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Nutrition, Epithelial Barrier Permeability and Chronic Disease: Basic Science and Clinical Implications

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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Prebiotics and Probiotics".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 29997

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Special Issue Editor

Dr. Jennifer M. Monk

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Guest Editor

Human Health & Nutritional Sciences, University Guelph, Guelph, ON N1G 2W1, Canada
Interests: epithelial barrier integrity; microbiome; mucosal immune function; immunological tolerance; inflammation; fatty acids; obesity
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Special Issue Information

Dear Colleagues,

Permeability or leakiness of the intestinal epithelial barrier contributes to the development and/or severity of multiple chronic diseases, including but not limited to obesity, diabetes, certain types of cancer, liver dysfunction and neurological conditions (via gut–brain axis). Furthermore, gastrointestinal function including epithelial cell integrity and turnover, regulation of mucus production, anti-microbial and mucosal immune defense, microbiome function and microbe–host communication not only contribute to epithelial barrier dysfunction but are also susceptible to dietary interventions. The aim of this Special Issue on “Nutrition, Epithelial Barrier Permeability and Chronic Disease: Basic Science and Clinical Implications” is to provide a comprehensive summary of current original research and review articles that highlight the critical role of nutrition in the regulation of epithelial barrier integrity and the implications for chronic disease susceptibility or severity. Authors are invited to submit manuscripts that are related to epithelial barrier function (or dysfunction) across a spectrum of research interests from basic science/mechanistic studies to clinical interventions, which will collectively highlight the importance of epithelial barrier integrity in both nutritional science and more broadly within biological science.

Dr. Jennifer M. Monk
Guest Editor

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Keywords

epithelial barrier permeability
leaky gut
obesity
diabetes
chronic disease
mucosal immune function
mucus barrier
anti-microbial defense
microbiota
microbial metabolites

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Published Papers (6 papers)

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Research

20 pages, 2567 KiB

Open AccessArticle

Navy Bean Supplementation in Established High-Fat Diet-Induced Obesity Attenuates the Severity of the Obese Inflammatory Phenotype

by Jennifer M. Monk, Wenqing Wu, Dion Lepp, K. Peter Pauls, Lindsay E. Robinson and Krista A. Power

Nutrients 2021, 13(3), 757; https://doi.org/10.3390/nu13030757 - 26 Feb 2021

Cited by 17 | Viewed by 4169

Abstract

Cooked common beans (Phaseolus vulgaris) improve intestinal health in lean mice and attenuate intestinal dysbiosis and inflammation when consumed concurrent with obesity development. We determined the effects of a high-fat (HF) bean supplemented diet in mice with established obesity (induced by 12 weeks of HF diet (60% fat as kcal)) compared to obese mice consuming a HF or low-fat (LF) weight loss control diet. Obese C57BL/6 male mice remained consuming HF for eight weeks or were randomly switched from HF to an isocaloric HF with 15.7% cooked navy bean powder diet (HF→HFB) or LF (11% fat as kcal; HF→LF) (n = 12/group). HF→HFB improved the obese phenotype, including (i) fecal microbiome (increased Prevotella, Akkermansia muciniphila, and short-chain fatty acid levels), (ii) intestinal health (increased ZO-1, claudin-2, Muc2, Relmβ, and Reg3γ expression), and (iii) reduced adipose tissue (AT) inflammatory proteins (NFκBp65, STAT3, IL-6, MCP-1, and MIP-1α), versus HF (p < 0.05). Conversely, HF→LF reduced body weight and circulating hormones (leptin, resistin, and PAI-1) versus HF and HF→HFB (p < 0.05); however, AT inflammation and intestinal health markers were not improved to the same degree as HF→HFB (p < 0.05). Despite remaining on a HF obesogenic diet, introducing beans in established obesity improved the obese phenotype (intestinal health and adipose inflammation) more substantially than weight loss alone. Full article

(This article belongs to the Special Issue Nutrition, Epithelial Barrier Permeability and Chronic Disease: Basic Science and Clinical Implications)

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15 pages, 759 KiB

Open AccessArticle

Functional Food Components, Intestinal Permeability and Inflammatory Markers in Patients with Inflammatory Bowel Disease

by Joana Franco Lacerda, Ana Catarina Lagos, Elisabete Carolino, Ana Santos Silva-Herdade, Manuel Silva and Catarina Sousa Guerreiro

