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Results for “Intestinal Barrier Function”

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PubMed2002

The effect of intestinal ischemia and reperfusion injury on ICAM-1 expression, endothelial barrier function, neutrophil tissue influx, and protease inhibitor levels in rats.

Multiple organ dysfunction syndrome (MODS) is mediated by complex mechanisms in which interactions between activated leukocytes and endothelial cells play a central role. ICAM-1 (intercellular adhesion molecule-1) mediates firm adhesion and transendothelial migration of activated leukocytes from postcapillary venules into the tissue. The present study evaluated the ICAM-1 expression in various organs after 40 min of intestinal ischemia and 1, 3, 6, 12 h of reperfusion (I/R) in the rat, using a dual monoclonal antibody technique (n = 36). Endothelial barrier permeability, using the vascular leakage of radiolabeled human serum albumin was also assessed (n = 12). Neutrophil sequestration in the lungs was quantitated by myeloperoxidase activity and plasma protease inhibitor levels were measured with electroimmunoassay. Significant regional differences were found in ICAM-1 expression between organs, both constitutively and after I/R-injury. The highest constitutive levels were observed in the liver and lungs, followed by the kidneys. The constitutive ICAM-1 expression in the intestines and in the heart was about 1/20 compared with that found in the liver and lungs. The brain and muscle had levels of about 1/150 of that in the liver and lungs. After intestinal I/R, significant increases (17-45%) were found in the lungs, intestines, brain, heart, and muscle. Albumin leakage index (ALI) in all examined organs and myeloperoxidase activity in the lungs increased after I/R-injury. Serum levels of albumin and most protease inhibitors decreased significantly after I/R challenge. Intestinal I/R results in an increase of systemic ICAM-1 expression with marked organ variability. The upregulation of ICAM-1 could represent a crucial step in the adherence- and migration process of activated leukocytes and potentially in the development of tissue injury.

Albumins↗

PubMed1977

Acute distal intestinal obstruction in gnotobiotic rats. Intestinal morphology and cell renewal.

1. Complete mechanical obstruction of the distal small intestine was produced in gnotobiotic rats. 72 h after the operation small intestinal morphology and epithelial cell renewal were investigated proximal and distal to the site of obstruction. 2. Proximal to the site of obstruction there were minor changes in villus height, base length and in villus cell number, a large increase in depth and diameter of the crypts and an approximately threefold increase in cell renewal. 3. Distal to the site of obstruction there were no differences between the intestines of rats with obstruction and controls. 4. The apparent lack of secretion by the goblet cells and the reduced number of intraepithelial leucocytes suggest that the barrier function of the small intestine is impaired in obstruction.

Animals↗

PubMed1995

Failure of intestinal amino acid absorptive mechanisms in sepsis.

BACKGROUND: Sepsis has been shown to impair the barrier function and metabolism of the intestine. This study was done to investigate the effect of sepsis on intestinal absorption of proline, leucine, glutamic acid, and aminoisobutyric acid. STUDY DESIGN: Rats (six per group) were studied 24 hours after cecal ligation and puncture (CLP) or six hours after intraperitoneal injection of lipopolysaccharide (LPS). Controls underwent sham laparotomy or saline solution injection. Four 7-cm everted proximal jejunal sacs were prepared from each rat and filled with 800 microL Krebs' bicarbonate buffer containing 100 mumol/L of amino acid. Paired sacs (septic and control) were incubated at 37 degrees C in flasks containing the same solution trace labeled with 3H containing the same solution trace labeled with 3H amino acid. Sac contents were aspirated 60 minutes later and amino acid uptake was determined by scintillation counting. RESULTS: Twenty-four hours after CLP and six hours after LPS administration there was significant impairment in the intestinal absorption of all amino acids studied. Absorption of glutamic acid was the least affected, followed by leucine, aminoisobutyric acid, and proline. CONCLUSIONS: Sepsis impairs the intestinal absorption of amino acids. The magnitude of this defect in absorption differed with the amino acid studied, suggesting that not all transport systems were affected equally. This differential response of transport systems to sepsis appears to be the inverse of what is observed after a period of starvation.

