Intestinal Function Research Articles

The regulatory effects of bioactive polysaccharides on intestinal function and bile acids: chemical structures, bioactivities, and mechanisms

Polysaccharides are one of the important components of the human diet, offering a wide range of biological activities, especially in improving inflammation in the digestive system and addressing metabolic diseases. Among all the reported bioactivities of polysaccharides, their regulation effects on intestinal function and bile acids (BAs) are gradually attracting the attention of more researchers. Bile acids, the main components of intestinal lipid digestive fluid, are also key signal factors for metabolic homeostasis and impact overall health. Polysaccharides usually interact directly or indirectly with the gut and gut microbiota to participate in the regulation process of reabsorption, metabolism, and excretion of bile acids in humans, thereby exerting their role in the intervention of human diseases. In this review, we comprehensively reviewed the effects of bioactive polysaccharides on the regulation of intestinal function and bile acids. The chemical structures, bioactivities, and potential mechanisms for their activities were also reviewed. This study aimed to provide a comprehensive reference for future research on the activities and mechanisms of polysaccharides, as well as to offer important strategies and insights for the development of bioactive polysaccharides to prevent inflammatory and metabolic diseases.

The Physiology of Enteric Glia.

Enteric glia are the partners of neurons in the enteric nervous system throughout the gastrointestinal tract. Roles fulfilled by enteric glia are diverse and contribute to maintaining intestinal homeostasis through interactions with neurons, immune cells, and the intestinal epithelium. Glial influences optimize physiological gut processes such as intestinal motility and epithelial barrier integrity through actions that regulate the microenvironment of the enteric nervous system, the activity of enteric neurons, intestinal epithelial functions, and immune response. Changes to glial phenotype in disease switch glial functions and contribute to intestinal inflammation, dysmotility, pain, neuroplasticity, and tumorigenesis. This review summarizes current concepts regarding the physiological roles of enteric glial cells and their potential contributions to gut disease. The discussion is focused on recent evidence that suggests important glial contributions to gastrointestinal health and pathophysiology.

Astragalus polysaccharide enhances maternal mucosal immunity against PEDV.

This study highlights the limitations of current porcine epidemic diarrhea virus (PEDV) vaccines in inducing sufficient maternal milk IgA, which is crucial for protecting neonatal piglets. By supplementing Astragalus polysaccharide (APS) into the vaccination regimen, we demonstrated a significant enhancement in milk PEDV-specific IgA levels, as well as improved cellular immune responses. APS also bolstered intestinal immune function and homeostasis in piglets. These findings suggest that APS supplementation could serve as an immune booster to enhance maternal immunity, offering a promising approach to better protect piglets against PEDV.

Maternal chitosan oligosaccharide supplementation during late gestation and lactation optimizes placental function in sows and intestinal function in 21-day-old IUGR suckling piglets

Maternal dietary supplementation with chitosan oligosaccharide (COS) has been considered as a potential intervention to mitigate the occurrence of intrauterine growth restriction (IUGR) and improve postnatal growth. The present study investigated the effect of COS as a dietary supplement for sows during late gestation and lactation on their productivity, placental function, and the intestinal health of IUGR piglets. From day (d) 85 of late gestation to d 21 of lactation, 30 sows were randomly divided into either a control group (basal diet) or a COS group (basal diet + 100 mg kg−1 COS). At d 21 of lactation, eight normal and eight IUGR littermates from eight litters belong to control sows, as well as eight IUGR littermates from COS sows, were selected for further analysis. The results showed a significant reduction in the number of stillbirths and mummies in COS groups (p < 0.05). Maternal dietary supplementation with COS also significantly up-regulated the expression levels of GLUT1, GLUT3, and VEGFA mRNA in the placenta of IUGR piglets compared to those in control group (p < 0.05). Furthermore, there was a significant decrease in MDA content and a significant increase in GSH content in the placenta of IUGR piglets from COS sows compared to those from control group (p < 0.05). Additionally, the expression levels of MUC2 and occludin mRNA as well as claudin1 protein significantly up-regulated in the jejunum of 21-day-old IUGR piglets from COS sows group compared to those from control group (p < 0.05). Moreover, IL-10 mRNA expression level was significantly increased while MDA content was significantly reduced in the jejunum of 21-day-old IUGR piglets from COS sows group compared to those from control group (p < 0.05). The results indicated that maternal dietary COS supplementation during late gestation effectively reduced the incidence of stillbirths and mummies, potentially linked to enhanced placental function, reduced oxidative stress, and improved immune status. Furthermore, maternal dietary COS supplementation exhibited positive impact on intestinal digestive and absorptive function, intestinal barrier integrity, intestinal antioxidant capacity and immune status in 21-day-old suckling IUGR piglets.

