• Gastric mucosal damage
• Glutamatergic neurons
• Insular cortex
• Nucleus tractus solitarius
• RWIS

• biochemistry
• human microbiota
• immunity
• metabolome
• microbiota’s crosstalk axis molecular biology
• probiotics

• Humans
• Dysbiosis/microbiology
• Gastrointestinal Microbiome
• Bacterial Translocation
• Sepsis/microbiology
• Animals

• Bariatric surgery
• Gut-brain-axis
• Microbiota
• Neurodegeneration
• Neuroendocrine
• Neurological disorders
• Neuropsychiatric
• Neurotransmitters

• Humans
• Bariatric Surgery
• Gastrointestinal Microbiome
• Weight Loss
• Nervous System Diseases/microbiology
• Animals

• Alzheimer Society of B.C.
• Canadian Institutes of Health Research

• Galacturonic acid
• Immunomodulation
• Methyl-esterification
• Pattern recognition receptors
• Pectin

• Humans
• Oligosaccharides/pharmacology
• Oligosaccharides/chemistry
• Hexuronic Acids/chemistry
• Hexuronic Acids/pharmacology
• Toll-Like Receptor 4/metabolism
• Esterification
• HEK293 Cells
• Toll-Like Receptor 2/metabolism
• Polymerization
• THP-1 Cells
• Immunomodulation/drug effects
• Cytokines/metabolism
• Pectins/chemistry
• Pectins/pharmacology
• Macrophages/drug effects
• Macrophages/metabolism
• Macrophages/immunology

• Coronary artery disease
• Cytokines
• Endotoxemia
• Intestinal hyperpermeability
• STEMI
• Tight junctions

• Humans
• Male
• Female
• Middle Aged
• ST Elevation Myocardial Infarction/blood
• ST Elevation Myocardial Infarction/surgery
• ST Elevation Myocardial Infarction/physiopathology
• Endotoxemia/blood
• Endotoxemia/therapy
• Percutaneous Coronary Intervention
• Inflammation/blood
• Aged
• Cytokines/blood
• Prospective Studies
• Endotoxins/blood
• Zonula Occludens-1 Protein/metabolism

• Bacillus tequilensis
• TLR4/NF-κB pathway
• colitis
• intestinal barriers

• Caco-2 cells
• epithelial barrier function
• gastrointestinal diseases
• hydrolysable tannins (HTs)
• oxidative stress
• zinc oxide (ZnO)

• Zinc Oxide/pharmacology
• Zinc Oxide/chemistry
• Caco-2 Cells
• Enterocytes/drug effects
• Enterocytes/metabolism
• Humans
• Hydrolyzable Tannins/pharmacology
• Hydrolyzable Tannins/chemistry
• Oxidative Stress/drug effects
• Tight Junction Proteins/metabolism

• Bacterial translocation
• Endotoxemia
• Intestinal barrier
• Intestinal permeability
• Liver transplantation
• Postoperative infections

• Humans
• Liver Transplantation/adverse effects
• Postoperative Complications/physiopathology
• Gastrointestinal Microbiome
• Bacterial Translocation

• University of Patras

• chronic kidney disease
• endotoxin
• intestinal barrier
• occludin
• tight junctions

• Alzheimer’s disease
• BBB
• Cellular junction
• Macromolecule

• Humans
• Alzheimer Disease/metabolism
• Blood-Brain Barrier/metabolism
• Brain/metabolism
• Signal Transduction/physiology
• Tight Junctions/metabolism
• Tight Junctions/pathology

• heart failure
• intestinal hyperpermeability
• systemic endotoxemia
• systemic inflammation
• tight junction dysfunction

• Histopathology
• Immunity
• Intestinal barrier
• Microbiota
• Pb

• Animals
• Coturnix
• Dysbiosis
• Ileum
• Immune System Diseases
• Lead/toxicity

• Angiotensin-converting enzyme 2
• COVID-19
• Gastrointestinal barrier dysfunction
• Immune cells
• Microbiome
• SARS-CoV-2

• Humans
• COVID-19
• SARS-CoV-2
• Gastrointestinal Diseases/diagnosis
• Diarrhea