Amino Acids↗

PubMed1997

The role of intravenous administration of dextran 70 in enteric bacterial translocation after partial hepatectomy in rats.

The aim of this study was to assess the effect of intravenous dextran on bacterial translocation and intestinal vascular endothelial and epithelial barrier function after experimental partial hepatectomy. We determined systemic arterial pressure, enteric bacterial growth (proximal and distal small intestine and colon) and bacterial translocation (BT) to mesenteric lymph nodes (MLN), liver, lungs, spleen, kidneys and blood, as well as intestinal vascular endothelial and epithelial barrier permeability, after sham operation or partial hepatectomy (50% and 90%) with preoperative intravenous administration of saline, albumin or dextran 70. Subtotal hepatectomy induced a significant decrease in arterial pressure and an increase in the number of Escherichia coli in the distal small intestine. BT was not observed in sham-operated animals or in rats with 50% hepatectomy administered dextran. The number of positive cultures of enteric bacteria was significantly increased after hepatectomy, whereas dextran treatment decreased the number of animals with BT. Increased permeability of the intestinal vascular endothelial and epithelial barriers was noted in hepatectomized animals, while dextran prevented hepatectomy-induced vascular endothelial barrier injury. Enteric bacterial translocation occurred following partial hepatectomy in the rat, associated with bacterial overgrowth in the distal small intestine. Intravenous administration of dextran 70 prevented bacterial overgrowth and translocation, at least in part, by maintaining gut vascular endothelial barrier integrity

Animals↗

PubMed2004

Germ warfare: probiotics in defense of the premature gut.

The potential benefits of a predominantly lactic acid bacterial flora include an improved balance of gut microbial ecology and decreased susceptibility of the gut mucosa to bacterial translocation via adherence to the intestinal mucosa, strengthening mucosal barrier function. These properties should be especially beneficial to the premature neonate with (1) delayed establishment of nor-mal flora, increasing the potential for proliferation of pathogenic bacteria and (2) immature development of the intestinal mucosa, rendering it more susceptible to the translocation of these pathogenic bacteria and leading to extra-intestinal spread and systemic disease. Early probiotic supplementation in preterm infants is theoretically sound and associated with minimal risk. Clinical data remain preliminary but are supportive of a reduction in feeding intolerance and NEC in this high-risk group.

Animals↗

PubMed1999

[Effects of basic fibroblast growth factor on repairing injury of intestinal mucosa in acute necrotic pancreatitis].

OBJECTIVE: To observe the effects of basic fibroblast growth factor (bFGF) on repairing injury of intestinal mucosa in acute necrotic pancreatitis (ANP). METHODS: Sixteen dogs of ANP animal model were made by injection of 5% sodium taurocholate (0.5 ml/kg) with 3,000 U/kg trypsin into the pancreatic duct. The mucosa structure, content of protein, DNA and malondiethylaldehyde (MDA) were observed after ANP and treatment with bFGF, and the plasma lipopolysaccharide and endothelin-1 were detected. The organs of dogs were made to bacterial culture. Ileal mucosa was collected for histological and ultrastructural studies. RESULTS: The results showed that after treatment with bFGF, the injury of intestinal mucosa in ANP was abated. The length, height and area of mucosa microvillus, the content of DNA and protein of ileal mucosa were significantly increased, while the plasma endothelin-1 and lipopolysaccharide were reduced. The organ bacterial translocation rate was also decreased in 50%. CONCLUSION: bFGF has good effects on abating injury of intestinal mucosa, protecting gut barrier function, reducing the incidence of lipopolysaccharide and bacterial translocation after ANP.

Animals↗

PubMed1998

Epithelial tight junction structure in the jejunum of children with acute and treated celiac sprue.

