The Intestinal Mucosa as a Habitat of the Gut Microbiota and a Rational Target for Probiotic Functionality and Safety

2004 ◽  
Vol 16 (2-3) ◽  
Author(s):  
Muriel Derrien ◽  
Diya Adawi ◽  
Siv Ahrné ◽  
Bengt Jeppsson ◽  
Göran Molin ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Mucosa

scholarly journals Nutritional intervention for the intestinal development and health of weaned pigs

2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 30-31 ◽  
Author(s):  
Yanhong Liu
Keyword(s):  
Gut Microbiota ◽  
Intestinal Mucosa ◽  
Barrier Function ◽  
Nutritional Intervention ◽  
Feed Additives ◽  
Intestinal Development ◽  
Intestinal Health ◽  
Gut Barrier ◽  
Weaned Pigs ◽  
Gut Barrier Function

Abstract Weaning imposes simultaneous stress, resulting in reduced feed intake and growth rate and increased morbidity and mortality of weaned pigs. Weaning impairs the intestinal integrity, disturbs digestive and absorptive capacity, and increases the intestinal oxidative stress and susceptibility of diseases in piglets. The improvement of intestinal development and health is critically important for enhancing nutrient digestibility capacity and disease resistance of weaned pigs, therefore, increasing their survival rate at this most vulnerable stage and overall productive performance during later stages. A healthy gut may include but not limited several important features: a healthy proliferation of intestinal epithelial cells, an integrated gut barrier function, a preferable or balanced gut microbiota, and a well-developed intestinal mucosa immunity. Burgeoning evidence suggested nutritional intervention are one of promising measures to enhance intestinal health of weaned pigs, although the exact protective mechanisms may vary and are still not completely understood. Previous research indicated that functional amino acids, such as arginine, cysteine, glutamine, or glutamate, may enhance intestinal mucosa immunity (i.e. increased sIgA secretion), reduce oxidative damage, stimulate proliferation of enterocytes, and enhance gut barrier function (i.e. enhanced expression of tight junction protein) of weaned pigs. A number of feed additives are marketed to assist in boosting intestinal immunity and regulating gut microbiota, therefore, reducing the negative impacts of weaning and other environmental challenges on piglets. The promising results have been demonstrated in antimicrobial peptides, clays, direct-fed microbials, micro-minerals, milk components, oligosaccharides, organic acids, phytochemicals, and many other feed additives. This review summarizes our current understanding of nutritional intervention on intestinal health and development of weaned pigs and the importance of mechanistic studies focusing on this research area.

The intestinal mucosa as a habitat of the gut microbiota and a rational target for probiotic functionality and safety

2004 ◽  
Vol 16 (2-3) ◽  
pp. 137-144 ◽  
Author(s):  
Muriel Derrien ◽  
Diya Adawi ◽  
Siv Ahrné ◽  
Bengt Jeppsson ◽  
Göran Molin ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Intestinal Mucosa

scholarly journals Exploring the Mechanism of Indigo Naturalis in the Treatment of Ulcerative Colitis Based on TLR4/MyD88/NF-κB Signaling Pathway and Gut Microbiota

2021 ◽  
Vol 12 ◽  
Author(s):  
Qi-yue Yang ◽  
Le-le Ma ◽  
Chen Zhang ◽  
Jun-zhi Lin ◽  
Li Han ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Signal Transduction ◽  
Gut Microbiota ◽  
Intestinal Mucosa ◽  
Activity Index ◽  
Intestinal Flora ◽  
Physiological Status ◽  
Inflammatory Factor ◽  
Pathological Section ◽  
Indigo Naturalis

Background: Clinical trials have proven that indigo naturalis is a candidate drug for treating ulcerative colitis (UC), but its therapeutic mechanism is still unclear.Purpose: This study aimed to evaluate the protective effect and mechanism of indigo naturalis to treat mice with dextran sulfate sodium (DSS)-induced UC.Methods: DSS-induced UC mice were treated with indigo naturalis (200 mg/kg), indigo (4.76 mg/kg), and indirubin (0.78 mg/kg) for 1 week. The anti-UC mechanism of indigo naturalis was studied by pathological section, inflammatory factor, western blot, and 16S rRNA sequencing.Results: According to body weight change, disease activity index, and colon length, indigo naturalis had the strongest anti DSS-induced UC effect, followed by indirubin and indigo. Pathological section showed that indigo naturalis, indigo, and indirubin could reduce the infiltration of inflammatory cells, increase the secretion of intestinal mucus, and repair the intestinal mucosa. Indigo naturalis, indigo, and indirubin could reduce IL-1β,IL-6, and TNF-α by inhibiting TLR4/MyD88/NF-κB signal transduction. Indigo naturalis and indigo could also reduce IgA and IgG both in serum and colon tissue. In addition, indigo naturalis, indigo, and indirubin could adjust the gut microbiota structure of DSS-induced UC mice, reducing the ratio of Firmicutes/Bacteroidetes and increasing the abundance of probiotics.Conclusion: Indigo and indirubin are one of the main anti-UC components of indigo naturalis. INN could regulate intestinal flora, reduce inflammation, repair intestinal mucosa, and improve the physiological status of DSS-induced UC mice and its anti-UC mechanism may be involved in inhibiting TLR4/MyD88/NF-κB signal transduction.