Establishment and validation of a nomogram for predicting postoperative intestinal adhesion in children with acute appendicitis.

This study aims to explore the value of multiple indicators in the evaluation of risk factors for intestinal adhesion (IA) after appendectomy in children with acute appendicitis (AA). A retrospective study was conducted on 608 patients who underwent appendectomy in the Department of Pediatric Surgery, Children's Medical Center of Jilin Province from January 2017 to April 2023, with a one-year follow-up period to record the occurrence of IA after appendectomy. Univariate and multivariate analysis were used to screen the risk factors of postoperative IA, and a prediction model was established to predict postoperative IA. There were 527 patients in the non-IA group and 81 patients in the IA group. Binary Logistic regression was used to determine the strength of correlation with postoperative intestinal adhesion. The risk factors identified were as follows: DS ≥ 43h (OR = 3.903, 5points), CRP ≥ 65mg/L (OR = 3.424, 4.5points), PCT ≥ 0.9µg/L (OR = 8.683, 8points), Surgical duration ≥ 100min (OR = 6.457, 7points), Appendiceal perforation (OR = 6.073, 6.5points), Postoperative exhaust time ≥ 55h (OR = 14.483, 10points). After test, the nomogram drawn based on binary logistic regression can obtain good prediction efficiency. In the training set, the area under the curve was 0.960, the sensitivity was 0.898, and the specificity was 0.905. In the test set, the area under the curve was 0.957, the sensitivity was 0.864, and the specificity was 0.906. Postoperative exhaust time ≥ 55h has a high risk of IA after appendicitis surgery in children. Early recovery of intestinal peristalsis function is essential. This scoring model is a novel and promising method for predicting postoperative IA.

MnNi@PVP Nanoenzyme Based on Regulating Inflammation and Immune Homeostasis for the Therapy of Inflammatory Bowel Disease.

Nanozymes exhibiting remarkable antioxidant capabilities represent an effective therapeutic approach for ulcerative colitis (UC). This study synthesized the MnNi@PVP nanoenzyme through high-temperature pyrolysis and the NaCl template method, which exhibited multienzyme activity comprising glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT). This study investigated the therapeutic effect of MnNi@PVP on colitis caused by sodium dextran sulfate (DSS). The findings indicated that MnNi@PVP notably decreased the disease activity index (DAI) score, which encompasses weight loss, colon shortening, and histopathological changes. MnNi@PVP showed effectiveness in addressing oxidative damage and suppressing the levels of proinflammatory markers, such as tumor necrosis factor (TNF-α), inducible nitric oxide synthase (iNOS), and interleukin (IL)-6, by inactivating the TLR4 pathway and macrophages. In addition, MnNi@PVP demonstrated the ability to repair tight junction proteins (occludin and ZO-1) and restore the intestinal barrier. The transcriptome sequencing demonstrated that MnNi@PVP could regulate inflammatory factor expression pathways and immune processes. Additionally, negatively charged MnNi@PVP can selectively bind to inflamed colonic tissues through electrostatic interactions, endowing it with targeted reparative capabilities at the location of intestinal inflammation. The MnNi@PVP, which possesses the reactive oxygen and nitrogen species (RONS) clearance capability examined in this section, is expected to provide the basis for the targeted repair of intestinal function.