Nutrients 2021, 13(2), 642; https://doi.org/10.3390/nu13020642 - 16 Feb 2021

Cited by 15 | Viewed by 4855

Abstract

Inflammatory bowel diseases (IBD) are characterized by a chronic inflammatory process that affects the intestinal barrier structure. Recent evidence suggests that some food components can influence the integrity of the intestinal barrier and thus its permeability. We aimed at assessing the effect of food components on the intestinal permeability (IP) and on inflammatory markers in individuals with IBD by a single-blind randomized clinical study. Of the 53 individuals included, 47% (n = 25) had been diagnosed with IBD. The participants were divided into 4 groups. IBD patients were allocated to intervention group (n = 14) vs. no intervention group (n = 11), and the same happened with 28 control participants without disease (n = 14 in intervention group vs. n = 14 without intervention). Symptomatology, nutritional status, biochemical parameters (specifically serum zonulin (ZO) to measure IP) were evaluated on all individuals on an eight week period following a diet plan with/without potentially beneficial foods for the IP. At the beginning of the study, there were no significant differences in ZO values between individuals with and without IBD (p > 0.05). The effect of specific food components was inconclusive; however, a trend in the reduction of inflammatory parameters and on the prevalence of gastrointestinal symptomatology was observed. More controlled intervention studies with diet plans, including food components potentially beneficial for the integrity of the intestinal barrier, are of the utmost importance. Full article

(This article belongs to the Special Issue Nutrition, Epithelial Barrier Permeability and Chronic Disease: Basic Science and Clinical Implications)

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11 pages, 648 KiB

Open AccessArticle

Effect of Xylo-Oligosaccharides Supplementation by Drinking Water on the Bone Properties and Related Calcium Transporters in Growing Mice

by Hang Gao and Zhenlei Zhou

Nutrients 2020, 12(11), 3542; https://doi.org/10.3390/nu12113542 - 19 Nov 2020

Cited by 15 | Viewed by 2916

Abstract

Xylo-oligosaccharides (XOS), non-digestible oligosaccharides, have the potential to regulate intestinal microorganisms, and thus, improve host health, but little evidence exists for the prebiotic effects on bone health. This study evaluates the dose-response effect of XOS supplementation on bone properties, the morphology of the intestine, cecum pH, and cecum wall weight, as well as the related calcium transporters. Ninety-six 28-day-old male mice were randomized into one of four groups, fed the same commercial diet, and given different types of deionized water containing 0, 1, 2, or 4% XOS by concentration for 30 days. Eight mice were randomly selected to accomplish particular tasks every 10 days. No significant differences in serum Ca and P levels and growth performance were observed among the four studied groups. XOS intervention significantly decreased cecum pH and increased cecum wall weight in a dose-dependent manner. At the late growth stage, compared with 0% XOS, the bone mineral density (BMD) and bone-breaking strength in 4% XOS were significantly higher. The bone crystallinity with 4% XOS, measured by Raman spectrum, was significantly enhanced compared to that with 0% XOS during later growth. The villus height and villus height to crypt depth (VH:CD) were enhanced with an increase of XOS concentration during the later stage of growth. The expression of transient receptor potential vanillin receptor 6 (TRPV6) and Na⁺/Ca²⁺ exchanger 1 (NCX1) in the duodenum were enhanced by XOS supplementation. XOS exerted a positive influence on bone properties by decreasing the cecum pH, increasing the cecum wall and villus structure, and upregulating the expression of related calcium transporters. Full article

(This article belongs to the Special Issue Nutrition, Epithelial Barrier Permeability and Chronic Disease: Basic Science and Clinical Implications)

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17 pages, 3763 KiB

Open AccessArticle

Opposing Effect of Naringenin and Quercetin on the Junctional Compartment of MDCK II Cells to Modulate the Tight Junction

by Mio Nakashima, Misaki Hisada, Natsuko Goda, Takeshi Tenno, Ayaka Kotake, Yuko Inotsume, Ikuo Kameoka and Hidekazu Hiroaki

Nutrients 2020, 12(11), 3285; https://doi.org/10.3390/nu12113285 - 27 Oct 2020

Cited by 19 | Viewed by 6427

Abstract

Maintaining tight junction (TJ) integrity is important for epithelial cell barriers. Previously, the enhancement of TJ integrity, induced by citrus-derived flavonoids, naringin (NRG) and hesperidin (HSD), was demonstrated, but the effects of their aglycones naringenin (NAR) and hesperetin (HST), and the mechanisms, have not been systematically investigated. Here we compared three series of flavonoids related to NAR, HST, quercetin (QUE) and their glycosides with the Madin–Darby canine kidney (MDCK) II cell monolayers. The effect of flavonoids on the protein expression level of claudin (CLD)-2 and its subcellular localization were investigated. NAR, NRG, and HSD increased the CLD-2 localization at the TJ compartment, and its protein expression level. QUE and HST showed TJ-mitigating activity. Narirutin (NRT), neohesperidin (NHD) and rutin (RUT) did not affect the TJ. In addition, NAR and QUE induced an increase or decrease of the transepithelial electrical resistance (TEER) values of the MDCK II monolayers. Two known signaling pathways, phosphatidyl-inositol-3 kinase (PI3K) and 5′-AMP-activated protein kinase (AMPK), were further compared with NAR. Two-dimensional polyacrylamide electrophoresis (2D PAGE) analysis of whole-cell proteins treated with NAR, AICA-riboside (AMPK activator) and LY294002 (PI3K inhibitor) showed in both a distinct pattern. This suggests the target of NAR’s CLD-2 or zonula occludens-1 (ZO-1) modulation was unique. Full article