Tight junction morphology was analyzed in freeze fracture electron micrographs from biopsies at two locations along the surface-crypt axis in the jejunum of children with treated and untreated sprue and in control subjects. In control jejunum, strand number, meshwork depth, and total depth of the tight junction decreased from surface to crypt, consistent with the concept of the crypt being more permeable than the surface epithelium. In acute sprue, strand number was reduced in all regions along the surface-crypt axis, from 5.5+/-0.2 to 3.4+/-0.3 (surface) and from 4.7+/-0.2 to 3.6+/-0.1 (crypt). Meshwork depth was also reduced at all regions along the surface-crypt axis. Strand discontinuities were more frequent in acute sprue. Aberrant strands appeared below the main meshwork of crypt tight junctions in acute sprue. In asymptomatic children treated with the gluten-free diet, jejunal tight junctional structure only partially recovered. Strand number was restored to normal at the surface, but was still decreased in the crypts, from 4.7+/-0.2 to 3.9+/-0.3. We conclude that the epithelial barrier function of the small intestine is seriously disturbed by structural modifications of the tight junction in acute symptomatic celiac disease, thereby accounting for increased ionic permeability noted in a parallel study on identical specimens. This epithelial barrier defect may contribute to diarrhea in celiac disease by a "leak flux mechanism." In children with sprue treated with a gluten-free diet, barrier dysfunction was only partly recovered, suggesting a level of "minimal damage."

Celiac Disease↗

PubMed1996

Infection of T84 cells with enteropathogenic Escherichia coli alters barrier and transport functions.

The effect of enteropathogenic Escherichia coli (EPEC) infection on electrophysiology of T84 cell monolayers was examined. After 18 h of infection with EPEC (E2348), transepithelial electrical resistance was decreased (30 +/- 5% of uninfected values) compared with monolayers infected with a nonpathogenic E. coli strain (104 +/- 13%). Resistance of monolayers infected with EPEC mutant strain CVD206, deficient in attaching and effacing lesion formation, was partially reduced (66 +/- 10%). In addition, permeability of EPEC-infected T84 monolayers increased compared with uninfected cells. Associated with these changes was an altered distribution of the tight junction protein, ZO-1. Taken together, these findings suggest that the barrier defect induced by EPEC was at the level of the tight junction. Adenosine 3'5'-cyclic monophosphate-stimulated chloride secretion was also diminished in EPEC-infected cells, whereas Ca2+ -dependent chloride secretion was not different from uninfected cells. These findings indicate that EPEC infection alters intestinal epithelial barrier and transport functions. Furthermore, these results provide a possible mechanism for EPEC-induced diarrheal disease.

Actins↗

PubMed2005

Roles of ZO-1, occludin, and actin in oxidant-induced barrier disruption.

Oxidants such as monochloramine (NH(2)Cl) decrease epithelial barrier function by disrupting perijunctional actin and possibly affecting the distribution of tight junctional proteins. These effects can, in theory, disturb cell polarization and affect critical membrane proteins by compromising molecular fence function of the tight junctions. To examine these possibilities, we investigated the actions of NH(2)Cl on the distribution, function, and integrity of barrier-associated membrane, cytoskeletal, and adaptor proteins in human colonic Caco-2 epithelial monolayers. NH(2)Cl causes a time-dependent decrease in both detergent-insoluble and -soluble zonula occludens (ZO)-1 abundance, more rapidly in the former. Decreases in occludin levels in the detergent-insoluble fraction were observed soon after the fall of ZO-1 levels. The actin depolymerizer cytochalasin D resulted in a decreased transepithelial resistance (TER) more quickly than NH(2)Cl but caused a more modest and slower reduction in ZO-1 levels and in occludin redistribution. No changes in the cellular distribution of claudin-1, claudin-5, or ZO-2 were observed after NH(2)Cl. However, in subsequent studies, the immunofluorescent cellular staining pattern of all these proteins was altered by NH(2)Cl. The actin-stabilizing agent phalloidin did not prevent NH(2)Cl-induced decreases in TER or increases of apical to basolateral flux of the paracellular permeability marker mannitol. However, it partially blocked changes in ZO-1 and occludin distribution. Tight junctional fence function was also compromised by NH(2)Cl, observed as a redistribution of the alpha-subunit of basolateral Na(+)-K(+)-ATPase to the apical membrane, an effect not found with the apical membrane protein Na(+)/H(+) exchanger isoform 3. In conclusion, oxidants not only disrupt perijunctional actin but also cause redistribution of tight junctional proteins, resulting in compromised intestinal epithelial barrier and fence function. These effects are likely to contribute to the development of malabsorption and dysfunction associated with mucosal inflammation of the digestive tract.