The intestinal lumen harbors a diverse consortium of microorganisms that participate in reciprocal crosstalk with intestinal immune cells and with epithelial and endothelial cells, forming a multi-layered barrier that enables the efficient absorption of nutrients without an excessive influx of pathogens. Despite being a lung-centered disease, severe coronavirus disease 2019 (COVID-19) affects multiple systems, including the gastrointestinal tract and the pertinent gut barrier function. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can inflict either direct cytopathic injury to intestinal epithelial and endothelial cells or indirect immune-mediated damage. Alternatively, SARS-CoV-2 undermines the structural integrity of the barrier by modifying the expression of tight junction proteins. In addition, SARS-CoV-2 induces profound alterations to the intestinal microflora at phylogenetic and metabolomic levels (dysbiosis) that are accompanied by disruption of local immune responses. The ensuing dysregulation of the gut-lung axis impairs the ability of the respiratory immune system to elicit robust and timely responses to restrict viral infection. The intestinal vasculature is vulnerable to SARS-CoV-2-induced endothelial injury, which simultaneously triggers the activation of the innate immune and coagulation systems, a condition referred to as “immunothrombosis” that drives severe thrombotic complications. Finally, increased intestinal permeability allows an aberrant dissemination of bacteria, fungi, and endotoxin into the systemic circulation and contributes, to a certain degree, to the over-exuberant immune responses and hyper-inflammation that dictate the severe form of COVID-19. In this review, we aim to elucidate SARS-CoV-2-mediated effects on gut barrier homeostasis and their implications on the progression of the disease.

• COVID-19
• SARS-CoV-2
• Intestinal barrier
• Dysbiosis
• Immunothrombosis
• Gut-lung axis

• dietary butyrate
• early weaning
• inflammation and appetite
• intestinal epithelial barrier
• microbe–gut–brain axis
• microbiome–metabolome

• IBD
• advanced glycation end-products
• enteric neurons
• gastrointestinal tract
• intestinal permeability
• microbiome

• Glycation End Products, Advanced/adverse effects
• Glycation End Products, Advanced/metabolism
• Maillard Reaction
• Diet
• Heart

• Mentha piperita leaf
• allergic rhinitis
• essential oils
• inflammation
• network pharmacology
• tight junction

The Wuji pill, also called Wuji Wan (WJW), is an effective traditional medicine for the clinical treatment of irritable bowel syndrome (IBS). It is principally composed of Rhizoma Coptidis, Fructus Evodiae Rutaecarpae, and Radix Paeoniae Alba. There have been no reports on the pharmacokinetics of WJW on IBS. Because it is more meaningful to study pharmacokinetics in relation to specific pathological conditions, our study investigated the pharmacokinetic differences of five representative components (berberine, palmatine, evodiamine, rutaecarpine, and paeoniflorin) in normal rats and chronic visceral hypersensitivity IBS (CVH-IBS) model rats after single dose and multiple doses of WJW using ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS). Transmission electron microscopy, immunohistochemistry, and immunofluorescence were used to explore mechanisms behind the pharmacokinetic differences in terms of tight junction proteins (Occludin and ZO-1), myosin light chain kinase (MLCK), and transporters including P-glycoprotein (P-gp), multidrug resistance associated protein 1 (MRP1), and multidrug resistance associated protein 2 (MRP2) in rat colons. After a single dose, for all components except rutaecarpine, significant differences were observed between normal and model groups. Compared with normal group, T_1/2 and AUC_0-t of berberine and palmatine in model group increased significantly (562.5 ± 237.2 vs. 1,384.9 ± 712.4 min, 733.8 ± 67.4 vs. 1,532.4 ± 612.7 min; 5,443.0 ± 1,405.8 vs. 9,930.8 ± 2,304.5 min·ng/ml, 2,365.5 ± 410.6 vs. 3,527.0 ± 717.8 min·ng/ml), while Cl/F decreased (840.7 ± 250.8 vs. 397.3 ± 142.7 L/h/kg, 427.7 ± 89.4 vs. 288.9 ± 114.4 L/h/kg). C_max and AUC_0-t of evodiamine in model group increased significantly (1.4 ± 0.6 vs. 2.4 ± 0.7 ng/ml; 573 ± 45.3 vs. 733.9 ± 160.2 min·ng/ml), while T_1/2, T_max, Cl/F, and Vd/F had no significant difference. T_max and AUC_0-t of paeoniflorin in model group increased significantly (21.0 ± 8.2 vs. 80.0 ± 45.8 min; 15,428.9 ± 5,063.6 vs. 33,140.6 ± 5,613.9 min·ng/ml), while Cl/F decreased (110.5 ± 48.1 vs. 43.3 ± 9.5 L/h/kg). However, after multiple doses, all five components showed significant differences between normal and model groups. Moreover, these differences were related to tight junction damage and the differential expression of transporters in the colon, suggesting that dose adjustment might be required during administration of WJW in the clinical treatment of IBS.