(This article belongs to the Special Issue Nutrition, Epithelial Barrier Permeability and Chronic Disease: Basic Science and Clinical Implications)

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13 pages, 1090 KiB

Open AccessArticle

Blends of Human Milk Oligosaccharides Confer Intestinal Epithelial Barrier Protection In Vitro

by Jane M. Natividad, Andreas Rytz, Sonia Keddani, Gabriela Bergonzelli and Clara L. Garcia-Rodenas

Nutrients 2020, 12(10), 3047; https://doi.org/10.3390/nu12103047 - 5 Oct 2020

Cited by 41 | Viewed by 5020

Abstract

Breastfeeding is integral in the proper maturation of the intestinal barrier and protection against inflammatory diseases. When human milk (HM) is not available, supplementation with HM bioactives like Human Milk Oligosaccharides (HMOs) may help in providing breastfeeding barrier-protective benefits. An increasing HMO variety is becoming industrially available, enabling approaching the HMO complexity in HM. We aimed at assessing the impact of blends of available HMOs on epithelial barrier function in vitro. The capacity of individual [2′-Fucosyllactose (2′FL), Difucosyllactose, Lacto-N-tetraose, Lacto-N-neotetraose, 3′-Siallylactose and 6′-Siallylactose] or varying combinations of 3, 5 and 6 HMOs to modulate fluorescein-isothiocyanate (FITC)-labelled Dextran 4 KDa (FD4) translocation and/or transepithelial resistance (TEER) was characterized in Caco-2: HT29- methotrexate (MTX) cell line monolayers before and after an inflammatory challenge with TNF-α and IFN-γ. The six HMO blend (HMO6) dose-dependently limited the cytokine-induced FD4 translocation and TEER decrease and increased TEER values before challenge. Similarly, 3 and 5 HMO blends conferred a significant protection against the challenge, with 2′FL, one of the most abundant but most variable oligosaccharides in HM, being a key contributor. Overall, our results suggest differential ability of specific HMOs in modulating the intestinal barrier and support the potential of supplementation with combinations of available HMOs to promote gut health and protect against intestinal inflammatory disorders. Full article

(This article belongs to the Special Issue Nutrition, Epithelial Barrier Permeability and Chronic Disease: Basic Science and Clinical Implications)

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15 pages, 3460 KiB

Open AccessArticle

In Vitro Effects of Live and Heat-Inactivated Bifidobacterium animalis Subsp. Lactis, BB-12 and Lactobacillus rhamnosus GG on Caco-2 Cells

by Vivian M. Castro-Herrera, Christine Rasmussen, Anja Wellejus, Elizabeth A. Miles and Philip C. Calder

Nutrients 2020, 12(6), 1719; https://doi.org/10.3390/nu12061719 - 8 Jun 2020

Cited by 23 | Viewed by 5753

Abstract

Probiotic–host interaction can be cell-to-cell or through metabolite production. Dead (inactive) organisms could interact with the host, leading to local effects and possible health benefits. This research examined the effects of live and heat-inactivated Bifidobacterium animalis subsp. lactis, BB-12 (BB-12) and Lactobacillus rhamnosus GG (LGG) on cultured Caco-2 cells focusing on epithelial integrity and production of inflammatory mediators. Live organisms increased transepithelial electrical resistance (TEER), a barrier-integrity marker, with LGG having a greater effect than BB-12. When mildly heat-treated, both organisms had a more modest effect on TEER than when alive. When they were heat-inactivated, both organisms had only a limited effect on TEER. Neither live nor heat-inactivated organisms affected production of six inflammatory mediators produced by Caco-2 cells compared to control conditions. Pre-treatment with heat-inactivated LGG or BB-12 did not alter the decline in TEER caused by exposure to an inflammatory cocktail of cytokines. However, pre-treatment of Caco-2 cells with heat-inactivated organisms alone or their combination decreased the production of interleukin (IL)-6, IL-18, and vascular endothelial growth factor. To conclude, while the live organisms improve the epithelial barrier using this model, neither live nor heat-inactivated organisms directly elicit an inflammatory response by the epithelium. Pre-treatment with heat-inactivated BB-12 or LGG can reduce some components of the response induced by an inflammatory stimulus. Full article

(This article belongs to the Special Issue Nutrition, Epithelial Barrier Permeability and Chronic Disease: Basic Science and Clinical Implications)

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