualized microbiome-based therapies and targeted mucosal treatments in IBD.

Prevention of age-related cognitive decline by tea consumption is of great interest. This study systematically compared the neuroprotective efficacy of raw Pu-erh tea (RPT) and ripened Pu-erh tea (FPT) against D-galactose-induced aging in mice, focusing on the modulation of the gut-brain axis. To enhance translational relevance, mice were provided with ad libitum access to RPT or FPT infusions, mimicking human drinking habits. Results showed that both RPT and FPT significantly ameliorated cognitive impairment and hippocampal damage in aging mice, with comparable efficacy despite their distinct phytochemical profiles. Both teas reversed gut microbiota dysbiosis, consistently enriching core taxa such as Lachnospiraceae_NK4A136_group and Alistipes, and restored host sphingolipid metabolism, leading to reduced cerebral ceramide levels and A&#x3b2; deposition. Notably, the key difference lay in polyphenol components: RPF acted mainly via native monomeric catechins, whereas FPT relied on fermentation-derived polymers (theaflavins, thearubigins, theabrownins) and gallic acid. Despite fundamental compositional differences imposed by pile fermentation, both teas provided similar protection against age-related cognitive decline, primarily through the gut microbiota-sphingolipid-brain axis. Our findings highlight that both RPT and FPT represent effective dietary interventions for cognitive health, with the choice being a matter of preference.

Children with painful disorders of gut brain interaction (DGBIs) report stigmatization from medical providers, school personnel, family members, and peers. The consequences of pain-related stigma include concealment of symptoms, lower mood, and poorer functioning. Stigma from other identities (e.g., race, gender) can intersect with pain-related stigma. Unfortunately, intersectional stigma remains understudied in the pediatric pain literature. Furthermore, chronic pain research tends to focus on deficits, rather than strengths. Thus, the current study aimed to understand the experiences of stigma and means of resilience in a sample of Black youth with painful DGBIs. Twenty Black youth between 8 and 18 years old completed semi-structured qualitative interviews. Thematic analysis was conducted via a combined deductive (a priori codes based on theory) and inductive (codes emerging from the data) approach. Codes were grouped into 4 major themes including 1) Experiences of Stigma, 2) Responses from Social Spheres of Influence, 3) Coping Strategies, and 4) Patient-centered Approaches to Treatment, and 8 subthemes. Overall, participants reported stigma from providers, teachers and nurses, family, and peers, while also relying on these groups for support. They were most sensitive to support from caregivers. Others' lack of knowledge about DGBIs appeared to be the largest risk factor for stigma, indicating a potential role for providers in mitigating stigma. Some youth also described the ways that intersecting identities (i.e., race, age, and gender) influenced how others viewed and interacted with their pain. Considerations for reducing stigma and facilitating coping are discussed. PERSPECTIVE: This article presents qualitative data on the experiences of Black youth with painful disorders of gut brain interaction. This study contributes to efforts to diversify pain research. Findings may aid in developing patient-centered interventions for chronic pain.

Pulmonary fibrosis (PF) is an irreversible chronic lung disease in which dysregulation of tissue repair leads to excessive deposition of extracellular matrix (ECM). Rosa roxburghii Tratt (RRT), which has anti-inflammatory and antioxidant properties, exhibits the potential to attenuate organ fibrosis. In this study, we evaluated the bioactive content and antioxidant capacity of different polar extracts of RRT (RRTEs), and explored the multi-target mechanism of the optimal extract in alleviating PF. The ethyl acetate extract of RRT (EAE) exhibited the highest bioactive content and the strongest antioxidant capacity. EAE intervention reshaped the gut microbiota composition in PF mice by enriching beneficial bacteria and reducing pathogenic taxa. Metabolomic analysis identified 11 potential serum biomarkers associated with PF, which were involved in 7 metabolic pathways. Notably, EAE attenuated the disruption of L-tryptophan metabolism, primarily through modulation of serotonin. Moreover, EAE was found to alleviate epithelial-mesenchymal transition (EMT) and inhibit inflammatory cytokine via the JAK2/STAT3 pathway. In conclusion, EAE may exert anti-PF effects associated with the structure of the gut microbiota, correction of amino acid metabolic disorders (notably tryptophan metabolism) and modulating JAK2/STAT3 signaling pathway in the lung. These findings provide new insights into the therapeutic potential of EAE against PF.

The microbiome of the honey bee is associated with immunity, oxidative state, and disease susceptibility. Here we investigated the effects of increased colony-level propolis exposure on gut microbiota and host worker immune and redox gene expression. Sampling pre-marked adult worker bees at 9-days post emergence revealed significantly larger populations of core microbiota in worker guts from propolis-rich colonies, but little change in taxonomic composition or relative structure. We found an overall trend towards decreased expression of immune genes in propolis-rich colonies. The expressions of both pro-phenol oxidase and catalase were significantly reduced in the worker fat body suggesting that propolis-rich colonies better support host redox balance in individual workers. Increased propolis levels resulted in greater expression of superoxide dismutase from the worker fat body and social head glands, consistent with tissue-specific expression considered beneficial in model organisms and humans. Our results suggest that propolis-rich conditions and social head gland secretions contribute to total redox activity throughout the niche space of social immunity. Moreover, our results are consistent with a companion paper that sampled the same colonies and age cohorts, reporting drastic increases in beneficial native bacteria and reduced pathogen prevalence on the mouthparts, a primary marker of social immunity.

Exposure to harmful environments during pregnancy and maternal nutritional status are key factors that affect offspring development; however, the underlying mechanisms of maternal-fetal interaction remain to be elucidated. In recent years, research on gut microbiota and epigenetics has provided new perspectives for understanding these mechanisms. This review systematically summarizes the potential mechanisms by which the maternal gut microbiota influences prenatal development from an epigenetic perspective. Furthermore, it discusses the role of personalized nutritional interventions in the prevention of non-communicable diseases during embryonic and fetal development, aiming to provide new insights and intervention targets for promoting healthy pregnancies and enabling early disease prevention.