scholarly journals Metabolic Influences of Gut Microbiota Dysbiosis on Inflammatory Bowel Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Salma Sultan ◽  
Mohammed El-Mowafy ◽  
Abdelaziz Elgaml ◽  
Tamer A. E. Ahmed ◽  
Hebatoallah Hassan ◽  
...  
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Disease Progression ◽  
Short Chain Fatty Acids ◽  
Host Immune System ◽  
Microbial Dysbiosis ◽  
Medical Disorders ◽  
Inflammatory Bowel ◽  
The Impact ◽  
Gut Microbiota Dysbiosis

Inflammatory bowel diseases (IBD) are chronic medical disorders characterized by recurrent gastrointestinal inflammation. While the etiology of IBD is still unknown, the pathogenesis of the disease results from perturbations in both gut microbiota and the host immune system. Gut microbiota dysbiosis in IBD is characterized by depleted diversity, reduced abundance of short chain fatty acids (SCFAs) producers and enriched proinflammatory microbes such as adherent/invasive E. coli and H2S producers. This dysbiosis may contribute to the inflammation through affecting either the immune system or a metabolic pathway. The immune responses to gut microbiota in IBD are extensively discussed. In this review, we highlight the main metabolic pathways that regulate the host-microbiota interaction. We also discuss the reported findings indicating that the microbial dysbiosis during IBD has a potential metabolic impact on colonocytes and this may underlie the disease progression. Moreover, we present the host metabolic defectiveness that adds to the impact of symbiont dysbiosis on the disease progression. This will raise the possibility that gut microbiota dysbiosis associated with IBD results in functional perturbations of host-microbiota interactions, and consequently modulates the disease development. Finally, we shed light on the possible therapeutic approaches of IBD through targeting gut microbiome.

scholarly journals The Microbiotic Highway to Health—New Perspective on Food Structure, Gut Microbiota, and Host Inflammation

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1590 ◽  
Author(s):  
Nina Hansen ◽  
Anette Sams
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Dietary Habits ◽  
Gut Hormones ◽  
Host Immune System ◽  
Inflammatory Conditions ◽  
Food Structure ◽  
New Perspective ◽  
And Function ◽  
The Impact

This review provides evidence that not only the content of nutrients but indeed the structural organization of nutrients is a major determinant of human health. The gut microbiota provides nutrients for the host by digesting food structures otherwise indigestible by human enzymes, thereby simultaneously harvesting energy and delivering nutrients and metabolites for the nutritional and biological benefit of the host. Microbiota-derived nutrients, metabolites, and antigens promote the development and function of the host immune system both directly by activating cells of the adaptive and innate immune system and indirectly by sustaining release of monosaccharides, stimulating intestinal receptors and secreting gut hormones. Multiple indirect microbiota-dependent biological responses contribute to glucose homeostasis, which prevents hyperglycemia-induced inflammatory conditions. The composition and function of the gut microbiota vary between individuals and whereas dietary habits influence the gut microbiota, the gut microbiota influences both the nutritional and biological homeostasis of the host. A healthy gut microbiota requires the presence of beneficial microbiotic species as well as vital food structures to ensure appropriate feeding of the microbiota. This review focuses on the impact of plant-based food structures, the “fiber-encapsulated nutrient formulation”, and on the direct and indirect mechanisms by which the gut microbiota participate in host immune function.

scholarly journals Inflammatory and Microbiota-Related Regulation of the Intestinal Epithelial Barrier

2021 ◽  
Vol 8 ◽  
Author(s):  
Giovanni Barbara ◽  
Maria Raffaella Barbaro ◽  
Daniele Fuschi ◽  
Marta Palombo ◽  
Francesca Falangone ◽  
...  
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Cell Damage ◽  
Short Chain Fatty Acids ◽  
The Body ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Inflammatory Bowel ◽  
Irritable Bowel

The intestinal epithelial barrier (IEB) is one of the largest interfaces between the environment and the internal milieu of the body. It is essential to limit the passage of harmful antigens and microorganisms and, on the other side, to assure the absorption of nutrients and water. The maintenance of this delicate equilibrium is tightly regulated as it is essential for human homeostasis. Luminal solutes and ions can pass across the IEB via two main routes: the transcellular pathway or the paracellular pathway. Tight junctions (TJs) are a multi-protein complex responsible for the regulation of paracellular permeability. TJs control the passage of antigens through the IEB and have a key role in maintaining barrier integrity. Several factors, including cytokines, gut microbiota, and dietary components are known to regulate intestinal TJs. Gut microbiota participates in several human functions including the modulation of epithelial cells and immune system through the release of several metabolites, such as short-chain fatty acids (SCFAs). Mediators released by immune cells can induce epithelial cell damage and TJs dysfunction. The subsequent disruption of the IEB allows the passage of antigens into the mucosa leading to further inflammation. Growing evidence indicates that dysbiosis, immune activation, and IEB dysfunction have a role in several diseases, including irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and gluten-related conditions. Here we summarize the interplay between the IEB and gut microbiota and mucosal immune system and their involvement in IBS, IBD, and gluten-related disorders.