Actins↗

PubMed2026

Probiotic-derived extracellular vesicles as food-based nanocarriers: Mechanisms, functional applications, and future perspectives in food systems.

Probiotic-derived extracellular vesicles (PDEVs) are a promising type of postbiotic nanoparticle derived by fermentation of probiotics, and have gained growing interest as a potential application in food science and nutrition. These are lipid bilayer vesicles of nanoscale, which are naturally released by probiotic cells and contain a wide variety of bioactive molecules, such as proteins, nucleic acids, and metabolites. Moreover, PDEVs are highly stable, biocompatible, and can be easily engineered to have surfaces with high functionality, which makes them good candidates in functional engineering. In contrast to traditional live probiotics, PDEVs overcome the difficulties of preserving microbial viability during processing and storage, thus providing superior safety, stability, and predictable biological performance. This is a systematic review of the various functions of PDEVs in food systems. We conclude on the processes through which PDEVs control intestinal barrier integrity, alter gut microbiota composition, and alter host immune responses, and their potential to enhance gut health when added to functional foods. In addition to their health-promoting effects, PDEVs have shown significant potential as natural antimicrobial agents to preserve food and as effective nanocarriers of hydrophobic bioactive compounds, including fucoxanthin, to improve their stability, bioavailability, and targeted delivery. Moreover, PDEVs can be used as new regulators of microbial fermentation. However, it should be noted that a lot of the evidence that is available is still preliminary and the effectiveness of these applications in real food-processing and storage conditions has not been fully proven. Although they have potential, there are a number of challenges that still hinder the widespread use of PDEVs in the food industry. These involve the creation of scalable and cost-effective production processes, batch-to-batch consistency, vesicle stability in a variety of food matrices, and regulatory and safety considerations. Other emerging engineering approaches, such as surface functionalization and cargo loading, are also discussed in this review and could further increase the specificity, functionality, and application versatility of PDEVs in food systems. Moving forward, the incorporation of PDEVs into the next generation functional foods, novel food preservation methods, and customized nutrition plans should be prioritized in future studies. Further developments in these fields can make PDEVs useful platforms at the interface of food microbiology, nanotechnology, and human health.

Probiotics↗

PubMed2026

Enterococcus faecalis GP1764 induces an early differential gene expression in the intestine on key pathways related to cellular immune response and gut barrier function in chickens.

The aim of the present study was to elucidate the mode of action of Enterococcus faecalis GP1764 in improving performance traits during the starter phase by analyzing genome-wide gene expression and its interaction with microbial populations in the intestine of chickens challenged with an NSP-rich diet. At day 7, microbiota populations from ileal and cecal contents and transcriptomics from jejunal and cecal mucosa were analyzed between Control (Ctrl) and Enterococcus faecalis GP1764 (EntF) groups. Results from microbiota analysis demonstrated that EntF shifted β-diversity indices in ileum (neutral (p= 0.006) and phylogenetic (p= 0.006)) and caecum (phylogenetic (p= 0.017)). Transcriptomics revealed 43 differentially expressed genes for EntF vs. Ctrl in the jejunal mucosa. Of these, MHCY-36 (MHC-I-Related), RAG2 and MUC19-like genes were upregulated in EntF vs. Ctrl, protein-coding genes with immunomodulatory capacities as supported by GSEA and Cytoscape-ClueGo pathway analyses. Results suggest an intestinal immunomodulation induced through presentation of B vitamins metabolites, synthetized by EntF, to an undescribed subset of innate-like unconventional T lymphocytes in chickens, similar to MAIT cells in mammals. These cells could contribute to antibacterial responses and repair of damaged barrier tissue after inflammatory processes. The upregulation of the MUC19-like gene expression observed in the jejunal mucosa can protect gut integrity via the promotion of mucus production by goblet cells. Finally, RAG2, involved in V(D)J coding segments recombination in B- and T-cells may provide a greater recognition of foreign invaders, allowing the animals to efficiently fight against pathogenic infections. Collectively, these results suggest an important role of EntF in promoting the capacity of animals to rapidly act against pathogenic challenges, herein, inducing resilience towards dietary ingredients with anti-nutritional activity that impart moderate inflammation in chickens.

