The GIT is a complex environment involving constant interaction between microbiota (infectious & commensal), mucus layer, epithelial cell layer (made of diverse secretory cells), mucosal immune system (innate & adaptive cells), and lymphatic system (Peyer’s patches). Mucus layer and epithelial barrier prevent the direct interaction of the contents with underlying layers, but regulate/modulate the passage of contents across the intestinal barrier. IBD is characterized by intestinal inflammation of unknown etiology. Various theories have been proposed to identify the immune cells, microbiome and elucidate pathways leading to chronic intestinal inflammation. Three main theories35 were proposed & investigated as underlying causes for IBD inflammation - 1.Reaction to persistent inflammation in intestine, 2.Defective intestinal barrier to luminal antigens and 3.Dysregulated host immune responses to normal GIT contents. The mucosal immune system of GIT has co-evolved with several layers to maintain the fine balance between tolerance and vigilance.36 Mucosal immune system and microbial flora of GIT have co-evolved36 and development of mucosal immune cells is dependent upon the presence of specific microbial species without which differentiation & functioning of immune cells is affected. For example differentiation of Th17 cells is dependent upon presence of single species of segmented filamentous bacteria Candidatus arthromitus.38,39 in mice studies. Animal model studies have also
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The relationship between the human gut microbiome to health and disease is strong. Human physiology, metabolism, nutrition, and immune function are all affected by the composition of the gut. If the composition of the gut microbiome is altered in a way that any of these functions are negatively affected, this can lead to disease. The developments of the microbiome, its complexity, and its functionality in health and disease have been extensively studied. In addition, the way in which it is altered has many implications in the cause of diseases, such as bowel disease, obesity, diabetes and cancer.
Crohn’s disease (CD) is a systemic auto-immune disease that is marked by abnormal inflammation of the gastrointestinal (GI) tract, it affects any part of the GI tract from mouth to anus. CD mainly presents in three areas: the small intestine, the colon, and the perianal region. CD mostly occurs between the ages of 15 and 30 years, or between the ages of 60 and 80 years of age. The exact etiology of Crohn’s disease is unknown. As stated by Mazal (2014) “Genetic predisposition—especially familial aggregation—seems to be the strongest independent indicator of which individuals will develop Crohn disease” (p.298). An increase diet in milk protein, milk protein and polysturated fatty acids is also a possible factor in disease incidences. Smoking may also double the risk of developing CD.
This review will explain Crohn’s disease and Ulcerative colitis, two types of inflammatory bowel disease that affect millions of people. These diseases are chronic that affects certain parts of the intestine gastrointestinal tract. People who has this disease are troubled with a variety of side effects that they will have to live with for the rest of their lives. To this day, there are no medical cure for these diseases, however there are several treatment options that are helpful. These diseases are still being studied for researchers to fully understand the causes, possible preventions, and cure for IBDs. Countless researches and studies are still under development, there have been many discoveries thus far, but nothing concrete.
Crohn’s Disease is a chronic inflammation of the gastrointestinal (“GI”) tract that can occur anywhere along the alimentary canal from the mouth to the anus. It is the second most common form of Inflammatory Bowel Disease (“IBD”) after Ulcerative Colitis and can be hard to distinguish from it due to the overlapping signs and symptoms. They are not, however, the same. With Crohn’s Disease the inflammation most often occurs in the small intestine at the end of the ileum and continues into the beginning of the colon, but inflammation may be found in multiple places along the digestive tract at the same time with normal, unaffected areas in between the distended areas. Furthermore, the disease will spread through every
The patient was presented to me with diagnosed crohn’s disease, in remission stage. Crohn’s disease is a chronic inflammatory disease of the intestines. Primarily, it causes ulcerations in the small and large intestines but has been seen to affect the digestive system anywhere from the oral cavity to the anus. The disease has no known cure but once the disease begins it proceeds to vary between periods of inactivity (remission) and activity (relapse). The cause of crohn’s disease is unknown but from research it is suspected that infections by certain bacterium could contribute to the disease. The activation of the immune system in the intestines is seen to be of importance to patients with crohn’s. The immune system causes inflammation within the tissues where it occurs. In normal cases the activation occurs when the body is exposed to harmful invaders. With patients with crohn’s disease the immune system is abnormally activated in the absence of any invader, thus resulting in chronic inflammation and ulceration as seen in the figure below. The disease causes abscesses and a cobble stone appearance to the infected area in the body, this infection causes the immune system to activate in an inflammatory response.