scholarly journals The role of microbiome in rheumatoid arthritis treatment

2019 ◽  
Vol 11 ◽  
pp. 1759720X1984463 ◽  
Author(s):  
Rahul Bodkhe ◽  
Baskar Balakrishnan ◽  
Veena Taneja
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune System ◽  
Gut Microbiota ◽  
Autoimmune Disorder ◽  
Host Immune System ◽  
Microbial Composition ◽  
Drug Induced ◽  
Partial Restoration ◽  
Genetic And Environmental Factors ◽  
The Impact

Rheumatoid arthritis (RA) is an autoimmune disorder with multifactorial etiology; both genetic and environmental factors are known to be involved in pathogenesis. Treatment with disease-modifying antirheumatic drugs (DMARDs) plays an essential role in controlling disease progression and symptoms. DMARDs have immunomodulatory properties and suppress immune response by interfering in various pro-inflammatory pathways. Recent evidence has shown that the gut microbiota directly and indirectly modulates the host immune system. RA has been associated with dysbiosis of the gut microbiota. Patients with RA treated with DMARDs show partial restoration of eubiotic gut microbiome. Hence, it is essential to understand the impact of DMARDs on the microbial composition and its consequent influences on the host immune system to identify novel therapies for RA. In this review, we discuss the importance of antirheumatic-drug-induced host microbiota modulations and possible probiotics that can generate eubiosis.

scholarly journals Changes of Gut-Microbiota-Liver Axis in Hepatitis C Virus Infection

Biology ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 55
Author(s):  
Mohammed El-Mowafy ◽  
Abdelaziz Elgaml ◽  
Mohamed El-Mesery ◽  
Salma Sultan ◽  
Tamer A. E. Ahmed ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Gut Microbiota ◽  
Disease Progression ◽  
Disease Status ◽  
Hcv Infection ◽  
Treatment Regimens ◽  
Liver Health ◽  
The Impact ◽  
Gut Microbiota Dysbiosis

The gut–liver-axis is a bidirectional coordination between the gut, including microbial residents, the gut microbiota, from one side and the liver on the other side. Any disturbance in this crosstalk may lead to a disease status that impacts the functionality of both the gut and the liver. A major cause of liver disorders is hepatitis C virus (HCV) infection that has been illustrated to be associated with gut microbiota dysbiosis at different stages of the disease progression. This dysbiosis may start a cycle of inflammation and metabolic disturbance that impacts the gut and liver health and contributes to the disease progression. This review discusses the latest literature addressing this interplay between the gut microbiota and the liver in HCV infection from both directions. Additionally, we highlight the contribution of gut microbiota to the metabolism of antivirals used in HCV treatment regimens and the impact of these medications on the microbiota composition. This review sheds light on the potential of the gut microbiota manipulation as an alternative therapeutic approach to control the liver complications post HCV infection.

scholarly journals Gut Microbiota and Dietary Factors as Modulators of the Mucus Layer in Inflammatory Bowel Disease

2021 ◽  
Vol 22 (19) ◽  
pp. 10224
Author(s):  
Samuel Fernández-Tomé ◽  
Lorena Ortega Moreno ◽  
María Chaparro ◽  
Javier P. Gisbert
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Dietary Factors ◽  
Host Immune System ◽  
Mucus Layer ◽  
Gut Health ◽  
Intestinal Mucus ◽  
Inflammatory Bowel ◽  
The Impact

The gastrointestinal tract is optimized to efficiently absorb nutrients and provide a competent barrier against a variety of lumen environmental compounds. Different regulatory mechanisms jointly collaborate to maintain intestinal homeostasis, but alterations in these mechanisms lead to a dysfunctional gastrointestinal barrier and are associated to several inflammatory conditions usually found in chronic pathologies such as inflammatory bowel disease (IBD). The gastrointestinal mucus, mostly composed of mucin glycoproteins, covers the epithelium and plays an essential role in digestive and barrier functions. However, its regulation is very dynamic and is still poorly understood. This review presents some aspects concerning the role of mucus in gut health and its alterations in IBD. In addition, the impact of gut microbiota and dietary compounds as environmental factors modulating the mucus layer is addressed. To date, studies have evidenced the impact of the three-way interplay between the microbiome, diet and the mucus layer on the gut barrier, host immune system and IBD. This review emphasizes the need to address current limitations on this topic, especially regarding the design of robust human trials and highlights the potential interest of improving our understanding of the regulation of the intestinal mucus barrier in IBD.