Plants, plant‐derived compounds, probiotics, and postbiotics as green agents to fight against poultry coccidiosis: A review

AbstractThe intestinal tract is the main place for animals to digest food and absorb nutrients, which also serves as the first line of defense against pathogens that invade the internal environment. Therefore, normal intestinal structure and function are essential for animal health. Poultry coccidiosis is an intestinal disease primarily caused by the parasitization of intestinal epithelial cells by protozoa of the genus Eimeria. The occurrence of coccidiosis not only compromises the intestinal integrity of poultry but also increases their disease susceptibility, thus posing a serious threat to the overall health and productivity of poultry. Nowadays, the primary methods for controlling and preventing coccidiosis in poultry are anticoccidial drugs or live oocyst vaccines. However, the use of the former may be associated with problems of resistance and drug residues, while the use of the latter may cause intestinal damage and significantly increase farming costs. For these reasons, it is critical to investigate green, safe, and cost‐effective natural alternative strategies such as phytochemicals and probiotics for controlling coccidiosis as well as mitigating the deleterious effects of coccidial infections in production. In this review, we aim to summarize the role, mechanisms, and therapeutic potential of natural products in the treatment of coccidiosis to lay a theoretical foundation for effective coccidiosis control.

Multi-Omics Reveal the Improvements of Nutrient Digestion, Absorption, and Metabolism and Intestinal Function via GABA Supplementation in Weanling Piglets

The nonprotein amino acid γ-aminobutyric acid (GABA) can enhance intestinal function in piglets; however, the mechanisms involved are not yet fully understood. To explore the effects of GABA and its underlying mechanisms, weanling piglets were randomly assigned to three groups, receiving either a basal diet or a basal diet supplemented with GABA (80 mg/kg or 120 mg/kg). The results demonstrated that dietary GABA improved growth performance and reduced diarrhea incidence (p < 0.05). Additionally, GABA supplementation decreased the serum and intestinal levels of pro-inflammatory cytokines (p < 0.05), and improved intestinal morphology. Multi-omics analyses were employed to explore the alterations caused by GABA supplementation and elucidate the related mechanisms. Microbiota profiling revealed improved beta-diversity and changes in the composition of ileal bacteria and fungi. Amino acid metabolism, lipid metabolism, and digestive processes were primarily enriched in the GABA group according to metabolomics analysis. A transcriptome analysis showed significant enrichment in ion transmembrane transport and nutrition absorption and digestion pathways in the ileum. Furthermore, increased lipase and trypsin activity, along with the elevated expression of tight junction proteins confirmed the beneficial effects of GABA on intestinal nutrient metabolism and barrier function. In conclusion, dietary 80 mg/kg GABA supplementation improved nutrient digestion and absorption and intestinal function in weanling piglets.

Utilizing the apical-out enteroids in vitro model to investigate intestinal glucose transport, barrier function, oxidative stress, and inflammatory responses in broiler chickens

IntroductionConventional 2D intestinal epithelial cell lines have been widely used in investigating intestinal functions, yet with limitations in recapitulating the in vivo gut physiology of chickens. A recently established chicken enteroid model with apical-out nature and the presence of leukocyte components represents intestinal mucosal functions. The objectives of this study were to 1) evaluate basic gut nutrient transport and barrier functions in this model and 2) identify the model’s effectiveness in studying inflammation and oxidative stress responses.MethodsEnteroids were generated from individual villus units isolated from the small intestine of Cobb500 broiler embryos. Enteroid viability, morphology, and epithelial cell markers were monitored; barrier function was evaluated based on the permeability to fluorescein isothiocyanate–dextran (FD4) with or without EDTA and lipopolysaccharide (LPS) challenges; nutrient transport was evaluated by fluorescence-labeled glucose (2NBD-G) with or without transporter blockade; the oxidative status was indicated by reactive oxygen species (ROS). Inflammatory and oxidative challenges were induced by LPS and menadione treatment, respectively. Selected marker gene expressions, including tight junction proteins (CLDN-1, CLDN-2, ZO-1, and OCCL), epithelial cell markers (Lgr-5, LYZ, and MUC-2), cytokines (IL-1β, IL-6, IL-8, IL-10, TNF-α, and INF-γ), and antioxidant enzymes (Nrf-2, catalase, and SOD), were determined by using RT-qPCR. Data were analyzed by one-way ANOVA among treatment groups.ResultsEnteroid cell activity was stable from day (d) 2 to d 6 and declined at d 7. Epithelial cell marker and cytokine expressions were stable from d 4 to d 6. FD4 permeability was increased after the EDTA treatment (P ≤ 0.05). Transporter-mediated 2NBD-G absorption was observed, which was reduced with glucose transporter blockade (P ≤ 0.05). Enteroids showed classic responses to LPS challenges, including upregulated gene expressions of IL-1β and IL-6, downregulated gene expressions of ZO-1 and OCCL, and increased FD4 permeability (P ≤ 0.05). Enteroids showed increased ROS generation (P ≤ 0.05) in response to oxidative stress.DiscussionIn conclusion, this apical-out enteroid model is a stable alternative in vitro model that exhibits intestinal barrier, nutrient transport, oxidation, and inflammation functions. With this enteroid model, we developed two challenge protocols for evaluating intestinal functions under oxidative stress and inflammation conditions.