Enterococcus faecalis↗

PubMed2006

Arachidonic acid cascade and epithelial barrier function during Caco-2 cell differentiation.

The small intestinal epithelium is a highly dynamic system continuously renewed by a process involving cell proliferation and differentiation. The intestinal epithelium constitutes a permeability barrier regulating the vectorial transport of ions, water, and solutes. Morphological changes during cell differentiation, as well as changes in the activity of brush-border enzymes and the expression of transport proteins, are well established. However, little is known about the arachidonic acid (AA) cascade underlying epithelial cell differentiation or its role in the development of epithelial barrier function. The main purpose of this study was to examine the activity of the high-molecular-weight phospholipases A(2) (PLA(2)) and cyclooxygenase (COX) pathway during differentiation, with particular emphasis on paracellular permeability. PLA(2) activity, AA release, COX-2 expression, prostaglandin E(2) (PGE(2)) production, and paracellular permeability were studied in preconfluent, confluent, and differentiated Caco-2 cell cultures. Our results show that Caco-2 differentiation induces a decrease in both calcium-independent PLA(2) activity and COX-2 expression and, consequently, a decrease in AA release and PGE(2) synthesis in parallel with a reduction in paracellular permeability. Moreover, the addition of PGE(2) to differentiated cells, at concentrations similar to those detected in nondifferentiated cultures, induces the disruption of epithelial barrier function. These results suggest that AA release by calcium-independent PLA(2), COX-2 expression, and subsequent PGE(2) release are important for the maintenance of paracellular permeability in differentiated Caco-2 cells.

Arachidonic Acid↗

PubMed1988

A single dose of endotoxin increases intestinal permeability in healthy humans.

To investigate the effects of endotoxin on gut barrier function, we performed paired studies of intestinal permeability in healthy humans (N = 12) receiving intravenous Escherichia coli endotoxin (4 ng/kg) or 0.9% saline solution. Two nonmetabolizable sugars, lactulose and mannitol, which are standard permeability markers, were administered orally, 30 minutes before and 120 minutes after the test injection. The 12-hour urinary excretion of these substances after endotoxin/saline solution administration was used to quantitate intestinal permeability. After endotoxin administration systemic absorption and excretion of lactulose increased almost two-fold (mean +/- SEM, 263 +/- 36 mumol per 12 hours vs 145 +/- 19 mumol per 12 hours during saline studies). Similar but less marked alterations in mannitol absorption and excretion occurred after endotoxin injection (5.7 +/- 0.3 mmol per 12 hours vs 4.9 +/- 0.3 mmol per 12 hours). When individual 12-hour lactulose excretion after endotoxin administration was related to the magnitude of systemic responses, a significant relationship occurred between lactulose excretion and elaboration of norepinephrine and between lactulose excretion and minimum white blood cell count. These data suggest that a brief exposure to circulating endotoxin increases the permeability of the normal gut. These observations are consistent with the hypothesis that during critical illness, prolonged or repeated exposure to systemic endotoxins or associated cytokines may significantly compromise the integrity of the gastrointestinal mucosal barrier.