scholarly journals The impact of metabolites derived from the gut microbiota on immune regulation and diseases

2020 ◽  
Vol 32 (10) ◽  
pp. 629-636
Author(s):  
Hiroshi Ohno
Keyword(s):  
Gut Microbiota ◽  
Short Chain Fatty Acids ◽  
Enterohemorrhagic Escherichia Coli ◽  
Cellular Functions ◽  
Secondary Bile Acid ◽  
Histone Deacetylase Inhibition ◽  
Microbial Dysbiosis ◽  
Escherichia Coli Infection ◽  
Integrated Omics ◽  
The Impact

Abstract Abstract The gut microbiota strongly impacts the physiology and pathology in the host. To understand the complex interactions between host and gut microbiota, an ‘integrated omics’ approach has been employed, where exhaustive analyses for the different layers of cellular functions, such as epigenomics, transcriptomics and metabolomics, in addition to metagenomics, are combined. With this approach, the mechanisms whereby short-chain fatty acids (SCFAs) regulate host defense and the immune system have been elucidated. In a gnotobiotic mouse model of enterohemorrhagic Escherichia coli infection, Bifidobacterium-derived acetate can protect from infection-mediated death by changing the gene expression profile of colonic epithelial cells. It has also been shown that gut microbiota-derived butyrate enhances colonic regulatory T-cell differentiation through its epigenetic modulatory ability via histone deacetylase inhibition. SCFAs are involved in many other immunomodulatory effects as well as host pathophysiological conditions. Dysbiosis in the gut has been implicated in the pathogenesis of many diseases. Although the causal relationship of gut microbial dysbiosis and/or metabolites with pathogenesis is mostly unknown, mechanistic insights have been elucidated in some cases. Metabolism in the gut microbiota and host liver produces trimethylamine N-oxide, which is known to aggravate atherosclerosis, and a secondary bile acid deoxycholate, which reportedly induces non-alcoholic steatohepatitis-related hepatocellular carcinoma. It has been reported that secondary bile acids could also induce the differentiation of peripherally derived regulatory T cells in the gut. Further studies on the interactions between the host and gut microbiota could lead to the development of new therapeutic strategies as well as in preventive medicine.

scholarly journals Crosstalks between helminthes and microbiota to improve gut health

QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
H S Elwakil
Keyword(s):  
Immune System ◽  
Intestinal Tract ◽  
Inflammatory Diseases ◽  
Short Chain Fatty Acids ◽  
Mammalian Host ◽  
Host Immune System ◽  
Helminth Parasites ◽  
Gut Health ◽  
Intestinal Microbes ◽  
Inflammatory Bowel

Abstract Intestinal helminths are potent regulators of their host’s immune system and can protect against Inflammatory bowel disease. This anti-inflammatory activity remains largely unknown. Is it purely intrinsic to helminths, or whether it also involved cross interaction with the local microbiota? Microbiota and helminths have coevolved within the mammalian host. Both have common strategies of establishing a new homeostasis in the host intestinal tract. These strategies include regulating host immunity to permit their survival through the induction of suppressive regulatory T cells ( Tregs ). Also, Short-Chain Fatty Acids (SCFAs) may be a possible another common pathway shared by microbiota and helminths. SCFAs are microbial metabolite that are derived from microbial fermentation of dietary fibers in the colon. Similarly, some helminth infection leads to SCFAs elevation in human. SCFAs can potentiate T regs generation and IL- 10 production in the periphery. Dissecting the multidirectional interactions among intestinal microbes, helminth parasites and their host immune system will hopefully enable the design of new therapeutic strategies to treat metabolic and inflammatory diseases

scholarly journals Gut Dysbiosis and Immune System in Atherosclerotic Cardiovascular Disease (ACVD)

2022 ◽  
Vol 10 (1) ◽  
pp. 108
Author(s):  
Ji Youn Yoo ◽  
Sarah Sniffen ◽  
Kyle Craig McGill Percy ◽  
Veera Bramhachari Pallaval ◽  
Bojjibabu Chidipi
Keyword(s):  
Cardiovascular Disease ◽  
Immune System ◽  
Gut Microbiota ◽  
Short Chain Fatty Acids ◽  
Low Grade ◽  
Host Immune System ◽  
Atherosclerotic Cardiovascular Disease ◽  
Gut Dysbiosis ◽  
Glucagon Like Peptide 1 ◽  
Inflammation Resolution

