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8137 KiB

Open AccessArticle

Dynamic In Vitro Models of the Human Gastrointestinal Tract as Relevant Tools to Assess the Survival of Probiotic Strains and Their Interactions with Gut Microbiota

by Charlotte Cordonnier, Jonathan Thévenot, Lucie Etienne-Mesmin, Sylvain Denis, Monique Alric, Valérie Livrelli and Stéphanie Blanquet-Diot

Microorganisms 2015, 3(4), 725-745; https://doi.org/10.3390/microorganisms3040725 - 23 Oct 2015

Cited by 67 | Viewed by 8281

Abstract

The beneficial effects of probiotics are conditioned by their survival during passage through the human gastrointestinal tract and their ability to favorably influence gut microbiota. The main objective of this study was to use dynamic in vitro models of the human digestive tract [...] Read more.

The beneficial effects of probiotics are conditioned by their survival during passage through the human gastrointestinal tract and their ability to favorably influence gut microbiota. The main objective of this study was to use dynamic in vitro models of the human digestive tract to investigate the effect of fasted or fed state on the survival kinetics of the new probiotic Saccharomyces cerevisiae strain CNCM I-3856 and to assess its influence on intestinal microbiota composition and activity. The probiotic yeast showed a high survival rate in the upper gastrointestinal tract whatever the route of admistration, i.e., within a glass of water or a Western-type meal. S. cerevisiae CNCM I-3856 was more sensitive to colonic conditions, as the strain was not able to colonize within the bioreactor despite a twice daily administration. The main bacterial populations of the gut microbiota, as well as the production of short chain fatty acids were not influenced by the probiotic treatment. However, the effect of the probiotic on the gut microbiota was found to be individual dependent. This study shows that dynamic in vitro models can be advantageously used to provide useful insight into the behavior of probiotic strains in the human digestive environment. Full article

(This article belongs to the Special Issue Host-Gut Microbiota Metabolic Interactions)

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Review

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493 KiB

Open AccessReview

Microbiome, Metabolome and Inflammatory Bowel Disease

by Ishfaq Ahmed, Badal C. Roy, Salman A. Khan, Seth Septer and Shahid Umar

Microorganisms 2016, 4(2), 20; https://doi.org/10.3390/microorganisms4020020 - 15 Jun 2016

Cited by 136 | Viewed by 14843

Abstract

Inflammatory Bowel Disease (IBD) is a multifactorial disorder that conceptually occurs as a result of altered immune responses to commensal and/or pathogenic gut microbes in individuals most susceptible to the disease. During Crohn’s Disease (CD) or Ulcerative Colitis (UC), two components of the [...] Read more.

Inflammatory Bowel Disease (IBD) is a multifactorial disorder that conceptually occurs as a result of altered immune responses to commensal and/or pathogenic gut microbes in individuals most susceptible to the disease. During Crohn’s Disease (CD) or Ulcerative Colitis (UC), two components of the human IBD, distinct stages define the disease onset, severity, progression and remission. Epigenetic, environmental (microbiome, metabolome) and nutritional factors are important in IBD pathogenesis. While the dysbiotic microbiota has been proposed to play a role in disease pathogenesis, the data on IBD and diet are still less convincing. Nonetheless, studies are ongoing to examine the effect of pre/probiotics and/or FODMAP reduced diets on both the gut microbiome and its metabolome in an effort to define the healthy diet in patients with IBD. Knowledge of a unique metabolomic fingerprint in IBD could be useful for diagnosis, treatment and detection of disease pathogenesis. Full article

(This article belongs to the Special Issue Host-Gut Microbiota Metabolic Interactions)

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547 KiB

Open AccessReview

Extensive Intestinal Resection Triggers Behavioral Adaptation, Intestinal Remodeling and Microbiota Transition in Short Bowel Syndrome

by Camille Mayeur, Laura Gillard, Johanne Le Beyec, André Bado, Francisca Joly and Muriel Thomas

Microorganisms 2016, 4(1), 16; https://doi.org/10.3390/microorganisms4010016 - 08 Mar 2016

Cited by 32 | Viewed by 7842

Abstract

Extensive resection of small bowel often leads to short bowel syndrome (SBS). SBS patients develop clinical mal-absorption and dehydration relative to the reduction of absorptive area, acceleration of gastrointestinal transit time and modifications of the gastrointestinal intra-luminal environment. As a consequence of severe [...] Read more.

