scholarly journals Immunological Aspect in Inflammatory Bowel Disease

2021 ◽  
Vol 9 (F) ◽  
pp. 708-711
Author(s):  
Darmadi Darmadi ◽  
Riska Habriel Ruslie
Keyword(s):  
Inflammatory Bowel Disease ◽  
Chronic Inflammation ◽  
Bowel Disease ◽  
Molecular Mimicry ◽  
Disease Incidence ◽  
Intestinal Barrier ◽  
Male Predominance ◽  
Inflammatory Bowel ◽  
External Risk ◽  
Antigen Presenting

Inflammatory bowel disease (IBD) is a chronic inflammation in the alimentary tract due to improper immune response toward external and internal antigens. The disease consists of 2 entities: ulcerative colitis (UC) and Crohn’s disease (CD). The disease’s prevalence is increasing worldwide due to westernization and industrialization. Europe still holds the highest prevalence of IBD in the world. There are 2 peaks of disease incidence. The first is in the third decade of life and the second is in the fourth decade. Slight male predominance is observed in IBD. Internal and external risk factors play important role in the occurrence of IBD including genetic, smoking, reduced fibre intake, less or absent breastfeeding, sedentary occupation, pollution exposure, and medications. The disease carries heavy economic burden and hampers patient’s quality of life. The immune concept of IBD was hypothesized in 1950s since the symptoms resolved with the administration of steroid. Innate and adaptive immune systems are involved in the pathogenesis of IBD. Antigen presenting cells are found hyperactive, intestinal barrier is disrupted, and autophagy activity is increased. Molecular mimicry occurs between foreign and self antigen. The activity of T helper (Th)1, Th2, and Th17 is amplified while regulatory T cell’s activity is suppressed. Pro-inflammatory cytokine production is elevated but anti-inflammatory cytokines is lowered. Finally, there is increased immunoglobulin G level in intestinal mucosa and imbalance of gut microorganism. All the above immune disturbances lead to chronic inflammation in IBD.

scholarly journals The Role of Ethnicity in Inflammatory Bowel Disease

2021 ◽  
Vol 9 (F) ◽  
pp. 342-346
Author(s):  
Gontar Alamsyah Siregar ◽  
Darmadi Darmadi ◽  
Riska Habriel Ruslie
Keyword(s):  
Inflammatory Bowel Disease ◽  
Genetic Susceptibility ◽  
Chronic Inflammation ◽  
Digestive Tract ◽  
Bowel Disease ◽  
Intestinal Barrier ◽  
Preventive Measure ◽  
Disease Course ◽  
Genetic Characteristics ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a chronic inflammation of the digestive tract which consists of ulcerative colitis and Crohn’s disease. The disease is previously recognized as a disease of Western countries but later it spreads all over the world across every ethnicity. The disease manifestations vary from intestinal to extra-intestinal manifestations. There are two risk factors related to the incidence of IBD: Internal and environmental factors. The internal factor is related to genetic susceptibility and genetic susceptibility is associated with ethnicity. Subject from Black ethnic has higher risk for suffering from IBD. Caucasians even have the lowest incidence compared to other ethnics. The disease course is also worse in Black and Hispanic ethnics. Asians have milder disease course. Immigrants tend to have higher risk for IBD compared to native subjects. Further investigations showed that ethnicity carries variable genetic characteristics which affect immune activity, intestinal barrier integrity, and autophagy. All the above mentioned will elicit inflammation if being unbalanced. Chronic inflammation particularly in digestive tract leads to IBD. Knowledge regarding the tendency of IBD in several ethnics raises awareness and will initiate earlier preventive measure against IBD.

scholarly journals Mucin-2 knockout is a model of intercellular junction defects, mitochondrial damage and ATP depletion in the intestinal epithelium

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Mariya A. Borisova ◽  
Kseniya M. Achasova ◽  
Ksenia N. Morozova ◽  
Evgeniya N. Andreyeva ◽  
Ekaterina A. Litvinova ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Chronic Inflammation ◽  
Knockout Mice ◽  
Bowel Disease ◽  
Intestinal Barrier ◽  
Mitochondrial Damage ◽  
Leaky Gut ◽  
Mucin 2 ◽  
Inflammatory Bowel