scholarly journals Two Weeks High Glucose is Enough to Induce Liver and Gut Lesion

2021 ◽  
Author(s):  
Cunyun Min ◽  
Tingting Fu ◽  
Yu Du ◽  
Wei Tan ◽  
Xiuhui Huang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Blood Sugar ◽  
Intestinal Mucosa ◽  
High Glucose ◽  
Serum Levels ◽  
Control Group ◽  
Small Intestinal Mucosa ◽  
Sd Rats ◽  
Small Intestinal ◽  
Short Time

Abstract Background: High glucose is critical for diabetes.But in which way it induces diabetes, and which organ trigger the formation of diabetes are not clear.This study is to evaluate the effect of shot time high glucose on different organs,to make clear this question.Methods: Twelve weeks old SD rats were randomly assigned to control group,high glucose infusion (HGI) group and oral high glucose (OHG) group.Fasten blood sugar,TNF-a and IL-6 were measured.Kidneys,intestine and liver samples were collected for pathological examination.Feces of rats were collected for gut microbiota tests.Results: The results indicated that short time high glucose induced hyperglycemia lasted for at least 2 weeks after ceasing of high glucose.It increased serum levels of IL-6 and TNF-a obviously.It led to small intestinal mucosa injury, obvious steatosis of hepatocytes, and broke the balance of gut microbiota.OHG led to swelling and necrosis of individual intestinal villi.HGI led to necrosis and disappearence of cells in the upper layer of intestinal mucosa.The lesion was confined to the mucosa.There is not obvious biopsy change in kidney and pancreas.Conclusions: Short time high glucose induced lesion of liver and intestine,broken the balance of gut microbiota.All of these led to inflammation and triggered diabetes.

scholarly journals Uncovering Bifidobacteria via Targeted Sequencing of the Mammalian Gut Microbiota

2019 ◽  
Vol 7 (11) ◽  
pp. 535 ◽  
Author(s):  
Gabriele Andrea Lugli ◽  
Sabrina Duranti ◽  
Christian Milani ◽  
Leonardo Mancabelli ◽  
Francesca Turroni ◽  
...  
Keyword(s):  
Gastrointestinal Tract ◽  
Gut Microbiota ◽  
Life Span ◽  
Relative Abundance ◽  
Intestinal Mucosa ◽  
Environmental Samples ◽  
Enrichment Method ◽  
Functional Roles ◽  
Genetic Features ◽  
Uptake Of Nutrients

Bifidobacteria are among the most prevalent gut commensals in mammals, playing crucial functional roles that start from their early colonization of the infant gastrointestinal tract and last throughout the life span of their host. Metagenomic approaches have been employed to unveil the genetic features of bifidobacteria in order to understand how they participate in the correct development of a healthy microbiome. Nevertheless, their low relative abundance in many environmental samples may represent a major limitation for metagenomics approaches. To overcome this restriction, we applied an enrichment method that allows amplification of bifidobacterial DNA obtained from human or animal fecal samples for up to 26,500-fold, resulting in the metagenomic reconstruction of genomes belonging to bifidobacterial strains, present at very low abundance in collected samples. Functional predictions of the genes from these reconstructed genomes allows us to identify unique signatures among members of the same bifidobacterial species, highlighting genes correlated with the uptake of nutrients and adhesion to the intestinal mucosa.

scholarly journals Intestinal Immunomodulatory Cells (T Lymphocytes): A Bridge between Gut Microbiota and Diabetes

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Qingwei Li ◽  
Zezheng Gao ◽  
Han Wang ◽  
Haoran Wu ◽  
Yanwen Liu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Immune System ◽  
T Lymphocytes ◽  
Gut Microbiota ◽  
Intestinal Mucosa ◽  
Human Immune System ◽  
Normal Functioning ◽  
Human Immune ◽  
Underlying Mechanisms

