scholarly journals Fructans in the diet cause alterations of intestinal mucosal architecture, released mucins and mucosa-associated bifidobacteria in gnotobiotic rats

2003 ◽  
Vol 89 (5) ◽  
pp. 597-606 ◽  
Author(s):  
Brigitta Kleessen ◽  
Ludger Hartmann ◽  
Michael Blaut
Keyword(s):  
Bacterial Colonization ◽  
Bifidobacterium Longum ◽  
Distal Colon ◽  
Goblet Cells ◽  
Mucosal Barrier ◽  
Standard Diet ◽  
Mucus Layer ◽  
Faecal Flora ◽  
Health Maintenance ◽  
Distal Jejunum

The effects of fructans in the diet on the mucosal morphometry (height of villi, depth of the crypts, number of goblet cells), the thickness of the epithelial mucus layer and the histochemical composition of intestinal mucosubstances in the distal jejunum and the distal colon were investigated by comparing germ-free (GF) rats, rats harbouringBacteroides vulgatusandBifidobacterium longum(diassociated (DA) rats), and rats with a human faecal flora (HFA). The rats were fed either a commercial standard diet (ST) or ST + (50 g oligofructose (OF)–long-chain inulin (lcIN))/kg. Changes in total bacteria, bifidobacteria andBacteroides–Prevotellain response to feeding these diets were investigated by fluorescentin situhybridization with 16S rRNA-targeted probes both in intestinal contents (lumen bacteria) and tissue sections (mucosa-associated bacteria). The OF–lcIN-containing diet resulted in higher villi and deeper crypts in bacteria-associated, but not in GF rats. In DA and HFA rats, the colonic epithelial mucus layer was thicker and the numbers of the goblet cells were greater than in GF rats. These effects were enhanced by the OF–lcIN-containing diet. In both dietary groups, bacterial colonization of GF rats caused an increase in neutral mucins in the distal jejunum and colon. Bacteria-associated rats had more acidic mucins in the colon than GF rats, and the OF–lcIN-containing diet stimulated sulfomucins as the predominant type of acidic mucins, while sialomucins dominated in the ST-fed groups. The number of mucosa-associated bifidobacteria detected in the colon of DA and HFA rats was greater with OF–lcIN than ST (4·9 and 5·4v. 3·5 and 4·0 log10/mm2mucosal surface respectively), whereas the number of luminal bifidobacteria was only affected by fructans in DA rats.Bacteroidesdid not differ between the groups. The stabilisation of the gut mucosal barrier, either by changes in the mucosal architecture itself, in released mucins or by stimulation of mucosal bifidobacteria with fructans, could become an important topic in the treatment and prophylaxis of gastrointestinal disorders and health maintenance.

scholarly journals Modulation of gut mucosal biofilms

2005 ◽  
Vol 93 (S1) ◽  
pp. S35-S40 ◽  
Author(s):  
Brigitta Kleessen ◽  
Michael Blaut
Keyword(s):  
Colonic Mucosa ◽  
Mucosal Barrier ◽  
Mucus Layer ◽  
Faecal Flora ◽  
New Approach ◽  
Serovar Typhimurium ◽  
Health Promoting ◽  
Gut Mucosal Barrier ◽  
Induced Changes ◽  
Stimulation Of

Non-digestible inulin-type fructans, such as oligofructose and high-molecular-weight inulin, have been shown to have the ability to alter the intestinal microbiota composition in such a way that members of the microbial community, generally considered as health-promoting, are stimulated. Bifidobacteria and lactobacilli are the most frequently targeted organisms. Less information exists on effects of inulin-type fructans on the composition, metabolism and healthrelated significance of bacteria at or near the mucosa surface or in the mucus layer forming mucosa-associated biofilms. Using rats inoculated with a human faecal flora as an experimental model we have found that inulin-type fructans in the diet modulated the gut microbiota by stimulation of mucosa-associated bifidobacteria as well as by partial reduction of pathogenicSalmonella enterica subsp. entericaserovar Typhimurium and thereby benefit health. In addition to changes in mucosal biofilms, inulin-type fructans also induced changes in the colonic mucosa stimulating proliferation in the crypts, increasing the release of mucins, and altering the profile of mucin components in the goblet cells and epithelial mucus layer. These results indicate that inulin-type fructans may stabilise the gut mucosal barrier. Dietary supplementation with these prebiotics could offer a new approach to supporting the barrier function of the mucosa.