AbstractThe disruption of the protective intestinal barrier—the ‘leaky gut’—is a common complication of the inflammatory bowel disease. There is limited data on the mechanisms of the intestinal barrier disruption upon low-grade inflammation characteristic of patients with inflammatory bowel disease in clinical remission. Thus, animal models that recapitulate the complexity of chronic intestinal inflammation in vivo are of particular interest. In this study, we used Mucin-2 (Muc2) knockout mice predisposed to colitis to study intestinal barrier upon chronic inflammation. We used 4-kDa FITC-Dextran assay and transmission electron microscopy to demonstrate the increased intestinal permeability and morphological defects in intercellular junctions in Muc2 knockout mice. Confocal microscopy revealed the disruption of the apical F-actin cytoskeleton and delocalization of tight junction protein Claudin-3 from the membrane. We further demonstrate mitochondrial damage, impaired oxygen consumption and the reduction of the intestinal ATP content in Muc2 knockout mice. Finally, we show that chemically induced mitochondrial uncoupling in the wild type mice mimics the intestinal barrier disruption in vivo and causes partial loss of F-actin and membrane localization of Claudin-3. We propose that mitochondrial damage and metabolic shifts during chronic inflammation contribute to the leaky gut syndrome in Muc2 knockout animal model of colitis.

scholarly journals Class A1 scavenger receptors mediated macrophages in impaired intestinal barrier of inflammatory bowel disease

2020 ◽  
Vol 8 (4) ◽  
pp. 106-106 ◽  
Author(s):  
Chenxi Xie ◽  
Yanyun Fan ◽  
Yinshi Huang ◽  
Shuangting Wu ◽  
Haimei Xu ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Barrier ◽  
Scavenger Receptors ◽  
Inflammatory Bowel

NOD-Like Receptors: Guardians of Intestinal Mucosal Barriers

Physiology ◽  
2015 ◽  
Vol 30 (3) ◽  
pp. 241-250 ◽  
Author(s):  
Anne-Kathrin Claes ◽  
Jun Yu Zhou ◽  
Dana J. Philpott
Keyword(s):  
Inflammatory Bowel Disease ◽  
Pattern Recognition ◽  
Potential Function ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Immune Defense ◽  
Intestinal Infections ◽  
Gut Homeostasis ◽  
Inflammatory Bowel

The NOD-like receptors (NLRs) are cytosolic pattern-recognition receptors, which are critically involved in mucosal immune defense. The association of the NLR, NOD2, with inflammatory bowel disease first pointed to the NLRs potential function as guardians of the intestinal barrier. Since then, several studies have emphasized the importance of NLRs in maintaining gut homeostasis and intestinal infections, and in shaping the microbiota. In this review, we will highlight the function of NLRs in intestinal inflammation.

Intestinal barrier integrity and inflammatory bowel disease: Stem cell‐based approaches to regenerate the barrier

2017 ◽  
Vol 12 (4) ◽  
pp. 923-935 ◽  
Author(s):  
Fredrik E.O. Holmberg ◽  
Jannie Pedersen ◽  
Peter Jørgensen ◽  
Christoffer Soendergaard ◽  
Kim B. Jensen ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Stem Cell ◽  
Bowel Disease ◽  
Intestinal Barrier ◽  
Barrier Integrity ◽  
Inflammatory Bowel ◽  
Intestinal Barrier Integrity

scholarly journals Inflammatory bowel disease: the role of inflammatory cytokine gene polymorphisms

2004 ◽  
Vol 13 (3) ◽  
pp. 181-187 ◽  
Author(s):  
Joanna Balding ◽  
Wendy J. Livingstone ◽  
Judith Conroy ◽  
Lesley Mynett-Johnson ◽  
Donald G. Weir ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Disease Incidence ◽  
Strong Association ◽  
Tnf Α ◽  
Genes Encoding ◽  
Inflammatory Processes ◽  
Inflammatory Bowel ◽  
Cytokine Gene Polymorphisms