Extensive resection of small bowel often leads to short bowel syndrome (SBS). SBS patients develop clinical mal-absorption and dehydration relative to the reduction of absorptive area, acceleration of gastrointestinal transit time and modifications of the gastrointestinal intra-luminal environment. As a consequence of severe mal-absorption, patients require parenteral nutrition (PN). In adults, the overall adaptation following intestinal resection includes spontaneous and complex compensatory processes such as hyperphagia, mucosal remodeling of the remaining part of the intestine and major modifications of the microbiota. SBS patients, with colon in continuity, harbor a specific fecal microbiota that we called “lactobiota” because it is enriched in the Lactobacillus/Leuconostoc group and depleted in anaerobic micro-organisms (especially Clostridium and Bacteroides). In some patients, the lactobiota-driven fermentative activities lead to an accumulation of fecal d/l-lactates and an increased risk of d-encephalopathy. Better knowledge of clinical parameters and lactobiota characteristics has made it possible to stratify patients and define group at risk for d-encephalopathy crises. Full article

(This article belongs to the Special Issue Host-Gut Microbiota Metabolic Interactions)

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566 KiB

Open AccessReview

Metabolic Interaction of Helicobacter pylori Infection and Gut Microbiota

by Yao-Jong Yang and Bor-Shyang Sheu

Microorganisms 2016, 4(1), 15; https://doi.org/10.3390/microorganisms4010015 - 16 Feb 2016

Cited by 42 | Viewed by 9538

Abstract

As a barrier, gut commensal microbiota can protect against potential pathogenic microbes in the gastrointestinal tract. Crosstalk between gut microbes and immune cells promotes human intestinal homeostasis. Dysbiosis of gut microbiota has been implicated in the development of many human metabolic disorders like [...] Read more.

As a barrier, gut commensal microbiota can protect against potential pathogenic microbes in the gastrointestinal tract. Crosstalk between gut microbes and immune cells promotes human intestinal homeostasis. Dysbiosis of gut microbiota has been implicated in the development of many human metabolic disorders like obesity, hepatic steatohepatitis, and insulin resistance in type 2 diabetes (T2D). Certain microbes, such as butyrate-producing bacteria, are lower in T2D patients. The transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome, but the exact pathogenesis remains unclear. H. pylori in the human stomach cause chronic gastritis, peptic ulcers, and gastric cancers. H. pylori infection also induces insulin resistance and has been defined as a predisposing factor to T2D development. Gastric and fecal microbiota may have been changed in H. pylori-infected persons and mice to promote gastric inflammation and specific diseases. However, the interaction of H. pylori and gut microbiota in regulating host metabolism also remains unknown. Further studies aim to identify the H. pylori-microbiota-host metabolism axis and to test if H. pylori eradication or modification of gut microbiota can improve the control of human metabolic disorders. Full article

(This article belongs to the Special Issue Host-Gut Microbiota Metabolic Interactions)

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Open AccessReview

Metabolic Interactions in the Gastrointestinal Tract (GIT): Host, Commensal, Probiotics, and Bacteriophage Influences

by Luis Vitetta, Sean Hall and Samantha Coulson

Microorganisms 2015, 3(4), 913-932; https://doi.org/10.3390/microorganisms3040913 - 17 Dec 2015

Cited by 8 | Viewed by 9355

Abstract

Life on this planet has been intricately associated with bacterial activity at all levels of evolution and bacteria represent the earliest form of autonomous existence. Plants such as those from the Leguminosae family that form root nodules while harboring nitrogen-fixing soil bacteria are [...] Read more.

