• Journal of Dairy Science and Biotechnology
• /
• v.28 no.2
• /
• pp.25-30
• /
• 2010

For centuries, probiotics have been known to promote health and prevent diseases. In recent times, modulation of diseases related to the immune function by probiotics has been recognized as very important to the health of the host's gut. Inflammatory bowel diseases (IBDs) are the most frequently studied diseases in which probiotic administration has been tested as a potential therapy. Various in vitro and in vivo studies have been performed. The studies discussed in this review suggest several mechanisms: probiotics could modulate the gut microflora by competing with disease-causing pathogenic bacteria and could directly regulate the mucosal immune system, which activates the innate and adaptive immune systems. In addition, human clinical trials have shown alleviation of disease symptoms of ulcerative colitis (UC), Crohn's disease, etc. This study aimed to understand the molecular mechanisms underlying immune modulation by probiotics and review studies on the functional aspect of IBD alleviation by probiotics. With more scientific studies confirming the effect of probiotics, this therapy holds promise for use in alternative medicine and/or pharmaceutical preparations, given the long history of safe consumption of probiotics.

• East Asian mathematical journal
• /
• v.32 no.1
• /
• pp.139-152
• /
• 2016

Inflammatory Bowel Disease(IBD) is chronic, relapsing, immune mediated disorder. The exact cause of IBD is still unknown. The immune system is known to play important role in the dynamics of IBD. We focus on relation between T cells and cytokines in immune system that leads to IBD. In this paper, we propose a mathematical model describing IBD under considering immune mediated disorder by using ordinary differential equations. The existence and stability of the model are established, where an applicable basin of attraction are calculated and examined. Some numerical simulations are presented to verify the proposed results and as changing parameter values given by sensitivity analysis, we show how to change dynamic behaviors of the model.

• Journal of Life Science
• /
• v.23 no.3
• /
• pp.448-461
• /
• 2013

Inflammatory bowel disease, known as Crohn's disease and ulcerative colitis, is an unexplained disease characterized by chronic inflammation that repeats a cycle of relapse, improvement, and complications. The cause of inflammatory bowel disease is not clearly known, but it is predicted that a complex of various factors precipitate its occurrence. In particular, inflammatory mediators, such as cytokine, induce an increase in cell-mediated inflammatory responses. Focal tissue damage then occurs in the intestinal mucosa because of the weakening of the immune-modulating functions of cotton. Immune and inflammatory responses do not decrease appropriately but continue until they lead to chronic inflammation. Current research has focused on the cytokine genes, which have important roles in these inflammatory responses. Cytokine is a glycoprotein that is produced mostly in activated immune cells. It connects the activation, multiplication, and differentiation between immune cells, which causes focal tissue damage and inflammatory response. Moreover, butyrate, which originates in dietary fiber and plays an important role in the structure and function of the intestinal area, shows control functions in the intestinal immune system by decreasing the proinflammatory cytokine and increasing the anti-inflammatory cytokine. Therefore, this research investigated the molecular mechanism of the anti-inflammatory effects of butyrate to comprehend the cytokine controlling abilities of butyrate in the immune cells. Butyrate is expected to have potential in new treatment strategies for inflammatory bowel disease.

• Clinical and Experimental Pediatrics
• /
• v.63 no.9
• /
• pp.337-344
• /
• 2020

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.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.16 no.1
• /
• pp.17-21
• /
• 2013

The gut mucosal barrier plays an important role in maintaining a delicate immune homeostasis. The pathogenesis of inflammatory bowel disease (IBD) is considered to involve a defective mucosal immunity along with a genetic predisposition. Recent views have suggested an excessive response to components of the gut microbiota in IBD. A condition of "dysbiosis", with alterations of the gut microbial composition, has been observed in patients with IBD. In this article, the author review recent studies of gut microbiota in IBD, particularly the importance of the gut microbiota in the pathogenesis of pediatric IBD.