scholarly journals Toxin-Mediated Effects on the Innate Mucosal Defenses: Implications for Enteric Vaccines

2009 ◽  
Vol 77 (12) ◽  
pp. 5206-5215 ◽  
Author(s):  
Gregory M. Glenn ◽  
David H. Francis ◽  
E. Michael Danielsen
Keyword(s):  
Protective Immunity ◽  
Bacterial Colonization ◽  
Fluid Secretion ◽  
Mucosal Barrier ◽  
Protective Effects ◽  
Mucus Layer ◽  
E Coli ◽  
Mediated Effects ◽  
Enteric Infections ◽  
The Common

ABSTRACT Recent studies have confirmed older observations that the enterotoxins enhance enteric bacterial colonization and pathogenicity. How and why this happens remains unknown at this time. It appears that toxins such as the heat-labile enterotoxin (LT) from Escherichia coli can help overcome the innate mucosal barrier as a key step in enteric pathogen survival. We review key observations relevant to the roles of LT and cholera toxin in protective immunity and the effects of these toxins on innate mucosal defenses. We suggest either that toxin-mediated fluid secretion mechanically disrupts the mucus layer or that toxins interfere with innate mucosal defenses by other means. Such a breach gives pathogens access to the enterocyte, leading to binding and pathogenicity by enterotoxigenic E. coli (ETEC) and other organisms. Given the common exposure to LT+ ETEC by humans visiting or residing in regions of endemicity, barrier disruption should frequently render the gut vulnerable to ETEC and other enteric infections. Conversely, toxin immunity would be expected to block this process by protecting the innate mucosal barrier. Years ago, Peltola et al. (Lancet 338:1285-1289, 1991) observed unexpectedly broad protective effects against LT+ ETEC and mixed infections when using a toxin-based enteric vaccine. If toxins truly exert barrier-disruptive effects as a key step in pathogenesis, then a return to classic toxin-based vaccine strategies for enteric disease is warranted and can be expected to have unexpectedly broad protective effects.

scholarly journals Differences in Intestinal Barrier Development between Intrauterine Growth Restricted and Normal Birth Weight Piglets

Animals ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 990 ◽  
Author(s):  
Jarosław Olszewski ◽  
Romuald Zabielski ◽  
Tomasz Skrzypek ◽  
Piotr Matyba ◽  
Małgorzata Wierzbicka ◽  
...  
Keyword(s):  
Intestinal Barrier ◽  
Goblet Cells ◽  
Normal Birth Weight ◽  
Intestinal Function ◽  
Gut Barrier ◽  
Intrauterine Growth ◽  
Normal Birth ◽  
Gut Mucosa ◽  
Average Size ◽  
Distal Jejunum

Intrauterine growth restricted (IUGR) piglets are born at term but have low birth mass and a characteristic shape of the head. Impaired general condition, especially in intestinal function, leads to an increase in the occurrence of diarrhoea and high mortality in the first days of life. So far, the mechanical and immunological gut barrier functions in IUGR are poorly understood. The aim of this study was to microscopically evaluate the early postnatal changes in the gut mucosa occurring in IUGR piglets. Whole-tissue small intestine samples were collected from littermate pairs (IUGR and normal) on postnatal day (PD) 7, 14 and 180 and analysed by light microscopy. We found that in the IUGR piglets, the percentage of intraepithelial leukocytes was reduced in the duodenum on PD 7, but it increased in the proximal and middle jejunum both on PD 7 and PD 14, which suggested the development of an inflammatory process. The number of goblet cells was also reduced on PD 14. The average size of the Peyer’s patches in the distal jejunum and ileum showed significant reduction on PD 7 as compared to normal pigs; however, on PD 14, it returned to normal. On PD 180, we did not find any differences in the measured parameters between the IUGR and the normal pigs. In conclusion, we found that in one-week-old IUGR pig neonates, the gut barrier and the immune system structures display signs of retarded development but recover within the second postnatal week of life.