Life on this planet has been intricately associated with bacterial activity at all levels of evolution and bacteria represent the earliest form of autonomous existence. Plants such as those from the Leguminosae family that form root nodules while harboring nitrogen-fixing soil bacteria are a primordial example of symbiotic existence. Similarly, cooperative activities between bacteria and animals can also be observed in multiple domains, including the most inhospitable geographical regions of the planet such as Antarctica and the Lower Geyser Basin of Yellowstone National Park. In humans bacteria are often classified as either beneficial or pathogenic and in this regard we posit that this artificial nomenclature is overly simplistic and as such almost misinterprets the complex activities and inter-relationships that bacteria have with the environment as well as the human host and the plethora of biochemical activities that continue to be identified. We further suggest that in humans there are neither pathogenic nor beneficial bacteria, just bacteria embraced by those that tolerate the host and those that do not. The densest and most complex association exists in the human gastrointestinal tract, followed by the oral cavity, respiratory tract, and skin, where bacteria—pre- and post-birth—instruct the human cell in the fundamental language of molecular biology that normally leads to immunological tolerance over a lifetime. The overall effect of this complex output is the elaboration of a beneficial milieu, an environment that is of equal or greater importance than the bacterium in maintaining homeostasis. Full article

(This article belongs to the Special Issue Host-Gut Microbiota Metabolic Interactions)

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346 KiB

Open AccessReview

Hydrogen Sulfide in Physiology and Diseases of the Digestive Tract

by Sudha B. Singh and Henry C. Lin

Microorganisms 2015, 3(4), 866-889; https://doi.org/10.3390/microorganisms3040866 - 12 Nov 2015

Cited by 160 | Viewed by 16083

Abstract

Hydrogen sulfide (H₂S) is a Janus-faced molecule. On one hand, several toxic functions have been attributed to H₂S and exposure to high levels of this gas is extremely hazardous to health. On the other hand, H₂S delivery [...] Read more.

Hydrogen sulfide (H₂S) is a Janus-faced molecule. On one hand, several toxic functions have been attributed to H₂S and exposure to high levels of this gas is extremely hazardous to health. On the other hand, H₂S delivery based clinical therapies are being developed to combat inflammation, visceral pain, oxidative stress related tissue injury, thrombosis and cancer. Since its discovery, H₂S has been found to have pleiotropic effects on physiology and health. H₂S is a gasotransmitter that exerts its effect on different systems, such as gastrointestinal, neuronal, cardiovascular, respiratory, renal, and hepatic systems. In the gastrointestinal tract, in addition to H₂S production by mammalian cystathionine-β-synthase (CBS), cystathionine-γ-lyase (CSE), H₂S is also generated by the metabolic activity of resident gut microbes, mainly by colonic Sulfate-Reducing Bacteria (SRB) via a dissimilatory sulfate reduction (DSR) pathway. In the gut, H₂S regulates functions such as inflammation, ischemia/ reperfusion injury and motility. H₂S derived from gut microbes has been found to be associated with gastrointestinal disorders such as ulcerative colitis, Crohn’s disease and irritable bowel syndrome. This underscores the importance of gut microbes and their production of H₂S on host physiology and pathophysiology. Full article

(This article belongs to the Special Issue Host-Gut Microbiota Metabolic Interactions)

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321 KiB

Open AccessReview

Gut Microbiota and Host Reaction in Liver Diseases

by Hiroshi Fukui

Microorganisms 2015, 3(4), 759-791; https://doi.org/10.3390/microorganisms3040759 - 28 Oct 2015

Cited by 43 | Viewed by 8283

Abstract

Although alcohol feeding produces evident intestinal microbial changes in animals, only some alcoholics show evident intestinal dysbiosis, a decrease in Bacteroidetes and an increase in Proteobacteria. Gut dysbiosis is related to intestinal hyperpermeability and endotoxemia in alcoholic patients. Alcoholics further exhibit reduced [...] Read more.