Gut microbiota modulates depressive-like behaviors induced by chronic ethanol exposure through short-chain fatty acids

BackgroundChronic ethanol exposure (CEE) is recognized as an important risk factor for depression, and the gut-brain axis has emerged as a key mechanism underlying chronic ethanol exposure-induced anxiety and depression-like behaviors. Short-chain fatty acids (SCFAs), which are the key metabolites generated by gut microbiota from insoluble dietary fiber, exert protective roles on the central nervous system, including the reduction of neuroinflammation. However, the link between gut microbial disturbances caused by chronic ethanol exposure, production of SCFAs, and anxiety and depression-like behaviors remains unclear.MethodsInitially, a 90-day chronic ethanol exposure model was established, followed by fecal microbiota transplantation model, which was supplemented with SCFAs via gavage. Anxiety and depression-like behaviors were determined by open field test, forced swim test, and elevated plus-maze. Serum and intestinal SCFAs levels were quantified using GC-MS. Changes in related indicators, including the intestinal barrier, intestinal inflammation, neuroinflammation, neurotrophy, and nerve damage, were detected using Western blotting, immunofluorescence, and Nissl staining.ResultsChronic ethanol exposure disrupted with gut microbial homeostasis, reduced the production of SCFAs, and led to anxiety and depression-like behaviors. Recipient mice transplanted with fecal microbiota that had been affected by chronic ethanol exposure exhibited impaired intestinal structure and function, low levels of SCFAs, intestinal inflammation, activation of neuroinflammation, a compromised blood-brain barrier, neurotrophic defects, alterations in the GABA system, anxiety and depression-like behaviors. Notably, the negative effects observed in these recipient mice were significantly alleviated through the supplementation of SCFAs.ConclusionSCFAs not only mitigate damage to intestinal structure and function but also alleviate various lesions in the central nervous system, such as neuroinflammation, and reduce anxiety and depression-like behaviors, which were triggered by transplantation with fecal microbiota that had been affected by chronic ethanol exposure, adding more support that SCFAs serve as a bridge between the gut and the brain.

Impacts of Nano-Composite of Copper and Carbon on Intestinal Luminal Micro-Ecosystem and Mucosal Homeostasis of Yellow-Feather Broilers

The present study was undertaken to evaluate the impacts of nano-composites of copper and carbon (NCCC) on the intestinal luminal micro-ecosystem and mucosal homeostasis of yellow-feather broilers. A total of two-hundred and forty 1-day-old male yellow-feather broilers were randomly allocated into four groups, each with five replications of twelve birds. The control (CON) group received a corn-soybean basal diet, while the N50, N100, and N200 groups were supplemented with 50, 100, and 200 mg/kg of NCCC in basal diets, respectively. The trial duration was 63 days. The findings demonstrated that there were slight impacts of NCCC addition on the intestinal luminal micro-ecosystem of broilers, with the fecal moisture content in the N100 group being slightly higher on Day 3 in the starter phase (p < 0.05). The cecal microbiota structure also did not obviously change (p > 0.05), in spite of the fall in the relative abundance of the Ruminococcus torques group in the N50 group and norank Clostridia UCG-014 in N200 group (p < 0.05). But for intestinal mucosal homeostasis, NCCC played a crucial part in jejunal morphology, tight junction, immunologic status, and antioxidant capacity. There was linear growth in villus height and a quadratic increase in villus height, crypt depth and their ratio with the increase in NCCC dosage (p < 0.05), and 100 mg/kg NCCC supplementation could intensify the expression of CLDN-3 genes (p < 0.05). In addition, IL-4 and IL-10 linearly increased after NCCC treatment (p < 0.05), along with some irregular changes in sIgA (p < 0.05). In addition, higher jejunal mucosal total antioxidant capacities in N50 and N200 groups were also observed (p < 0.05). Overall, NCCC treatment optimized the intestinal mucosa function of broilers in terms of physical barrier and immune and antioxidant capacities, but exerted subtle influence in the luminal environment of yellow-feather broilers. More precisely, dietary supplementation with 50 mg/kg NCCC is recommended for intestinal homeostasis of broilers.