THE mechanisms responsible for development of inflammatory bowel disease (IBD) have not been fully elucidated, although the main cause of disease pathology is attributed to up-regulated inflammatory processes. The aim of this study was to investigate frequencies of polymorphisms in genes encoding pro-inflammatory and anti-inflammatory markers in IBD patients and controls. We determined genotypes of patients with IBD (n=172) and healthy controls (n=389) for polymorphisms in genes encoding various cytokines (interleukin (IL)-1β, IL-6, tumour necrosis factor (TNF), IL-10, IL-1 receptor antagonist). Association of these genotypes to disease incidence and pathophysiology was investigated. No strong association was found with occurrence of IBD. Variation was observed between the ulcerative colitis study group and the control population for the TNF-α-308 polymorphism (p=0.0135). There was also variation in the frequency of IL-6-174 and TNF-α-308 genotypes in the ulcerative colitis group compared with the Crohn's disease group (p=0.01). We concluded that polymorphisms in inflammatory genes are associated with variations in IBD phenotype and disease susceptibility. Whether the polymorphisms are directly involved in regulating cytokine production, and consequently pathophysiology of IBD, or serve merely as markers in linkage disequilibrium with susceptibility genes remains unclear.

scholarly journals Thrombotic Complications in Inflammatory Bowel Disease

2019 ◽  
Vol 29 (2) ◽  
pp. 23-26
Author(s):  
A. V. Borota ◽  
A. A. Borota ◽  
E. V. Onishchenko
Keyword(s):  
Inflammatory Bowel Disease ◽  
Chronic Inflammation ◽  
Bowel Disease ◽  
Intestinal Wall ◽  
Coagulation Cascade ◽  
Coagulation System ◽  
Primary Disease ◽  
Prevention And Treatment ◽  
Thrombotic Complications ◽  
Inflammatory Bowel

The risk of thrombotic complications is known to be 3 times higher in patients with inflammatory bowel disease (IBD) than in healthy individuals, with the relative risk being 15 times higher during the periods of relapses. Aim. To study and generalize literature data available on the prevention and treatment of IBD thrombotic complications.Key findings. In the сonditions under study, the presence of chronic inflammation and increased bleeding of the intestinal wall is shown to activate the coagulation system, impair the fibrinolysis system and reduce the activity of natural anticoagulation mechanisms. The concentration of fibrinogen — a protein of the acute inflammation phase — increases significantly. This results in an imbalance of the blood coagulation system with a tendency to hypercoagulation, which significantly increases the risk of thrombotic complications and the disseminated intravascular coagulation syndrome. In turn, the activation of the coagulation cascade may trigger the inflammatory response, which eventually leads to the formation of a vicious circle between chronic inflammation and thrombosis. The pathogenesis of thrombosis in inflammatory colon diseases is a multifactor process, which remains to be understood.Conclusion.The management of patients with IBD in combination with thromboembolic complications requires an individual multidisciplinary approach. Taking into account the pathogenetic factors, the following options are possible in the prevention and treatment of thrombotic complications in IBD: strengthening the basic therapy of the primary disease; administration of prophylactic doses of anticoagulants under dynamic continuous laboratory control in the acute period using the methods of conservative therapy of thrombotic complications (elastic compression of the lower extremities) in the period of exacerbation of the primary disease.

scholarly journals Serum bile acid profiling reflects enterohepatic detoxification state and intestinal barrier function in inflammatory bowel disease

2009 ◽  
Vol 15 (25) ◽  
pp. 3134 ◽  
Author(s):  
Carsten Gnewuch ◽  
Gerhard Liebisch ◽  
Thomas Langmann ◽  
Benjamin Dieplinger ◽  
Thomas Mueller ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Bowel Disease ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Serum Bile Acid ◽  
Inflammatory Bowel
Sign in / Sign up

Export Citation Format

Share Document