Absorption of Protein and Protein Fragments in the Developing Intestine: Role in Immunologic/Allergic Reactions

PEDIATRICS ◽  
1985 ◽  
Vol 75 (1) ◽  
pp. 167-171
Author(s):  
W. Allan Walker
Keyword(s):  
Human Milk ◽  
Defense Mechanisms ◽  
Bacterial Colonization ◽  
Newborn Infants ◽  
Mucosal Barrier ◽  
Protein Fragments ◽  
Susceptibility To Infection ◽  
Impermeable Barrier ◽  
Other Substances ◽  
Life Threatening

An important adaptation of the gastrointestinal tract to the extrauterine environment is its development of a mucosal barrier against the penetration of proteins and protein fragments. To combat the potential danger of invasion across the mucosal barrier the newborn infant must develop within the lumen and on the luminal mucosal surface an elaborate system of defense mechanisms which act to control and maintain the epithelium as an impermeable barrier to the uptake of macromolecular antigens. As a result of a delay in the maturation of the mucosal barrier, newborn infants are particularly vulnerable to pathologic penetration by harmful intraluminal substances. The consequences of altered defense are susceptibility to infection and the potential for hypersensitivity reactions and the formation of immune complexes. With these reactions comes the potential for developing life-threatening diseases such as necrotizing enterocolitis, sepsis, and hepatitis. Fortunately, "nature" has provided a means for passively protectecting the "vulnerable" newborn against the dangers of a deficient intestinal defense system, namely human milk. It is now increasingly apparent that human milk contains not only antibodies and viable leukocytes but many other substances that can interfere with bacterial colonization and prevent antigen penetration.

POTENTIAL OF ETHANOL EXTRACT OF MAHKOTA DEWA LEAVES (PHALERIA MACROCARPA (SCHECFF.) BOERL.) TO INHIBIT INFLAMMATION IN MOUSE DISTAL COLON INDUCED BY DEXTRAN SODIUM SULFATE (DSS) AND AZOXYMETHANE (AOM)

2020 ◽  
pp. 101-105
Author(s):  
MUHAMMAD ILHAM DHIYA RAKASIWI ◽  
KUSMARDI KUSMARDI ◽  
ARI ESTUNINGTYAS ◽  
ARYO TEDJO
Keyword(s):  
Leaf Extract ◽  
Histopathological Examination ◽  
Ethanol Extract ◽  
Distal Colon ◽  
Goblet Cells ◽  
Sodium Sulphate ◽  
Dextran Sodium Sulphate ◽  
Phaleria Macrocarpa ◽  
Hematoxylin Eosin

Objective: To demonstrates the ability of P. macrocarpa leaf extract to reduce inflammation of the distal colon in DSS/AOM-induced mice. Methods: In vivo experimental research using Balb/c mice induced by 0.2 ml azoxymethane (AOM) 0.1% once and 1% dextran sodium sulphate (DSS) for one week; additionally, ethanol extract of P. macrocarpa leaves, 25 mg and 50 mg, and 0.84 mg acetosal were given orally. The mice were sacrificed after 20 w. Histopathological examination (hematoxylin-eosin staining) was conducted by counting the average number of goblet cells per crypt, inflammatory focus and angiogenesis. Results: Ethanol extract of P. macrocarpa leaves was able to prevent the decrease in the number of goblet cells (p<0.05). However, the administration of ethanol P. macrocarpa leaf extract could not reduce focal inflammation and angiogenesis in inflammation of the distal colon. Conclusion: Ethanol extract of the Mahkota Dewa leaves is able to prevent inflammation of the distal colon by preventing the decrease in the number of goblet cells.

scholarly journals Draft Genome Sequence of Bifidobacterium longum BB-79, a Strain That Produces Acid Exopolysaccharide

2018 ◽  
Vol 7 (19) ◽  
Author(s):  
Linyan Cao ◽  
Junlin Yu ◽  
Huahai Chen ◽  
Yeshi Yin
Keyword(s):  
Genome Sequence ◽  
Immune Modulation ◽  
Bacterial Colonization ◽  
Bifidobacterium Longum ◽  
Draft Genome ◽  
Draft Genome Sequence ◽  
Content Type

The surface exopolysaccharide of Bifidobacterium spp. was found to be involved in many processes, including bacterial colonization and host immune modulation.

scholarly journals Obesity-associated microbiota contributes to mucus layer defects in genetically obese mice

2020 ◽  
Vol 295 (46) ◽  
pp. 15712-15726
Author(s):  
Bjoern O. Schroeder ◽  
George M. H. Birchenough ◽  
Meenakshi Pradhan ◽  
Elisabeth E. L. Nyström ◽  
Marcus Henricsson ◽  
...  
Keyword(s):  
Growth Rate ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Intermediate Phenotype ◽  
Mucosal Barrier ◽  
Mucus Layer ◽  
Dietary Interventions ◽  
High Blood Glucose ◽  
Glucose Levels ◽  
Intestinal Mucus

