scholarly journals Increasing incidence of inflammatory bowel disease in children and adolescents: significance of environmental factors

2020 ◽  
Vol 63 (9) ◽  
pp. 337-344 ◽  
Author(s):  
Sowon Park ◽  
Yunkoo Kang ◽  
Hong Koh ◽  
Seung Kim
Keyword(s):  
Inflammatory Bowel Disease ◽  
Environmental Factors ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Intestinal Tract ◽  
Immune Dysregulation ◽  
Immune Mediated ◽  
Inflammatory Bowel ◽  
Dietary Treatments

Inflammatory bowel disease (IBD) is a chronic relapsing immune-mediated disease of the intestinal tract. Although its prevalence is reportedly lower in Asia than in Western countries, the rapid increase in the incidence of IBD has drawn attention to its etiology, including genetic susceptibility and environmental factors. Specifically, recent studies concerning dietary treatments and intestinal microbiota suggest that these factors may interact with the immune system, and the imbalance of this relationship may lead to immune dysregulation in IBD. Changes in diet or alterations in the composition of the intestinal microbiota may be associated with the increasing incidence of IBD in Asia. Here, we aim to review recent studies on the role of diet and intestinal microbiota in IBD pathogenesis and the results of the investigations performed to modulate these factors.

scholarly journals Role of intestinal microbiota in pathogenesis of inflammatory bowel disease

2016 ◽  
Vol 24 (33) ◽  
pp. 4505
Author(s):  
Jing-Zhi Zhang ◽  
Chun-Hui Bao ◽  
Zheng Shi ◽  
Zhi-Jun Weng ◽  
Xiao-Mei Wang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Role of intestinal microbiota and metabolites in inflammatory bowel disease

2019 ◽  
Vol 132 (13) ◽  
pp. 1610-1614 ◽  
Author(s):  
Li-Na Dong ◽  
Mu Wang ◽  
Jian Guo ◽  
Jun-Ping Wang
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Inflammatory Bowel

Extra-articular manifestations: inflammatory bowel disease

2016 ◽  
Author(s):  
Dirk Elewaut ◽  
Heleen Cypers ◽  
Matthew L. Stoll ◽  
Charles O. Elson
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Intestinal Barrier ◽  
Innate Immune ◽  
Intestinal Barrier Function ◽  
Innate Immune Responses ◽  
Susceptible Host ◽  
Inflammatory Bowel

A significant overlap exists between spondyloarthritis (SpA) and inflammatory bowel disease (IBD), particularly in the IL-23/IL-17 pathway. Shared immunologic mechanisms include aberrant innate immune responses, an excess of Th1/Th17-mediated immunity, and inadequate immune regulation. Many genetic factors associated with IBD are involved in host–pathogen interactions and intestinal barrier function, and the intestinal microbiota do appear to play an important role in disease development. Hence the current hypothesis for IBD pathogenesis is that it stems from a dysregulated immune response to intestinal microbiota in a genetically susceptible host. In SpA, evidence for a role of intestinal microbiota is less abundant, but given the overlap with IBD, it is plausible that gut microbiota are important players in SpA pathogenesis as well. However, there are significant genetic differences between these two conditions, as well as differing responses to biologic therapy.

Inflammatory bowel disease: the role of environmental factors

2004 ◽  
Vol 3 (5) ◽  
pp. 394-400 ◽  
Author(s):  
Silvio Danese ◽  
Miquel Sans ◽  
Claudio Fiocchi
Keyword(s):  
Inflammatory Bowel Disease ◽  
Environmental Factors ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Selective Tyrosine Kinase 2 Inhibition for Treatment of Inflammatory Bowel Disease: New Hope on the Rise

2021 ◽  
Author(s):  
Silvio Danese ◽  
Laurent Peyrin-Biroulet
Keyword(s):  
Inflammatory Bowel Disease ◽  
Tyrosine Kinase ◽  
Bowel Disease ◽  
Inflammatory Diseases ◽  
Janus Kinase ◽  
Type I ◽  
Tyrosine Kinase 2 ◽  
Immune Mediated ◽  
Inflammatory Bowel

Abstract Conventional systemic and biologic agents are the mainstay of inflammatory bowel disease (IBD) management; however, many of these agents are associated with loss of clinical response, highlighting the need for effective, novel targeted therapies. Janus kinase (JAK) 1-3 and tyrosine kinase 2 (TYK2) mediate signal transduction events downstream of multiple cytokine receptors that regulate targeted gene transcription, including the interleukin-12, interleukin-23, and type I interferon receptors for TYK2. This review summarizes the role of TYK2 signaling in IBD pathogenesis, the differential selectivity of TYK2 inhibitors, and the potential clinical implications of TYK2 inhibition in IBD. A PubMed literature review was conducted to identify studies of JAK1-3 and TYK2 inhibitors in IBD and other immune-mediated inflammatory diseases. Key efficacy and safety information was extracted and summarized. Pan-JAK inhibitors provide inconsistent efficacy in patients with IBD and are associated with toxicities resulting from a lack of selectivity at therapeutic dosages. Selective inhibition of TYK2 signaling via an allosteric mechanism, with an agent that binds to the regulatory (pseudokinase) domain, may reduce potential toxicities typically associated with JAK1-3 inhibitors. Deucravacitinib, a novel, oral, selective TYK2 inhibitor, and brepocitinib and PF-06826647, TYK2 inhibitors that bind to the active site in the catalytic domain, are in development for IBD and other immune-mediated inflammatory diseases. Allosteric TYK2 inhibition is more selective than JAK1-3 inhibition and has the potential to limit toxicities typically associated with JAK1-3 inhibitors. Future studies will be important in establishing the role of selective, allosteric TYK2 inhibition in the management of IBD.