Although alcohol feeding produces evident intestinal microbial changes in animals, only some alcoholics show evident intestinal dysbiosis, a decrease in Bacteroidetes and an increase in Proteobacteria. Gut dysbiosis is related to intestinal hyperpermeability and endotoxemia in alcoholic patients. Alcoholics further exhibit reduced numbers of the beneficial Lactobacillus and Bifidobacterium. Large amounts of endotoxins translocated from the gut strongly activate Toll-like receptor 4 in the liver and play an important role in the progression of alcoholic liver disease (ALD), especially in severe alcoholic liver injury. Gut microbiota and bacterial endotoxins are further involved in some of the mechanisms of nonalcoholic fatty liver disease (NAFLD) and its progression to nonalcoholic steatohepatitis (NASH). There is experimental evidence that a high-fat diet causes characteristic dysbiosis of NAFLD, with a decrease in Bacteroidetes and increases in Firmicutes and Proteobacteria, and gut dysbiosis itself can induce hepatic steatosis and metabolic syndrome. Clinical data support the above dysbiosis, but the details are variable. Intestinal dysbiosis and endotoxemia greatly affect the cirrhotics in relation to major complications and prognosis. Metagenomic approaches to dysbiosis may be promising for the analysis of deranged host metabolism in NASH and cirrhosis. Management of dysbiosis may become a cornerstone for the future treatment of liver diseases. Full article

(This article belongs to the Special Issue Host-Gut Microbiota Metabolic Interactions)

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Open AccessReview

The Gut Microbiota as a Therapeutic Target in IBD and Metabolic Disease: A Role for the Bile Acid Receptors FXR and TGR5

by Annemarie Baars, Annemarie Oosting, Jan Knol, Johan Garssen and Jeroen Van Bergenhenegouwen

Microorganisms 2015, 3(4), 641-666; https://doi.org/10.3390/microorganisms3040641 - 10 Oct 2015

Cited by 60 | Viewed by 10094

Abstract

The gut microbiota plays a crucial role in regulating many physiological systems of the host, including the metabolic and immune system. Disturbances in microbiota composition are increasingly correlated with disease; however, the underlying mechanisms are not well understood. Recent evidence suggests that changes [...] Read more.

The gut microbiota plays a crucial role in regulating many physiological systems of the host, including the metabolic and immune system. Disturbances in microbiota composition are increasingly correlated with disease; however, the underlying mechanisms are not well understood. Recent evidence suggests that changes in microbiota composition directly affect the metabolism of bile salts. Next to their role in digestion of dietary fats, bile salts function as signaling molecules for bile salt receptors such as Farnesoid X receptor (FXR) and G protein-coupled bile acid receptor (TGR5). Complementary to their role in metabolism, FXR and TGR5 are shown to play a role in intestinal homeostasis and immune regulation. This review presents an overview of evidence showing that changes in bile salt pool and composition due to changes in gut microbial composition contribute to the pathogenesis of inflammatory bowel disease and metabolic disease, possibly through altered activation of TGR5 and FXR. We further discuss how dietary interventions, such as pro- and synbiotics, may be used to treat metabolic disease and inflammatory bowel disease (IBD) through normalization of bile acid dysregulation directly or indirectly through normalization of the intestinal microbiota. Full article

(This article belongs to the Special Issue Host-Gut Microbiota Metabolic Interactions)

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618 KiB

Open AccessReview

Does the Gut Microbiota Contribute to Obesity? Going beyond the Gut Feeling

by Marisol Aguirre and Koen Venema

Microorganisms 2015, 3(2), 213-235; https://doi.org/10.3390/microorganisms3020213 - 27 Apr 2015

Cited by 29 | Viewed by 10831

Abstract

Increasing evidence suggests that gut microbiota is an environmental factor that plays a crucial role in obesity. However, the aetiology of obesity is rather complex and depends on different factors. Furthermore, there is a lack of consensus about the exact role that this [...] Read more.

Increasing evidence suggests that gut microbiota is an environmental factor that plays a crucial role in obesity. However, the aetiology of obesity is rather complex and depends on different factors. Furthermore, there is a lack of consensus about the exact role that this microbial community plays in the host. The aim of this review is to present evidence about what has been characterized, compositionally and functionally, as obese gut microbiota. In addition, the different reasons explaining the so-far unclear role are discussed considering evidence from in vitro, animal and human studies. Full article

(This article belongs to the Special Issue Host-Gut Microbiota Metabolic Interactions)

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