scholarly journals Diet–Microbiota Interactions in Inflammatory Bowel Disease

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1533
Author(s):  
Kohei Sugihara ◽  
Nobuhiko Kamada
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Current Knowledge ◽  
Chronic Inflammatory Disease ◽  
Host Cells ◽  
Intestinal Homeostasis ◽  
New Therapeutic Approaches ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract. Although the precise etiology of IBD is largely unknown, it is widely thought that diet contributes to the development of IBD. Diet shapes the composition of the gut microbiota, which plays critical roles in intestinal homeostasis. In contrast, intestinal inflammation induces gut dysbiosis and may affect the use of dietary nutrients by host cells and the gut microbiota. The interaction of diet and the gut microbiota is perturbed in patients with IBD. Herein, we review the current knowledge of diet and gut microbiota interaction in intestinal homeostasis. We also discuss alterations of diet and gut microbiota interaction that influence the outcome and the nutritional treatment of IBD. Understanding the complex relationships between diet and the gut microbiota provides crucial insight into the pathogenesis of IBD and advances the development of new therapeutic approaches.

scholarly journals Alteration of Gut Microbiota in Inflammatory Bowel Disease (IBD): Cause or Consequence? IBD Treatment Targeting the Gut Microbiome

Pathogens ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 126 ◽  
Author(s):  
Israr Khan ◽  
Naeem Ullah ◽  
Lajia Zha ◽  
Yanrui Bai ◽  
Ashiq Khan ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Current Knowledge ◽  
Pathological Condition ◽  
Gut Flora ◽  
Core Microbiome ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a chronic complex inflammatory gut pathological condition, examples of which include Crohn’s disease (CD) and ulcerative colitis (UC), which is associated with significant morbidity. Although the etiology of IBD is unknown, gut microbiota alteration (dysbiosis) is considered a novel factor involved in the pathogenesis of IBD. The gut microbiota acts as a metabolic organ and contributes to human health by performing various physiological functions; deviation in the gut flora composition is involved in various disease pathologies, including IBD. This review aims to summarize the current knowledge of gut microbiota alteration in IBD and how this contributes to intestinal inflammation, as well as explore the potential role of gut microbiota-based treatment approaches for the prevention and treatment of IBD. The current literature has clearly demonstrated a perturbation of the gut microbiota in IBD patients and mice colitis models, but a clear causal link of cause and effect has not yet been presented. In addition, gut microbiota-based therapeutic approaches have also shown good evidence of their effects in the amelioration of colitis in animal models (mice) and IBD patients, which indicates that gut flora might be a new promising therapeutic target for the treatment of IBD. However, insufficient data and confusing results from previous studies have led to a failure to define a core microbiome associated with IBD and the hidden mechanism of pathogenesis, which suggests that well-designed randomized control trials and mouse models are required for further research. In addition, a better understanding of this ecosystem will also determine the role of prebiotics and probiotics as therapeutic agents in the management of IBD.

scholarly journals Unraveling the Role of ACE2, the Binding Receptor for SARS-CoV-2, in Inflammatory Bowel Disease

2020 ◽  
Vol 26 (12) ◽  
pp. 1787-1795 ◽  
Author(s):  
Mariana Ferreira-Duarte ◽  
Maria Manuela Estevinho ◽  
Margarida Duarte-Araújo ◽  
Fernando Magro ◽  
Manuela Morato
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Current Knowledge ◽  
Renin Angiotensin System ◽  
Biologic Drugs ◽  
Multifunctional Protein ◽  
Expression Activity ◽  
Inflammatory Bowel ◽  
The Impact

Abstract Angiotensin-converting enzyme 2 (ACE2) has been highlighted for its role as a receptor for SARS-CoV-2, responsible for the current COVID-19 pandemic. This review summarizes current knowledge about ACE2 as a multifunctional protein, focusing on its relevance in inflammatory bowel disease (IBD). As an enzyme, ACE2 may be protective in IBD because it favors the counter-regulatory arm of the renin-angiotensin system or deleterious because it metabolizes other anti-inflammatory/repairing elements. Meanwhile, as a receptor for SARS-CoV-2, the impact of ACE2 expression/activity on infection is still under debate because no direct evidence has been reported and, again, both protective and deleterious pathways are possible. Research has shown that ACE2 regulates the expression of the neutral amino acid transporter B0AT1, controlling tryptophan-associated intestinal inflammation and nutritional status. Finally, intact membrane-bound or shed soluble ACE2 can also trigger integrin signaling, modulating the response to anti-integrin biologic drugs used to treat IBD (such as vedolizumab) and fibrosis, a long-term complication of IBD. As such, future studies on ACE2 expression/activity in IBD can improve monitoring of the disease and explore an alternative pharmacological target.

scholarly journals Roles of Autophagy-Related Genes in the Pathogenesis of Inflammatory Bowel Disease

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 77 ◽  
Author(s):  
Sup Kim ◽  
Hyuk Eun ◽  
Eun-Kyeong Jo
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Paneth Cell ◽  
Conditional Knockout ◽  
Intestinal Homeostasis ◽  
Genetic Studies ◽  
Inflammatory Bowel ◽  
Direct Targeting ◽  
Catabolic Process