Administration, Oral↗

PubMedDate not supplied

[Bacterial translocation: the effect of supplements with dietary fiber in enteral diets in an experimental model of methotrexate-induced enterocolitis].

Bacterial translocation, described by 1979 by Berg and Garlington as the movement of viable bacteria through anatomically intact intestinal mucosa to the mesenteric ganglia, is suspected of playing an important role in the development of sepsis with no apparent focus, fundamentally in polytraumatized and sever surgical patients: even now, with the wide range of antibiotic and chemotherapy agents available for treatment, this sepsis represents a high rate of hospital morbid-mortality. To assess the function as barrier of the intestinal mucosa and the influence of dietary fiber thereon, we studied bacterial translocation measured as positive cultures of the mesenteric lymphatic ganglia in an experiment model of enterocolitis induced by the intraperitoneal injection of 20 mg/kg of Methotrexate (MTX), using 72 male S-D rats, half of which were used as control group. These animals were sub-divided into four series according to the diet they were to receive. In addition to bacterial translocation, we examined the intestinal mucous parameters (mucosa weight, protein and DNA content, and number of mitoses) to quantify the potential trophic effect of dietary fiber on the intestinal mucosa. In the group subject to enterocolitis, there were no significant differences in the bacterial translocation with the series fed with defined-formula diets supplemented or otherwise with dietary fiber. Only the series receiving standard feed showed a significant reduction of bacterial translocation. pectin improved all mucous parameters when compared with the other diets studied. In the control group, the bacterial translocation rate was zero in all dietary series.

Analysis of Variance↗

PubMed1999

Human colonic subepithelial myofibroblasts modulate transepithelial resistance and secretory response.

The epithelium of the gastrointestinal tract transports ions and water but excludes luminal microorganisms and toxic molecules. The factors regulating these important functions are not fully understood. Intestinal myofibroblasts lie subjacent to the basement membrane, at the basal surface of epithelial cells. We recently showed that primary cultures of adult human colonic subepithelial myofibroblasts express cyclooxygenase (COX)-1 and COX-2 enzymes and release bioactive transforming growth factor-beta (TGF-beta). In this study we have investigated the role of normal human colonic subepithelial myofibroblasts in the regulation of transepithelial resistance and secretory response in HCA-7 and T84 colonic epithelial cell lines. Cocultures of epithelial cells-myofibroblasts and medium conditioned by myofibroblasts enhanced transepithelial resistance and delayed mannitol flux. A panspecific antibody to TGF-beta (but not piroxicam) antagonized this effect. In HCA-7 cells, myofibroblasts downregulated secretagogue-induced change in short-circuit current, and this effect was reversed by pretreatment of myofibroblasts with piroxicam. In contrast to HCA-7 cells, myofibroblasts upregulated the agonist-induced secretory response in T84 cells. This study shows that intestinal subepithelial myofibroblasts enhance barrier function and modulate electrogenic chloride secretion in epithelial cells. The enhancement of barrier function was mediated by TGF-beta. In contrast, the modulation of agonist-induced change in short-circuit current was mediated by cyclooxygenase products. These findings suggest that colonic myofibroblasts regulate important functions of epithelial cells via distinct secretory products.

Biological Transport↗

PubMed2004

Heparin-binding epidermal growth factor-like growth factor and intestinal ischemia-reperfusion injury.

Intestinal ischemia/reperfusion (I/R) injury affects patients of different ages, especially premature babies and the elderly. The outcome after intestinal I/R is often dismal, which may be attributed to loss of the barrier and immune functions of the intestines, as well as development of secondary injury in remote organs. The available treatment for advanced gut ischemia mandates extensive resection, which may cause growth retardation in infants and nutritional problems in the elderly. Throughout the past decade we have been investigating the potential therapeutic role of heparin-binding epidermal growth factor-like factor (HB-EGF) in intestinal I/R. The mitogenic and chemoattractant functions of HB-EGF formed the initial rationale for our investigations. In addition, HB-EGF is a potent antiapoptotic protein that enables cells and tissues exposed to different apoptotic stimuli to survive hypoxic, oxidative, and nutritional stresses. HB-EGF is known to have a vital role in wound healing and postischemic regeneration in different organs. In the current review, we summarize the results of our findings of the beneficial effects of HB-EGF in intestinal I/R, supported by additional evidence from the literature and an explanation of different possible mechanisms of its actions. Collectively, the data strongly suggest a potential therapeutic role for the use of HB-EGF to treat intestinal ischemic diseases such as I/R and necrotizing enterocolitis.