The intestinal mucus layer is a physical barrier separating the tremendous number of gut bacteria from the host epithelium. Defects in the mucus layer have been linked to metabolic diseases, but previous studies predominantly investigated mucus function during high-caloric/low-fiber dietary interventions, thus making it difficult to separate effects mediated directly through diet quality from potential obesity-dependent effects. As such, we decided to examine mucus function in mouse models with metabolic disease to distinguish these factors. Here we show that, in contrast to their lean littermates, genetically obese (ob/ob) mice have a defective inner colonic mucus layer that is characterized by increased penetrability and a reduced mucus growth rate. Exploiting the coprophagic behavior of mice, we next co-housed ob/ob and lean mice to investigate if the gut microbiota contributed to these phenotypes. Co-housing rescued the defect of the mucus growth rate, whereas mucus penetrability displayed an intermediate phenotype in both mouse groups. Of note, non-obese diabetic mice with high blood glucose levels displayed a healthy colonic mucus barrier, indicating that the mucus defect is obesity- rather than glucose-mediated. Thus, our data suggest that the gut microbiota community of obesity-prone mice may regulate obesity-associated defects in the colonic mucosal barrier, even in the presence of dietary fiber.

scholarly journals A52 BUTYRATE SUPPLEMENTATION AMELIORATES DAMAGE CAUSED BY ENTERIC CITROBACTER RODENTIUM INFECTION

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 61-62
Author(s):  
L S Celiberto ◽  
G Healey ◽  
J Xu ◽  
L Xia ◽  
B Vallance
Keyword(s):  
Butyric Acid ◽  
Tissue Damage ◽  
Intestinal Inflammation ◽  
Bacterial Colonization ◽  
Clinical Signs ◽  
Host Susceptibility ◽  
Mucus Layer ◽  
Citrobacter Rodentium ◽  
Oral Gavage ◽  
Intestinal Mucus

Abstract Background Patients with inflammatory bowel disease (IBD) often display a dysbiotic microbiome as well as a defective intestinal mucus layer, which appears thinner and more penetrable than the mucus layer of healthy subjects. Tributyrin (TB), a prodrug of butyric acid, has shown beneficial effects in models of IBD due to its anti-inflammatory effects. We previously showed that mice lacking the major intestinal mucin Muc2 (Muc2-/-) or lacking the “Core1” enzyme responsible for glycosylating Muc2 (C1galt1-/-) were highly susceptible to infection by Citrobacter rodentium, a murine model of intestinal inflammation. Aims The study explored the role of gut mucus in providing host defense against C. rodentium, as well as the effects of TB supplementation in the prevention of mucosal damage in this model. Methods Six to ten week old wildtype (WT), Muc2-/-, flox control (C1galt1f/f) and C1galt1-/- mice were infected with C. rodentium (∼2.5 × 108 CFU) by oral gavage. For TB supplementation experiments, mice received 100µL of TB or glycerol as a control by oral gavage every other day starting on day 1 post infection. Mice were monitored daily throughout the experiment and were euthanized at day 6 of infection. Several tissues of interest were collected to verify bacterial colonization in the gut and at systemic sites as well as histological tissue damage. Cecal contents were collected for the analysis of short chain fatty acids, while blood was collected by cardiac puncture after oral gavage with FITC-dextran to measure intestinal permeability. Results While WT and C1galt1f/f mice were only modestly susceptible to C. rodentium infection, Muc2-/- and C1galt1-/- mice displayed dramatically (100 fold) increased pathogen burdens, significantly greater intestinal macroscopic and histopathology scores, and heightened barrier disruption as compared to controls. Moreover, Muc2-/- and C1galt1-/- mice showed significantly lower levels of butyric acid as compared to control mice under baseline conditions. Interestingly, when supplemented with TB, Muc2-/- and C1galt1-/- proved less susceptible to C. rodentium infection, as indicated by reduced weight loss and clinical signs of colitis, while pathogen burdens were greatly reduced as was histological tissue damage, and epithelial barrier dysfunction. The same protection was conferred when TB was administered as a dietary supplementation, thus confirming its beneficial effect in protecting mice against C. rodentium infection. Conclusions These findings demonstrate that intestinal mucus controls host susceptibility to C. rodentium infection via control over butyrate levels, and highlight the need to explore the mechanisms by which gut mucus modulates the resident microbiota and its metabolites. Funding Agencies CCC, CIHR

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