Metagenomics reveals the divergence of gut microbiome composition and function in two common pika species (Ochotona curzoniae, Ochotona daurica) in China.

Gut microbiome plays crucial roles in animal adaptation and evolution. However, research on adaptation and evolution of small wild high-altitude mammals from the perspective of gut microbiome is still limited. In this study, we compared difference in intestinal microbiota composition and function in Plateau pikas (Ochotona curzoniae) and Daurian pikas (Ochotona daurica) using metagenomic sequencing. Our results showed that microbial community structure had distinct differences in different pika species. Prevotella, Methanosarcina, Rhizophagus and Podoviridae were abundant bacteria, archaea, eukaryotes and viruses in Plateau pikas, respectively. However, Prevotella, Methanosarcina, Ustilago and Retroviridae were dominated in Daurian pikas. Functional pathways related to carbohydrate metabolism that refer to utilization of pectin, hemicellulose and debranching enzymes were abundant in Plateau pikas, while the function for degradation of chitin, lignin and cellulose was more concentrated in Daurian pikas. Pika gut had abundant multidrug resistance genes, followed by glycopeptide and beta-lactamase resistance genes, as well as high-risk ARGs, such as mepA, tetM and bacA. Escherichia coli and Klebsiella pneumoniae may be potential hosts of mepA. This research provided new insights for adaptation and evolution of wild animals from perspective of gut microbiome, and broadened our understanding of high-risk ARGs and potential pathogens of wild animals.

Chronic constipation: focus on microbiome-targeted therapies with prebiotics, probiotics, and synbiotics

Chronic constipation is a global medical, social, and economic problem due to its negative impact on patients’ quality of life and increased risk of colorectal cancer, cardiovascular and cerebrovascular disorders. The gut microbiota plays an important role in the pathophysiology of constipation through its interplay with the immune system, enteral and central nervous system, representing a promising therapeutic target. Gut dysbiosis in patients with constipation is characterized by reduced relative numbers of bacteria producing lactate (Lactobacillaceae, Bifidobacteriaceae) and butyrate (Lachnospiraceae, Oscillospiraceae), as well as with increased numbers of those producing hydrogen sulfide (Desulfovibrionaceae) and methanogenic archaea (Methanobacteriaceae). The leading pathogenetic mechanism related to intestinal dysbiosis in chronic constipation, can be microbial metabolic abnormalities (metabolic dysbiosis) characterized by altered production of short-chain fatty acid, methane, hydrogen sulfide, tryptophan metabolites and by abnormal bile acid biotransformation. It has been proven that dysbiotic abnormalities of the intestinal microbiome play a role in the pathophysiology of constipation, which allows for the use of prebiotics, probiotics, and synbiotics for effective microbiome-modulating therapy in patients with chronic constipation. The proven role of dysbiotic abnormalities of the intestinal microbiome in the pathophysiology of chronic constipation determines the effectiveness of microbiome-modulating therapy (prebiotics, probiotics, synbiotics) in patients with this syndrome. Inulin is the most studied preboitic; it is a soluble food fiber that markedly contributes to the regulation of intestinal microbiota, stimulates the growth of beneficial bacteria, and production of anti-inflammatory metabolites. Inulin normalized the intestinal function in patients with chronic constipation increasing the stool frequency, softening the stool, and reducing the intestinal transit time. In addition, inulin modulates the immune response and impacts the absorption of minerals, appetite, and satiety. Treatment with probiotics is also associated with reduced intestinal transit time, compared to controls. According to a systematic review and meta-analysis of 30 randomized controlled trials, only Bifidobacterium lactis strains (but not other probiotics) significantly increase stool frequencies in chronic constipation in adults. Clinical studies have shown that the targeted probiotic Bifidobacterium lactis HN019 can significantly increase the stool frequencies in patients with low (≤ 3 per week) stool frequency up to 4.7–5.0 per week, reduce the intestinal transit time and the rate of functional gastroenterological symptoms in adults with constipation. Beyond its clinical effects, Bifidobacterium lactis HN019 leads to beneficial changes in intestinal microbiota, significantly increasing the bifidobacteria and decreasing the enterobacteria numbers. The results of trials confirm the importance of synbiotic correction of dysbiotic microbiota in all patients with constipation to increase stool frequencies and improve fecal consistency, as well as to prevent the chronic disorders associated with constipation. Synbiotics, such as a combination of Bifidobacterium lactis HN019 and inulin, with the properties of both complementary and synergic synbiotic, may have the greatest microbiome-modulating and functional potential to significantly improve clinical outcomes in patients with chronic constipation compared to probiotics or prebiotics used alone.