• National Natural Science Foundation of China

A considerable proportion of patients with severe COVID-19 meet Sepsis-3 criteria and share common pathophysiological mechanisms of multiorgan injury with bacterial sepsis, in absence of secondary bacterial infections, a process characterized as “viral sepsis”. The intestinal barrier exerts a central role in the pathophysiological sequence of events that lead from SARS-CoV-2 infection to severe systemic complications. Accumulating evidence suggests that SARS-CoV-2 disrupts the integrity of the biological, mechanical and immunological gut barrier. Specifically, microbiota diversity and beneficial bacteria population are reduced, concurrently with overgrowth of pathogenic bacteria (dysbiosis). Enterocytes’ tight junctions (TJs) are disrupted, and the apoptotic death of intestinal epithelial cells is increased leading to increased gut permeability. In addition, mucosal CD4(+) and CD8(+) T cells, Th17 cells, neutrophils, dendritic cells and macrophages are activated, and T-regulatory cells are decreased, thus promoting an overactivated immune response, which further injures the intestinal epithelium. This dysfunctional gut barrier in SARS-CoV-2 infection permits the escape of luminal bacteria, fungi and endotoxin to normally sterile extraintestinal sites and the systemic circulation. Pre-existing gut barrier dysfunction and endotoxemia in patients with comorbidities including cardiovascular disease, obesity, diabetes and immunosuppression predisposes to aggravated endotoxemia. Bacterial and endotoxin translocation promote the systemic inflammation and immune activation, which characterize the SARS-CoV-2 induced “viral sepsis” syndrome associated with multisystemic complications of severe COVID-19.

In recent years, antimicrobial (AM) use in poultry farming has been attracting attention worldwide mainly due to AM resistance spreading. The role of AM prophylaxis in the modulation of gut microbiota, as well as of gut health, is still not clearly understood. Therefore, this study aimed to investigate the role of different prophylaxis protocols in the modulation of the gut barrier in broilers by applying a histopathological approach. Intestinal tissue samples were collected from a total of 240 male broilers (Ross 306), reared and treated with different AM protocols. Haematoxylin and Eosin (HE) staining and a multiple scoring system were used to evaluate the presence of lesions in ileum, cecum and colon of treated broilers. Moreover, immunohistochemistry (IHC) was performed to assess the expression of claudin-3 and ZO-1 proteins in intestinal tissues. The application of a semi-quantitative scoring system was used in IHC stained samples. HE results revealed that intestinal tissues were mainly characterized by epithelial detachment and fusion of the intestinal villi, but also by the presence of lymphocytic infiltrate in the mucosa and submucosa of AM-treated broilers. However, the IHC approach for the evaluation of claudin-3 and ZO-1 proteins showed that their expression was not affected by the different AM treatments. Nevertheless, the presence of intestinal lesions highlighted by histopathology suggests that AM treatments could harm the gut health of broilers, inducing an inflammatory response and consequent epithelial lesions. In order to clarify the role of AM treatments in the modulation of gut barrier in broilers, further studies are needed.