• IMMUNE NETWORK
• /
• v.22 no.6
• /
• pp.46.1-46.25
• /
• 2022

T-helper-17 (Th17) cells and related IL-17-producing (type17) lymphocytes are abundant at the epithelial barrier. In response to bacterial and fungal infection, the signature cytokines IL-17A/F and IL-22 mediate the antimicrobial immune response and contribute to wound healing of injured tissues. Despite their protective function, type17 lymphocytes are also responsible for various chronic inflammatory disorders, including inflammatory bowel disease (IBD) and colitis associated cancer (CAC). A deeper understanding of type17 regulatory mechanisms could ultimately lead to the discovery of therapeutic strategies for the treatment of chronic inflammatory disorders and the prevention of cancer. In this review, we discuss the current understanding of the development and function of type17 immune cells at the intestinal barrier, focusing on the impact of microbiota-immune interactions on intestinal barrier homeostasis and disease etiology.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.11 no.sup2
• /
• pp.59-66
• /
• 2008

Genome-wide association studies using large case-control samples and several hundred thousand genetic markers efficiently and powerfully assay common genetic variations. The application of these studies to inflammatory bowel disease has led to the identification of susceptibility genes and affirmed the importance of innate and adaptive immunity in the pathogenesis of disease. Efforts directed towards the identification of environmental factors have implicated commensal bacteria as determinants of dysregulated immunity and inflammatory bowel disease. Host genetic polymorphisms most likely interact with functional bacterial changes to stimulate aggressive immune responses that lead to chronic tissue injury.

• Biomolecules & Therapeutics
• /
• v.29 no.6
• /
• pp.582-595
• /
• 2021

Researchers have endeavored to identify the etiology of inflammatory bowel diseases, including Crohn's disease and ulcerative colitis. Though the pathogenesis of inflammatory bowel diseases remains unknown, dysregulation of the immune system in the host gastrointestinal tract is believed to be the major causative factor. Omics is a powerful methodological tool that can reveal biochemical information stored in clinical samples. Lipidomics is a subset of omics that explores the lipid classes associated with inflammation. One objective of the present systematic review was to facilitate the identification of biochemical targets for use in future lipidomic studies on inflammatory bowel diseases. The use of high-resolution mass spectrometry to observe alterations in global lipidomics might help elucidate the immunoregulatory mechanisms involved in inflammatory bowel diseases and discover novel biomarkers for them. Assessment of the characteristics of previous clinical trials on inflammatory bowel diseases could help researchers design and establish patient selection and analytical method criteria for future studies on these conditions. In this study, we curated literature exclusively from four databases and extracted lipidomics-related data from literature, considering criteria. This paper suggests that the lipidomics approach toward research in inflammatory bowel diseases can clarify their pathogenesis and identify clinically valuable biomarkers to predict and monitor their progression.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.15 no.1
• /
• pp.13-18
• /
• 2012

The pathogenesis of inflammatory bowel diseases is not very well understood; it is currently thought to be caused by the interaction between genetic factors, environmental factors, intestinal microbes, and immune factors. Biological agents such as anti-tumor necrosis factor (anti-TNF) are widely being used as therapeutic agents. Infliximab, a chimeric monoclonal IgG1 antibody against tumor necrosis factor, has been demonstrated to have an effect in the induction and maintenance of remission in Crohn's disease in children. The effects of biological agents, typified by anti-TNFs, in inflammatory bowel disease in children; the recent concern on the administration of biological agents in combination with immunomodulators; and 'Top-down' therapy are some of the topics covered in this review.

• The Korean Journal of Physiology and Pharmacology
• /
• v.18 no.4
• /
• pp.279-288
• /
• 2014

Ulcerative colitis and Crohn's disease are a set of chronic, idiopathic, immunological and relapsing inflammatory disorders of the gastrointestinal tract referred to as inflammatory bowel disorder (IBD). Although the etiological factors involved in the perpetuation of IBD remain uncertain, development of various animal models provides new insights to unveil the onset and the progression of IBD. Various chemical-induced colitis models are widely used on laboratory scale. Furthermore, these models closely mimic morphological, histopathological and symptomatical features of human IBD. Among the chemical-induced colitis models, trinitrobenzene sulfonic acid (TNBS)-induced colitis, oxazolone induced-colitis and dextran sulphate sodium (DSS)-induced colitis models are most widely used. TNBS elicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response of Th-2 phenotype. DSS-induced colitis model also induces changes in Th-1/Th-2 cytokine profile. The present review discusses the methodology and rationale of using various chemical-induced colitis models for evaluating the pathogenesis of IBD.