Autophagy is an intracellular catabolic process that is essential for a variety of cellular responses. Due to its role in the maintenance of biological homeostasis in conditions of stress, dysregulation or disruption of autophagy may be linked to human diseases such as inflammatory bowel disease (IBD). IBD is a complicated inflammatory colitis disorder; Crohn’s disease and ulcerative colitis are the principal types. Genetic studies have shown the clinical relevance of several autophagy-related genes (ATGs) in the pathogenesis of IBD. Additionally, recent studies using conditional knockout mice have led to a comprehensive understanding of ATGs that affect intestinal inflammation, Paneth cell abnormality and enteric pathogenic infection during colitis. In this review, we discuss the various ATGs involved in macroautophagy and selective autophagy, including ATG16L1, IRGM, LRRK2, ATG7, p62, optineurin and TFEB in the maintenance of intestinal homeostasis. Although advances have been made regarding the involvement of ATGs in maintaining intestinal homeostasis, determining the precise contribution of autophagy has remained elusive. Recent efforts based on direct targeting of ATGs and autophagy will further facilitate the development of new therapeutic opportunities for IBD.

scholarly journals Proposed grading scheme for inflammatory bowel disease in ferrets and correlation with clinical signs

2019 ◽  
Vol 32 (1) ◽  
pp. 17-24
Author(s):  
Paola Cazzini ◽  
Megan K. Watson ◽  
Nicole Gottdenker ◽  
Joerg Mayer ◽  
Drury Reavill ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Clinical Utility ◽  
Intestinal Inflammation ◽  
Companion Animals ◽  
Clinical Signs ◽  
Chronic Inflammatory Disease ◽  
Mustela Putorius ◽  
Crypt Abscess ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is an idiopathic, chronic, inflammatory disease of the gastrointestinal tract of companion animals, including ferrets ( Mustela putorius furo). Clinical signs of IBD are nonspecific, and intestinal biopsies are necessary for a definitive diagnosis. A grading scheme has not been established for ferrets. Additionally, the association between histologic severity and clinical signs in ferrets is unknown. We evaluated enteric samples from ferrets diagnosed with IBD, compared histologic grading schemes, and correlated the results with the severity of clinical signs. Enteric sections from 23 ferrets with IBD were analyzed using grading schemes for intestinal inflammation in cats and dogs, and a correlation with clinical signs was evaluated. After dividing the histologic samples into groups based on the severity of clinical signs, main histologic differences were identified. Age and sex were also assessed for correlation with clinical signs. No significant correlation was found between the 2 grading schemes and clinical signs (rho = 0.02, p = 0.89; rho = 0.26, p = 0.18, respectively). Degree of villus fusion, hemorrhage and/or fibrin, epithelial damage, inflammation density, and crypt abscess formation were used retrospectively to create a ferret IBD grading scheme, which was significantly correlated with the severity of clinical signs (rho = 0.48, p = 0.01). A positive correlation was observed between age ( p = 0.04) and females ( p = 0.007) with severity of clinical signs. Our ferret grading scheme may have clinical utility in providing a more objective, consistent evaluation of IBD in ferrets.

Protective Mechanisms of Butyrate on Inflammatory Bowel Disease

2019 ◽  
Vol 24 (35) ◽  
pp. 4154-4166 ◽  
Author(s):  
João P.B. Silva ◽  
Kely C. Navegantes-Lima ◽  
Ana L.B. Oliveira ◽  
Dávila V.S. Rodrigues ◽  
Sílvia L.F. Gaspar ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Current Knowledge ◽  
In Vivo Studies ◽  
Whole Body ◽  
Protective Mechanisms ◽  
Mucus Production ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a multifactorial chronic disease, commonly associated with alteration in the composition and function of gut microbiota. This process can lead to a decreased production of short chain fatty acids (SCFAs) by the gut microbiota, mainly butyrate, which is an important immunomodulatory molecule in the intestine. Butyrogenic bacteria normally produces butyrate through carbohydrate fermentation or amino acids degradation pathways. This molecule plays an important protective role in intestinal homeostasis acting in both adaptive immunity and innate immunity. This review summarizes the current knowledge about the role of butyrate on the development of IBD and the protective mechanisms of this metabolite on the intestinal mucosa and the whole body, as reported by in vitro and in vivo studies. Thus, butyrate can regulate the activation of regulatory T cells, increasing the acetylation of histones and decreasing the activation of NF-κB. In addition, it can also stimulate the mucus production from epithelial cells and the rearrangement of tight junction proteins.