• Ministero dell'Istruzione, dell'Università e della Ricerca

• COVID-19
• ZO1
• bacterial translocation
• endotoxin
• gut barrier
• pneumonia

This paper explores the effects of wine polyphenols on intestinal permeability in in vitro conditions. A red wine (2500 mg/L of gallic acid equivalents) was sequentially subjected to gastrointestinal and colonic digestion in the Dynamic Gastrointestinal Simulator (simgi^®) to obtain two simulated fluids: intestinal-digested wine (IDW) and colonic-digested wine (CDW). The two fluids were incubated with Caco-2 cell monolayers grown in Transwell^® inserts, and paracellular permeability was measured as transport of FITC-dextran. Non-significant decreases (p > 0.05) in paracellular permeability were found, which was attributed to the relatively low phenolic concentration in the solutions tested (15.6 and 7.8 mg of gallic acid equivalents/L for IDW and CDW, respectively) as quercetin (200 µM) and one of its microbial-derived phenolic metabolites, 3,4-dihydroxyphenylacetic acid (200 µM), led to significant decreases (p < 0.05). The expression of tight junction (TJ) proteins (i.e., ZO-1 and occludin) in Caco-2 cells after incubation with IDW and CDW was also determined. A slight increase in mRNA levels for occludin for both IDW and CDW fluids, albeit without statistical significance (p > 0.05), was observed. Analysis of the microbiome and microbial activity during wine colonic fermentation revealed relevant changes in the relative abundance of some families/genera (i.e., reduction in Bacteroides and an increase in Veillonella, Escherichia/Shigella and Akkermansia) as well as in the microbial production of SCFA (i.e., a significant increase in propionic acid in the presence of IDW), all of which might affect paracellular permeability. Both direct and indirect (microbiota-mediated) mechanisms might be involved in the protective effects of (wine) polyphenols on intestinal barrier integrity. Overall, this paper reinforces (wine) polyphenols as a promising dietary strategy to improve gut functionality, although further studies are needed to evaluate the effect on the intestinal barrier under different conditions.

• gut permeability
• microbiota
• simulated digestion
• tight junctions
• wine polyphenols

• Chicken
• Embryo
• Enterocyte
• Immunofluorescence
• Primary culture

• In vitro toxicology
• Intestinal co-cultures
• Intestine-specific functional endpoints
• Structure–activity relationships
• Synthetic amorphous silica (E551)

• Caco-2 Cells
• Coculture Techniques
• Dose-Response Relationship, Drug
• Food Additives/administration & dosage
• Food Additives/toxicity
• HT29 Cells
• Humans
• Intestinal Mucosa/drug effects
• Intestinal Mucosa/metabolism
• Silicon Dioxide/administration & dosage
• Silicon Dioxide/toxicity

• Competence Centre for Materials Science and Technology
• Evonik Industries AG
• Empa - Swiss Federal Laboratories for Materials Science and Technology

The intestinal barrier plays a crucial role in the absorption of nutrients and in preventing the entry of pathogenic microorganisms and toxic molecules. Several studies have shown a compromised intestinal barrier associated with low-grade inflammation in the small intestinal mucosa in celiac disease, inflammatory bowel disease, and irritable bowel syndrome (IBS), particularly in IBS with diarrhea (IBS-D). In light of these new data, IBS is no longer considered a functional disease but rather a heterogeneous syndrome that has yet to be carefully studied. Therefore, investigating the integrity and function of the intestinal barrier is now essential to improving knowledge of the pathophysiology of IBS-D and to improving the management of IBS-D patients. However, the study of the intestinal barrier must clarify some still unsolved methodological aspects and propose standardised assays before becoming a useful diagnostic tool. In this framework, this review will discuss data about the tests that noninvasively evaluate the integrity and functionality of the human intestinal barrier, paying particular attention to patients with IBS-D, in both clinical and research situations.

• bioactive peptides
• marine
• marine waste
• mechanism of activity
• proline
• secondary structure

• Animals
• Aquatic Organisms/chemistry
• Food
• Humans
• Peptides/chemistry
• Peptides/isolation & purification
• Peptides/pharmacology
• Protein Conformation
• Protein Stability
• Structure-Activity Relationship

• 316004 Seventh Framework Programme
• BIOWAFER POR-FESR Regione Emilia-Romagna

Grape polyphenols have previously been shown to improve gut health and attenuate the symptoms of metabolic syndrome; however, the mechanism of these beneficial effects is still debated. In this study, we investigated the protective effect of proanthocyanidin-rich grape seed extract (GSE) on bacterial lipopolysaccharide (LPS)-induced oxidative stress, inflammation, and barrier integrity of human Caco-2 colon cells. GSE significantly reduced the LPS-induced intracellular reactive oxygen species (ROS) production and mitochondrial superoxide production, and upregulated the expression of antioxidant enzyme genes. GSE also restored the LPS-damaged mitochondrial function by increasing mitochondrial membrane potential. In addition, GSE increased the expression of tight junction proteins in the LPS-treated Caco-2 cells, increased the expression of anti-inflammatory cytokines, and decreased pro-inflammatory cytokine gene expression. Our findings suggest that GSE exerts its beneficial effects on metabolic syndrome by scavenging intestinal ROS, thus reducing oxidative stress, increasing epithelial barrier integrity, and decreasing intestinal inflammation.