Dietary supplementation with Rehmannia glutinosa catalpol improves broiler performance by regulating intestinal immune microenvironment

Plant extracts have been widely considered as a feed additive. Rehmannia glutinosa catalpol can promote the growth performance of the host, improve the immune response, and strengthen the intestinal barrier function of the host. The broilers were fed with Rehmannia glutinosa catalpol (0.01%), and the composition of caecum microbiota in broilers was explored by 16S rRNA gene sequencing. Finally, the changes of intestinal mucosa morphology and immune function were analysed by tissue staining and RT-qPCR. The proportion of thick-walled bacteria in the treatment group was higher than that in the control group. At the genus level, the relative abundance of Faecalibacterium, Paraacteroides and Barnesiella increased after the addition of Rehmannia glutinosa catalpol. The function prediction results of PICRUSt2 showed that the microbiota mainly participated in the biosynthesis and degradation/utilization/association pathway. The results of tissue staining and RT-qPCR showed that the caecum tissue morphology and immune barrier function of broilers were significantly improved after the addition of catalpol. The results of this study show that Rehmannia glutinosa catalpol in the diet may be beneficial to the intestinal health of broilers, which may be achieved by regulating the intestinal microbiota and enhancing the immune function of broilers.

The vital role of melatonin in the intestinal mucosal barrier integrity in chick

BackgroundThe intestinal tract, as the main place for nutrient digestion and absorption, is closely related to the health of livestock and poultry. Melatonin secreted by the pineal gland acts as an endocrine transport signaling molecule to regulate intestinal function. However, the effect on intestinal function after pineal removal is unclear. MethodsWe raised 24 chicks under 400-700 nm white light with or without pinealectomy for 21 days. We used electron microscopy, HE staining, PAS staining, immunohistochemistry, immunofluorescence staining and western blot to detect intestinal physical and to explore the effect of melatonin secreted by the pineal gland on the intestinal mucosa barrier function. ResultsThe results showed that after pineal gland removal, the structure of the intestinal villi is severely damaged. Moreover, there was an obviously down-regulation in the villi length, the number of goblet cells and and its secretion of MUC2 protein, the expression level of tight junction proteins (Occludin and ZO-1) and lysozyme secreted by paneth cells, number of PCNA positive cells and macrophage, and an up-regualtion in crypt depth and apoptosis level after pinealectomy, suggesting pinealectomy-mediated melatonin level decrease damaged the intestinal physical, chemical and immune barriers. ConclusionOur findings provide new theoretical support for the future use of melatonin in intestinal development and new ideas about the relationship between endocrine hormone and intestinal physiology.

Conservative Management of Bowel Endometriosis: Cross-Sectional Analysis for Assessing Clinical Outcomes and Quality-of-Life.