Ganoderma applanatum polysaccharides and ethanol extracts promote the recovery of colitis through intestinal barrier protection and gut microbiota modulations

2021 ◽  
Author(s):  
Miaoyu Li ◽  
Leilei Yu ◽  
Qixiao Zhai ◽  
Bingshu Liu ◽  
Jianxin Zhao ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Protective Effect ◽  
Bowel Disease ◽  
Intestinal Barrier ◽  
Intestinal Homeostasis ◽  
Ganoderma Applanatum ◽  
Inflammatory Bowel ◽  
Ethanol Extracts ◽  
Gut Microbiota Dysbiosis

Inflammatory bowel disease is associated with intestinal homeostasis dysregulation and gut microbiota dysbiosis. This study aimed to investigate the protective effect of Ganoderma applanatum extracts (G. applanatum polysaccharides (GAP) and...

scholarly journals Innate Lymphoid Cells in Intestinal Homeostasis and Inflammatory Bowel Disease

2021 ◽  
Vol 22 (14) ◽  
pp. 7618
Author(s):  
Angela Saez ◽  
Raquel Gomez-Bris ◽  
Beatriz Herrero-Fernandez ◽  
Claudia Mingorance ◽  
Cristina Rius ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Intestinal Homeostasis ◽  
Mucosal Homeostasis ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

Inflammatory bowel disease (IBD) is a heterogeneous state of chronic intestinal inflammation of unknown cause encompassing Crohn’s disease (CD) and ulcerative colitis (UC). IBD has been linked to genetic and environmental factors, microbiota dysbiosis, exacerbated innate and adaptive immunity and epithelial intestinal barrier dysfunction. IBD is classically associated with gut accumulation of proinflammatory Th1 and Th17 cells accompanied by insufficient Treg numbers and Tr1 immune suppression. Inflammatory T cells guide innate cells to perpetuate a constant hypersensitivity to microbial antigens, tissue injury and chronic intestinal inflammation. Recent studies of intestinal mucosal homeostasis and IBD suggest involvement of innate lymphoid cells (ILCs). These lymphoid-origin cells are innate counterparts of T cells but lack the antigen receptors expressed on B and T cells. ILCs play important roles in the first line of antimicrobial defense and contribute to organ development, tissue protection and regeneration, and mucosal homeostasis by maintaining the balance between antipathogen immunity and commensal tolerance. Intestinal homeostasis requires strict regulation of the quantity and activity of local ILC subpopulations. Recent studies demonstrated that changes to ILCs during IBD contribute to disease development. A better understanding of ILC behavior in gastrointestinal homeostasis and inflammation will provide valuable insights into new approaches to IBD treatment. This review summarizes recent research into ILCs in intestinal homeostasis and the latest advances in the understanding of the role of ILCs in IBD, with particular emphasis on the interaction between microbiota and ILC populations and functions.

scholarly journals Dietary Composition and Effects in Inflammatory Bowel Disease

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1398 ◽  
Author(s):  
Fernando Castro ◽  
Heitor S. P. de Souza
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Dietary Habits ◽  
Intestinal Inflammation ◽  
Dietary Factors ◽  
Food Components ◽  
Increased Risk ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

Dramatic changes in the environment and human lifestyle have been associated with the rise of various chronic complex diseases, such as inflammatory bowel disease (IBD). A dysbiotic gut microbiota has been proposed as a crucial pathogenic element, contributing to immune imbalances and fostering a proinflammatory milieu, which may be associated with disease relapses or even the initiation of IBD. In addition to representing important regulators of the mucosal immunity and the composition of the gut microbiota, food components have been shown to be potential environmental triggers of epigenetic modifications. In the context of chronic intestinal inflammation, dietary habits and specific food components have been implicated as important modulators of epigenetic mechanisms, including DNA methylation, which may predispose a person to the increased risk of the initiation and evolution of IBD. This review provides novel insights about how dietary factors may interact with the intestinal mucosa and modulate immune homeostasis by shaping the intestinal ecosystem, as well as the potential influence of diet in the etiopathogenesis and management of IBD.

scholarly journals The Multifaceted Role of Serotonin in Intestinal Homeostasis

2021 ◽  
Vol 22 (17) ◽  
pp. 9487
Author(s):  
Nienke Koopman ◽  
Drosos Katsavelis ◽  
Anne S. ten Hove ◽  
Stanley Brul ◽  
Wouter J. de Jonge ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Current Knowledge ◽  
Bacterial Species ◽  
Disease Course ◽  
Intestinal Homeostasis ◽  
Wide Range ◽  
Range Of Functions ◽  
Inflammatory Bowel

The monoamine serotonin, 5-hydroxytryptamine (5-HT), is a remarkable molecule with conserved production in prokaryotes and eukaryotes and a wide range of functions. In the gastrointestinal tract, enterochromaffin cells are the most important source for 5-HT production. Some intestinal bacterial species are also able to produce 5-HT. Besides its role as a neurotransmitter, 5-HT acts on immune cells to regulate their activation. Several lines of evidence indicate that intestinal 5-HT signaling is altered in patients with inflammatory bowel disease. In this review, we discuss the current knowledge on the production, secretion, and signaling of 5-HT in the intestine. We present an inventory of intestinal immune and epithelial cells that respond to 5-HT and describe the effects of these signaling processes on intestinal homeostasis. Further, we detail the mechanisms by which 5-HT could affect inflammatory bowel disease course and describe the effects of interventions that target intestinal 5-HT signaling.

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