• antioxidant
• inflammation
• polyphenol
• proanthocyanidin
• tight junction

• Anti-Inflammatory Agents
• Antioxidants
• Caco-2 Cells
• Cytokines/genetics
• Cytokines/metabolism
• Gene Expression/drug effects
• Grape Seed Extract/pharmacology
• Grape Seed Extract/therapeutic use
• Humans
• Inflammation Mediators/metabolism
• Intestinal Mucosa/cytology
• Intestinal Mucosa/metabolism
• Membrane Potential, Mitochondrial/drug effects
• Mitochondria/metabolism
• Oxidative Stress/drug effects
• Proanthocyanidins/pharmacology
• Proanthocyanidins/therapeutic use
• Reactive Oxygen Species/metabolism
• Superoxides/metabolism
• Tight Junctions/metabolism

• T32 AT004094 NCCIH NIH HHS
• IR, 1R01AT008618-01 NIH HHS

A high-fat diet (HFD) or obesity-promoting diet is closely associated with metabolic diseases and intestinal tumors, particularly in middle-aged individuals (typically 45–64 years old). The intestinal epithelium constitutes a barrier that separates the host from the food and microbiota in the gut, and thus, a dysfunctional epithelium is associated with a number of diseases. However, the changes caused to the function of intestinal epithelium in response to an HFD have not been well-studied to date. In the present study, middle-aged female mice (12 months old) fed an HFD for a period of 14 weeks were used to determine the effects of HFD on the intestine. Characteristics including the body weight, fat deposition, glucose metabolism, inflammatory state and intestinal morphology were assessed, while the intestinal stem cell (ISC) counts and the ability of isolated intestinal crypts to form organoid bodies in 3D culture were examined. Intestinal epithelial barrier function, including secretory defense, tight junctions and cell apoptosis, were also studied. Morphologically, the HFD resulted in a mild reduction in the length of villi of the small intestine, the colon length and the depth of colon crypts. In addition, the ISC counts were increased in the small intestine and colon in HFD-fed mice. The ability of crypts to grow into organoids (mini-guts) was also increased in crypts obtained from mice fed an HFD, while HFD compromised the epithelial barrier function of the colon. These results demonstrated how an HFD affects the intestinal epithelium and highlighted the need to carefully consider dietary patterns.

• Cross talk
• Gut microbiota
• Immune system
• Inflammatory bowel diseases
• Pathogenesis
• Treatment

• Animals
• Dysbiosis/microbiology
• Dysbiosis/therapy
• Fecal Microbiota Transplantation
• Gastrointestinal Microbiome
• Humans
• Inflammatory Bowel Diseases/microbiology
• Inflammatory Bowel Diseases/therapy

• Caco-2 cells
• Free fatty acids
• High-fat diet
• Intestinal epithelial barrier
• Paracellular permeability
• Tight junction
• Type 2 diabetes mellitus

• Candida albicans
• adherence
• damage
• enterocyte
• infection models
• interaction
• intestinal barrier
• invasion

• Candida albicans/metabolism
• Host-Pathogen Interactions/immunology
• Humans
• Intestinal Mucosa/physiopathology