Atherosclerosis is a leading cause of cardiovascular disease and mortality worldwide. Alterations in the gut microbiota composition, known as gut dysbiosis, have been shown to contribute to atherosclerotic cardiovascular disease (ACVD) development through several pathways. Disruptions in gut homeostasis are associated with activation of immune processes and systemic inflammation. The gut microbiota produces several metabolic products, such as trimethylamine (TMA), which is used to produce the proatherogenic metabolite trimethylamine-N-oxide (TMAO). Short-chain fatty acids (SCFAs), including acetate, butyrate, and propionate, and certain bile acids (BAs) produced by the gut microbiota lead to inflammation resolution and decrease atherogenesis. Chronic low-grade inflammation is associated with common risk factors for atherosclerosis, including metabolic syndrome, type 2 diabetes mellitus (T2DM), and obesity. Novel strategies for reducing ACVD include the use of nutraceuticals such as resveratrol, modification of glucagon-like peptide 1 (GLP-1) levels, supplementation with probiotics, and administration of prebiotic SCFAs and BAs. Investigation into the relationship between the gut microbiota, and its metabolites, and the host immune system could reveal promising insights into ACVD development, prognostic factors, and treatments.

scholarly journals The Gut Dysbiosis and Immune System in Atherosclerotic Cardiovascular Disease (ACVD)

2021 ◽  
Author(s):  
Ji Youn Yoo ◽  
Sarah Sniffen ◽  
Kyle McGill Percy ◽  
Bojji Babu Chidipi ◽  
Veera Bramhachari Pallaval
Keyword(s):  
Cardiovascular Disease ◽  
Immune System ◽  
Gut Microbiota ◽  
Short Chain Fatty Acids ◽  
Low Grade ◽  
Host Immune System ◽  
Atherosclerotic Cardiovascular Disease ◽  
Gut Dysbiosis ◽  
Glucagon Like Peptide 1 ◽  
Inflammation Resolution

Atherosclerosis is a leading cause of cardiovascular disease and mortality worldwide. Alterations in the gut microbiota composition, known as gut dysbiosis, have been shown to contribute to atherosclerotic cardiovascular disease (ACVD) development through several pathways. Disruptions in gut homeostasis are associated with activation of immune processes and systemic inflammation. The gut microbiota produces several metabolic products, namely trimethylamine (TMA), which is used to produce the proatherogenic metabolite trimethylamine-N-oxide (TMAO). Short chain fatty acids (SCFAs), including acetate, butyrate, and propionate, and certain bile acids (BAs) produced by the gut microbiota lead to inflammation resolution and decrease atherogenesis. Chronic low-grade inflammation is associated to common risk factors for atherosclerosis, including metabolic syndrome, type 2 diabetes mellitus (T2DM), and obesity. Novel strategies for reducing ACVD include the use of nutraceuticals such as resveratrol, modification of glucagon-like peptide 1 (GLP-1) levels, supplementation with probiotics, and administration of prebiotic SCFAs and BAs. Investigation into the relationship between the gut microbiota and its metabolites, and the host immune system could reveal promising insight into ACVD development, prognostic factors, and treatments.

scholarly journals Mold, Mycotoxins and a Dysregulated Immune System: A Combination of Concern?

2021 ◽  
Vol 22 (22) ◽  
pp. 12269
Author(s):  
Stephanie Kraft ◽  
Lisa Buchenauer ◽  
Tobias Polte
Keyword(s):  
Immune System ◽  
Disease Progression ◽  
Inflammatory Diseases ◽  
Host Immune System ◽  
System A ◽  
Immunodeficiency Virus ◽  
Mold Exposure ◽  
The Impact

Fungi represent one of the most diverse and abundant eukaryotes on earth. The interplay between mold exposure and the host immune system is still not fully elucidated. Literature research focusing on up-to-date publications is providing a heterogenous picture of evidence and opinions regarding the role of mold and mycotoxins in the development of immune diseases. While the induction of allergic immune responses by molds is generally acknowledged, other direct health effects like the toxic mold syndrome are controversially discussed. However, recent observations indicate a particular importance of mold/mycotoxin exposure in individuals with pre-existing dysregulation of the immune system, due to exacerbation of underlying pathophysiology including allergic and non-allergic chronic inflammatory diseases, autoimmune disorders, and even human immunodeficiency virus (HIV) disease progression. In this review, we focus on the impact of mycotoxins regarding their impact on disease progression in pre-existing immune dysregulation. This is complemented by experimental in vivo and in vitro findings to present cellular and molecular modes of action. Furthermore, we discuss hypothetical mechanisms of action, where evidence is missing since much remains to be discovered.

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