Background/Objectives: Bowel endometriosis (BE) is characterized by the presence of endometrial-like tissue within the muscular layer of the bowel wall. When BE does not result in the severe obstruction to fecal transit and in the absence of (sub)occlusive symptoms, the decision to perform surgery can be challenging, as intestinal procedures are associated with higher complication rates and long-term bowel dysfunction. This cross-sectional study aims to evaluate the quality of life (QoL) in patients with BE who avoided surgery, as well as to investigate the impact of the characteristics of BE nodules on the QoL and intestinal function. Methods: A retrospective cross-sectional analysis was conducted involving 580 patients with BE who did not undergo surgery but were treated conservatively with medical therapy or expectant management between January 2017 and August 2022. The diagnosis of BE was established through transvaginal ultrasound and confirmed via double contrast barium enema. After at least one year of follow-up, the QoL and intestinal function were assessed using the Endometriosis Health Profile-5 (EHP-5) questionnaire and the Bowel Endometriosis Symptom (BENS) score, while pain symptoms were quantified with the Visual Analog Scale (VAS 0-10). Statistical analyses were performed to explore potential associations between the QoL and the characteristics of BE nodules (size, location, and evidence of stenosis), as well as the type and duration of medical therapy. Results: Patients with BE reported a satisfactory overall QoL, with a mean EHP-5 score of 105.42 ± 99.98 points and a VAS score below three across all pain domains. They did not demonstrate significant impairment in bowel function, as indicated by a mean BENS score of 4.89 ± 5.28 points. Notably, patients receiving medical therapy exhibited a better QoL compared to those not receiving treatment (p < 0.05), with the exception of postmenopausal patients, who reported the highest QoL overall (p < 0.05). Among the characteristics of BE, nodule location significantly impacted the QoL and symptom intensity, with low (rectal or rectosigmoid) nodules less tolerated compared to sigmoid nodules, particularly regarding non-menstrual pelvic pain (NMPP), dyschezia, and psychological impact on daily life (p < 0.05). Conclusions: Women can effectively manage BE conservatively in the absence of (sub)occlusive symptoms, even when large nodules are present, causing significant radiological stenosis. The characteristics of BE nodules do not significantly affect the QoL or symptom intensity; however, the location of BE nodules is a crucial factor negatively influencing these outcomes. Medical therapy may confer a beneficial impact on patients of reproductive age with BE, but its use should be carefully considered for those approaching menopause, weighing the risks and benefits.

Bacterial cellulose is a desirable biological macromolecule that can prevent obesity via modulating lipid metabolism and gut microbiota

Obesity has attracted great concern because of its undesirable effects on our life quality. Bacterial cellulose (BC) is a biological macromolecule that can improve gut homeostasis and lipid metabolism. However, its potential role in preventing obesity and associated mechanisms is still poorly understood. Herein, a supplement of BC was used to fully evaluate how it prevents obesity based on physio-biochemical and gut microbial analyses. Results showed that BC consumption helped decrease body and liver weight, and fat accumulation in kidney and epididymis. Correspondingly, glucose concentrations, total triglycerides, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol were reversed to the control levels. Consuming BC also improved liver fat metabolism and intestinal function, and alleviated ileum and epididymis inflammation. High-throughput sequencing suggested that a high-fat diet significantly decreased gut microbiota diversity, which could be reversed by consuming BC. A decreased Firmicutes and Proteobacteria and an increased Bacteroidetes following BC consumption were observed. The OTU-based analysis identified that Lachnospiraceae, Desulfovibrio, Lachnoclostridium, Blautia, Anaerotruncus, Bacteroides, Faecalibaculum, Bacteroidales S24–7 group, Prevotellaceae UCG-001 group, and Alloprevotella might be involved in obesity development or prevention. Our data suggest that BC is a good insoluble dietary fiber to prevent obesity via regulating lipid metabolism and gut microbiota.

Magnolol preserves the integrity of the intestinal epithelial barrier and mitigates intestinal injury through activation of PPAR γ in COPD rat