Lactobacillus reuteri is an inhabitant of the gastrointestinal (GI) tract of mammals and birds and several strains of this species are known to be effective probiotics. The mechanisms by which L. reuteri confers its health‐promoting effects are far from being fully understood, but protection of the mucosal barrier is thought to be important. Leaky gut is a state of abnormal intestinal permeability with implications for the pathophysiology of various gastrointestinal disorders. Enterotoxigenic Escherichia coli (ETEC) can invade the intestinal mucosa and induce changes in barrier function by producing enterotoxin or by direct invasion of the intestinal epithelium. Our hypothesis was that L. reuteri can protect the mucosal barrier, and the goal of the study was to challenge this hypothesis by monitoring the protective effect of L. reuteri strains on epithelial dysfunction caused by ETEC. Using an infection model based on the porcine intestinal cell line IPEC‐J2, it was demonstrated that pretreatment of the cells with human‐derived L. reuteri strains (ATCC PTA 6475, DSM 17938 and 1563F) and a rat strain (R2LC) reduced the detrimental effect of ETEC in a dose‐dependent manner, as monitored by permeability of FITC‐dextran and transepithelial electrical resistance (TEER). Moreover, the results revealed that ETEC upregulated proinflammatory cytokines IL‐6 and TNFα and decreased expression of the shorter isoform of ZO‐1 (187 kDa) and E‐cadherin. In contrast, pretreatment with L. reuteri DSM 17938 and 1563F downregulated expression of IL‐6 and TNFα, and led to an increase in production of the longer isoform of ZO‐1 (195 kDa) and maintained E‐cadherin expression. Interestingly, expression of ZO‐1 (187 kDa) was preserved only when the infected cells were pretreated with strain 1563F. These findings demonstrate that L. reuteri strains exert a protective effect against ETEC‐induced mucosal integrity disruption.

• Lactobacillus reuteri
• Enterotoxigenic Escherichia coli (ETEC)
• IPEC-J2
• mucosal integrity

Protein diets are well known for body maintenance and weight loss.

• Bacterial translocation
• Danger-associated molecular patterns
• Gut-lymph hypothesis
• Gut-origin sepsis
• ICU
• Intestinal barrier
• Intestinal permeability

• Animals
• Biomarkers
• Critical Illness
• Gastrointestinal Microbiome
• Humans
• Intestinal Diseases/complications
• Intestinal Diseases/microbiology
• Multiple Organ Failure/etiology
• Multiple Organ Failure/microbiology
• Sepsis/etiology
• Sepsis/microbiology
• Sepsis/physiopathology
• Sepsis/therapy

• amino acids
• food processing
• functional food
• health effect
• in vivo activity

• Human endometrium
• Intestinal permeability
• Recurrent pregnancy loss
• inflammasome

• Celiac disease
• Diagnosis
• Epidemiology
• Pathogenesis
• Treatment

Maintaining a healthy gut environment is a prerequisite for sustainable animal production. The gut plays a key role in the digestion and absorption of nutrients and constitutes an initial organ exposed to external factors influencing bird’s health. The intestinal epithelial barrier serves as the first line of defense between the host and the luminal environment. It consists of a continuous monolayer of intestinal epithelial cells connected by intercellular junctional complexes which shrink the space between adjacent cells. Consequently, free passing of solutes and water via the paracellular pathway is prevented. Tight junctions (TJs) are multi-protein complexes which are crucial for the integrity and function of the epithelial barrier as they not only link cells but also form channels allowing permeation between cells, resulting in epithelial surfaces of different tightness. Tight junction’s molecular composition, ultrastructure, and function are regulated differently with regard to physiological and pathological stimuli. Both in vivo and in vitro studies suggest that reduced tight junction integrity greatly results in a condition commonly known as “leaky gut”. A loss of barrier integrity allows the translocation of luminal antigens (microbes, toxins) via the mucosa to access the whole body which are normally excluded and subsequently destroys the gut mucosal homeostasis, coinciding with an increased susceptibility to systemic infection, chronic inflammation and malabsorption. There is considerable evidence that the intestinal barrier dysfunction is an important factor contributing to the pathogenicity of some enteric bacteria. It has been shown that some enteric pathogens can induce permeability defects in gut epithelia by altering tight junction proteins, mediated by their toxins. Resolving the strategies that microorganisms use to hijack the functions of tight junctions is important for our understanding of microbial pathogenesis, because some pathogens can utilize tight junction proteins as receptors for attachment and subsequent internalization, while others modify or destroy the tight junction proteins by different pathways and thereby provide a gateway to the underlying tissue. This review aims to deliver an overview of the tight junction structures and function, and its role in enteric bacterial pathogenesis with a special focus on chickens. A main conclusion will be that the molecular mechanisms used by enteric pathogens to disrupt epithelial barrier function in chickens needs a much better understanding, explicitly highlighted for Campylobacter jejuni, Salmonella enterica and Clostridium perfringens. This is a requirement in order to assist in discovering new strategies to avoid damages of the intestinal barrier or to minimize consequences from infections.

• chickens
• enteric pathogens
• gut health
• intestinal barrier
• leaky gut
• paracellular permeability
• tight junction