Animals↗

PubMedDate not supplied

Glutamine-supplemented parenteral nutrition improves gut mucosa integrity and function in endotoxemic rats.

The effects of glutamine-supplemented parenteral nutrition on protein metabolism, small intestinal mucosal metabolism, morphology, and barrier function were studied in endotoxin-treated rats. Forty-six male Wistar rats were randomized to two groups of 23 animals each and received total parenteral nutrition solutions supplemented with either glutamine (GLN group) or glycine (GLY group) at 2% wt/vol. Endotoxemia was induced by continuous intravenous infusion of endotoxin at a dose of 2 mg/kg per day throughout the 4-day study period. The GLN group had a less-negative cumulative nitrogen balance (-14.0 +/- 132.8 mg of nitrogen in the GLN group and -86.8 +/- 161.7 mg of nitrogen in the GLY group, p < .05) and less cumulative excretion of urinary 3-methylhistidine (2910 +/- 593 nmol) than the GLY group (4447 +/- 933 nmol, p < .01). Jejunal mucosal glutaminase activity and the arterio-portal venous blood glutamine concentration differences were significantly higher in the GLN group compared with the GLY group (15.6 +/- 2.3 vs 11.1 +/- 1.9 mumol/g per minute, p < .05, and 181 +/- 52 vs 147 +/- 36 nmol/mL, p < .05, respectively). The morphology of the jejunal mucosa in the GLN group was significant for having greater mucosal weight (23.4 +/- 3.1 vs 17.6 +/- 2.5 mg/cm), villus height (445 +/- 75 vs 357 +/- 57 microns), crypt depth (197 +/- 34 vs 161 +/- 28 microns), and wall thickness (751 +/- 77 vs 648 +/- 102 microns) than the GLY group (p < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2026

Graded Mulberry Leaf Supplementation Shapes Gut Microbiota, Reprograms Intestinal Metabolism, and Maintains Intestinal Chemical-Immune Barrier Homeostasis in Amur Sturgeon: A Multi-Omics Study.

Mulberry leaf contains abundant phytochemicals with antioxidant and immunomodulatory activities. However, systematic insight into its dose-dependent regulatory effects on the intestinal health of Amur sturgeon remains limited. In the present study, multi-omics approaches, including 16S rRNA gene sequencing, untargeted metabolomics, transcriptomics, together with RT-qPCR, were applied to investigate graded dietary mulberry leaf supplementation in Acipenser schrenckii. Juvenile sturgeons were fed four experimental diets containing 0%, 2%, 4% and 6% mulberry leaf over a 10-week feeding trial. Dietary mulberry leaf caused no adverse impacts on growth performance or intestinal digestive capacity. Although the overall structure of the intestinal microbiota remained stable, beneficial bacterial taxa were enriched in a dose-dependent manner. Intestinal metabolism underwent hierarchical remodelling: low inclusion levels supported basal nutrient metabolism, medium inclusion strengthened antioxidant capacity, and high inclusion reprogrammed lipid metabolism and immune function. Mulberry leaf reinforced the intestinal chemical barrier by balancing redox homeostasis and reducing mucosal epithelial permeability. Moreover, intestinal immunity was modulated through three sequential phases: initial innate immune priming, B-cell homing, and the establishment of sustained immune tolerance. In conclusion, mulberry leaf maintains intestinal chemical-immune barrier homeostasis in a dosage-tunable manner, supporting its potential application as a functional aquafeed ingredient.

Amur sturgeon (Acipenser schrenckii)↗