scholarly journals The Role of Vitamin D in the Pathogenesis of Inflammatory Bowel Disease

2019 ◽  
Vol 1 (1) ◽  
pp. 231-240 ◽  
Author(s):  
Stefano Nobile ◽  
Michela Tenace ◽  
Helen Pappa
Keyword(s):  
Inflammatory Bowel Disease ◽  
Vitamin D ◽  
Immune System ◽  
Bowel Disease ◽  
Immune Dysregulation ◽  
Proof Of Concept ◽  
Search Terms ◽  
System Components ◽  
Inflammatory Bowel

Vitamin D has a complex role in the pathogenesis of inflammatory bowel disease (IBD), which is still under investigation. We conducted a literature search using PubMed through December 2018 through the use of relevant search terms. We found an abundance of evidence to support the role of vitamin D in regulating the innate and adaptive arms of the immune system. The pathogenesis of IBD implicates the immune dysregulation of these immune system components. Proof of concept of the vitamin’s role in the pathogenesis of IBD is the mapping of the vitamin D receptor in a region of chromosome 12, where IBD is also mapped, and specific VDR polymorphisms’ link to IBD phenotypes. Further research is needed to better delineate vitamin D’s role in preventing IBD and its potential as a therapeutic target for this disease.

scholarly journals Bases for the Adequate Development of Nutritional Recommendations for Patients with Inflammatory Bowel Disease

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1062 ◽  
Author(s):  
Esteban Sáez-González ◽  
Beatriz Mateos ◽  
Pedro López-Muñoz ◽  
Marisa Iborra ◽  
Inés Moret ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune System ◽  
Environmental Factors ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Nutritional Intervention ◽  
Host Cells ◽  
Host Immune System ◽  
Intestinal Immunity ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory condition of the gastrointestinal tract; it is a heterogeneous and multifactorial disorder resulting from a complex interplay between genetic variation, intestinal microbiota, the host immune system and environmental factors such as diet, drugs, breastfeeding and smoking. The interactions between dietary nutrients and intestinal immunity are complex. There is a compelling argument for environmental factors such as diet playing a role in the cause and course of IBD, given that three important factors in the pathogenesis of IBD can be modulated and controlled by diet: intestinal microbiota, the immune system and epithelial barrier function. The aim of this review is to summarize the epidemiological findings regarding diet and to focus on the effects that nutrients exert on the intestinal mucosa–microbiota–permeability interaction. The nature of these interactions in IBD is influenced by alterations in the nutritional metabolism of the gut microbiota and host cells that can influence the outcome of nutritional intervention. A better understanding of diet–host–microbiota interactions is essential for unravelling the complex molecular basis of epigenetic, genetic and environmental interactions underlying IBD pathogenesis as well as for offering new therapeutic approaches for the treatment of IBD.

Targeting Enteric Neurons and Plexitis for the Management of Inflammatory Bowel Disease

2020 ◽  
Vol 21 (14) ◽  
pp. 1428-1439
Author(s):  
Rhian Stavely ◽  
Raquel Abalo ◽  
Kulmira Nurgali
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Tract ◽  
Intestinal Inflammation ◽  
Neuronal Loss ◽  
Predictive Marker ◽  
Enteric Neurons ◽  
Inflammatory Bowel ◽  
Molecular Expression

Ulcerative colitis (UC) and Crohn’s disease (CD) are pathological conditions with an unknown aetiology that are characterised by severe inflammation of the intestinal tract and collectively referred to as inflammatory bowel disease (IBD). Current treatments are mostly ineffective due to their limited efficacy or toxicity, necessitating surgical resection of the affected bowel. The management of IBD is hindered by a lack of prognostic markers for clinical inflammatory relapse. Intestinal inflammation associates with the infiltration of immune cells (leukocytes) into, or surrounding the neuronal ganglia of the enteric nervous system (ENS) termed plexitis or ganglionitis. Histological observation of plexitis in unaffected intestinal regions is emerging as a vital predictive marker for IBD relapses. Plexitis associates with alterations to the structure, cellular composition, molecular expression and electrophysiological function of enteric neurons. Moreover, plexitis often occurs before the onset of gross clinical inflammation, which may indicate that plexitis can contribute to the progression of intestinal inflammation. In this review, the bilateral relationships between the ENS and inflammation are discussed. These include the effects and mechanisms of inflammation-induced enteric neuronal loss and plasticity. Additionally, the role of enteric neurons in preventing antigenic/pathogenic insult and immunomodulation is explored. While all current treatments target the inflammatory pathology of IBD, interventions that protect the ENS may offer an alternative avenue for therapeutic intervention.

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