Diabetes mellitus (DM) is one of the most familiar chronic diseases threatening human health. Recent studies have shown that the development of diabetes is closely related to an imbalance of the gut microbiota. Accordingly, there is increasing interest in how changes in the gut microbiota affect diabetes and its underlying mechanisms. Immunomodulatory cells play important roles in maintaining the normal functioning of the human immune system and in maintaining homeostasis. Intestinal immunomodulatory cells (IICs) are located in the intestinal mucosa and are regarded as an intermediary by which the gut microbiota affects physiological and pathological properties. Diabetes can be regulated by IICs, which act as a bridge linking the gut microbiota and DM. Understanding this bridge role of IICs may clarify the mechanisms by which the gut microbiota contributes to DM. Based on recent research, we summarize this process, thereby providing a basis for further studies of diabetes and other similar immune-related diseases.

scholarly journals Immune System, Microbiota, and Microbial Metabolites: The Unresolved Triad in Colorectal Cancer Microenvironment

2021 ◽  
Vol 12 ◽  
Author(s):  
Michelle Hanus ◽  
Daniela Parada-Venegas ◽  
Glauben Landskron ◽  
Ana Maria Wielandt ◽  
Claudia Hurtado ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Microenvironment ◽  
Gut Microbiota ◽  
Tumor Progression ◽  
Intestinal Mucosa ◽  
Immune Cells ◽  
Close Contact ◽  
Colorectal Carcinogenesis ◽  
Microbial Metabolites ◽  
Ample Evidence

Colorectal cancer (CRC) is one of the most common cancers worldwide. As with other cancers, CRC is a multifactorial disease due to the combined effect of genetic and environmental factors. Most cases are sporadic, but a small proportion is hereditary, estimated at around 5-10%. In both, the tumor interacts with heterogeneous cell populations, such as endothelial, stromal, and immune cells, secreting different signals (cytokines, chemokines or growth factors) to generate a favorable tumor microenvironment for cancer cell invasion and metastasis. There is ample evidence that inflammatory processes have a role in carcinogenesis and tumor progression in CCR. Different profiles of cell activation of the tumor microenvironment can promote pro or anti-tumor pathways; hence they are studied as a key target for the control of cancer progression. Additionally, the intestinal mucosa is in close contact with a microorganism community, including bacteria, bacteriophages, viruses, archaea, and fungi composing the gut microbiota. Aberrant composition of this microbiota, together with alteration in the diet‐derived microbial metabolites content (such as butyrate and polyamines) and environmental compounds has been related to CRC. Some bacteria, such as pks+ Escherichia coli or Fusobacterium nucleatum, are involved in colorectal carcinogenesis through different pathomechanisms including the induction of genetic mutations in epithelial cells and modulation of tumor microenvironment. Epithelial and immune cells from intestinal mucosa have Pattern-recognition receptors and G-protein coupled receptors (receptor of butyrate), suggesting that their activation can be regulated by intestinal microbiota and metabolites. In this review, we discuss how dynamics in the gut microbiota, their metabolites, and tumor microenvironment interplays in sporadic and hereditary CRC, modulating tumor progression.

Activation of isolated heterophils from chicks stimulated in vivo with salmonella enteritidis-immune lymphokines

1996 ◽  
Vol 54 ◽  
pp. 760-761
Author(s):  
R. B. Moyes ◽  
R. E. Droleskey ◽  
M. H. Kogut ◽  
J. R. DeLoach
Keyword(s):  
Lamina Propria ◽  
Intestinal Mucosa ◽  
Salmonella Enteritidis ◽  
Intestinal Tract ◽  
Polymorphonuclear Cells ◽  
Subclinical Infection ◽  
Egg Products ◽  
Immune Lymphokines ◽  
Organ Invasion

Salmonella enteritidis (SE) is of great concern to the poultry industry due to the organism's ability to penetrate the intestinal mucosa of the laying hen and subsequently colonize the ovaries and yolk membrane. The resultant subclinical infection can lead to SE infection of raw eggs and egg products. Interference with the ability of the organism to invade has been linked to the activation and recruitment of inflammatory polymorphonuclear cells, heterophils, to the lamina propria of the intestinal tract.Recently it has been established that heterophil activation and increased resistance to SE organ invasion can be accomplished by the administration of SE-immune lymphokines (SE-ILK) obtained from supernatants of concanavalin-A stimulated SE immune T lymphocytes from SE hyperimmunized hens. Invasion of SE into the lamina propria provides a secondary signal for directing activated heterophils to the site of SE invasion.

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