Ethnopharmacological relevanceMagnolia officinalis Rehder & E.H. Wilson is traditionally used in the treatment of gastrointestinal disorders, diarrhea, and cough. Its main active ingredient, magnolol, exhibits protective effects on the lungs and gastrointestinal tract, including the inhibition of inflammation in these organs. Aim of the studyThis work aims to explore the molecular mechanism by which magnolol suppressed Chronic obstructive pulmonary disease (COPD) intestinal damage by improving the intestinal epithelial barrier. Materials and methodsThe study focused on investigating the mitigation effect of magnolol on intestinal injury and epithelial barrier in a COPD rat. Caco-2 cells were induced with TNF-α or IL-1β to establish the barrier injury model in order to explore the direct protective effect of magnolol on the intestinal barrier and elucidate the molecular mechanism by which it activates peroxisome proliferators-activated receptors-γ (PPARγ). ResultsMagnolol significantly improves pulmonary function and tissue damage in COPD rats by inhibiting inflammation, protease imbalance, and oxidative stress. It also suppresses colon tissue damage and inflammation, and protects colon epithelial barrier function by suppressing the decline of tight junction proteins, reducing colon epithelial permeability. In Caco-2 cells, magnolol directly reduces monolayer permeability, increases TEER, and upregulates tight junction protein expression induced by TNF-α or IL-1β. Drug Affinity Responsive Target Stability (DARTS) and thermal shift assays show that magnolol effectively binds to SRC, activating PPARγ signaling in Caco-2 cells and colon tissues of COPD rats. Furthermore, magnolol enhances the binding of PPARγ and RXRα, promoting their activation and entry into the nucleus. The PPARγ inhibitor GW9662 can reverse the effects of magnolol on PPARγ activation and tight junction protein upregulation in IL-1β or TNF-α induced Caco-2 cells. ConclusionsThis work demonstrates that magnolol enhances lung and intestinal functions in COPD rats, and elucidates its mechanism of action in protecting the intestinal epithelial barrier by activating PPARγ.

1α,25-hydroxyvitamin D3 alleviated rotavirus infection induced ferroptosis in IPEC-J2 cells by regulating the ATF3-SLC7A11-GPX4 axis

Rotavirus (RV) mainly infects mature intestinal epithelial cells and impairs intestinal absorption function, which leads to the death of infected cells and eventually fatal diarrhea. Ferroptosis is a novel regulatory cell death pattern, which can be caused by virus infection. 1α,25-hydroxyvitamin D3 (1,25D3) has an anti-RV infection effect and can regulate ferroptosis. However, whether RV infection can induce ferroptosis, and whether 1,25D3 can inhibit RV infection by regulating ferroptosis has not yet been studied. Present study shows that RV infection or erastin treatment induces IPEC-J2 cell death, which results in mitochondrial shrinkage, decreased mitochondrial membrane potential (MMP) and glutathione (GSH) content, increased MMP, intracellular Fe2+, reactive oxygen species (ROS), and malondialdehyde (MDA) contents. Meanwhile, ferrostatin-1 (Fer-1), liproxstatin-1 (Lip-1), and deferoxamine (DFO) treatment can effectively reverse the increase of intracellular Fe2+, ROS and MDA levels induced by RV infection. Moreover, RV infection increases activating transcription factor 3 (ATF3) mRNA and protein expressions, and inhibited SLC7A11 and glutathione peroxidase 4 (GPX4) expressions, which was partially alleviated by siATF3. 1,25D3 treatment significantly eliminates RV induced ferroptosis via ATF3-SLC7A11-GPX4 axis. Therefore, our results reveals that RV infection induces ferroptosis in IPEC-J2 cell and 1,25D3 alleviates RV induced ferroptosis by regulating the ATF3-SLC7A11-GPX4 axis.

Dietary nucleic acids promote oral tolerance through innate sensing pathways in mice

Oral tolerance is essential for intestinal homeostasis and systemic immune function. However, our understanding of how oral tolerance is maintained is inadequate. Here we report that food-derived nucleic acids promote oral tolerance through innate sensing pathways. We find that dietary nucleic acids, but not microbiota, expand the natural intraepithelial lymphocyte (IEL) pool, specifically in the small intestine. TGF-β1, produced by natural IELs, then promotes activation of gut CD103+ dendritic cells to support the induction of antigen-specific Treg cells in a mouse model of OVA-induced oral tolerance. Mechanistically, MAVS and STING are redundantly required for sensing dietary RNAs and DNAs to activate downstream TBK1 signalling to induce IL-15 production, which results in the accumulation of natural IELs. Thus, our study demonstrates a key role of food-triggered innate sensing pathways in the maintenance of natural IELs and oral tolerance.