Crohn’s Disease is an inflammatory disease that affects the digestive system. According to an international team of researchers, it is now believed that a fungus in the gut helps develop the disease. Researchers found that those with Crohn’s were more likely to have one type of fungus (Candida Tropicalis) and two types of bacteria in their body. It was found that the fungus and bacteria work together to create a bacteria that sticks to the intestines and cause it to become inflamed.
Crohn’s Disease is an intestinal disease first discovered by and named after Dr. Burrill B. Crohn, “who first described the disease in 1932 along with colleagues Dr. Leon Ginzburg and Dr. Gordon D. Oppenheimer.” (Foundation, 2015) Konkel (2015) refers to this disease as belonging “to a group of conditions called inflammatory bowel diseases (IBD)” (Konkel, 2015) CD is
The use of the first form of microbe-based therapeutics, probiotics, is beneficial for preventing disease. These live microorganisms are known to strengthen the equilibrium of the gut flora by the development of healthy gut
IBD is the result of an abnormal innate repsonce to antigens in the intestinal flora, thus activating the adaptive immune repsinse; a process in which genome wide stidues have implicated several genes such as NOD2 and ATG16L1, both involved in the intracellular processing of bacterial antigens. PSC has shown similar mechanisms characterized by Th1 cytokines and structuring. However, PSC has aslo shown close association with classic autoimmune diseases such as type 1 diabetes, rheumatoid arthiritis, and others; has shown a strong association with the human leukocyte antigen(HLA) DRB1*0301 haplotype; and has shown a variety of autoantigens to neutrophils and biliary epithelial cells (BEC). (1) Thus suggesting the immunopathogenesis of PSC is complicated and may have more than one cause.
Crohn’s disease is an inflammatory condition that is immunologically mediated. Even though the etiology of the disease is not yet determined, results from different researches such as human genetics, clinical tests and basic science have given significant insights in the inflammatory disease pathogenesis. In addition, the studies reports that Crohn’s disease is heterogeneous disease that is characterized by different genetic abnormalities that results to T cells responses. The research paper has highlighted various signs of the disease that indicates that T cells usually response to the environment. For instance, the paper states that T cells are important to an individual’s immunity and has both protective and harmful immune response. The research paper has a purpose statement that provides the theme or the question that is being examined in the paper. The paper also reviews both the Crohn’s mechanism and the assumed pathophysiological mechanisms. Assumed pathophysiological mechanisms include intestinal permeability, infectious agents, pro-inflammatory moles and the abnormal immunological response. On the other hand, signs and symptoms of the Crohn’s disease include diarrhea, weight loss, abdominal pain and fever.
Crohn’s disease (CD) is a life-long, chronic, idiopathic inflammatory condition of the intestines that is characterized by frequent symptomatic relapse and remission. It involves inflammation and ulceration of various regions of the gastrointestinal tract (GI tract) lining, which often extends deep into the layers of the affected areas. The associated inflammation and ulceration of the disease affects various segments of the intestines with unaffected bowel occuring between the diseased areas. CD can involve any area of the GI tract, ranging from the mouth to the anus. However, it frequently affects the jejunum, terminal ileum (regional enteritis), and proximal colon (granulomatous colitis) (Schub, 2016).
Crohn’s disease (CD) is an Inflammatory bowel disease (IBD), which is caused by the inflammation of gastrointestinal (GI) tract. IBD is known as the complex disease and the mechanism of progression remains as secret. Microbial imbalance expected to be the main cause of the inflammation. Gut microbiota takes a crucial importance in the intestinal diseases. Patients affected with the IBD are expected to have reduced biodiversity of commensal bacteria, such as Bacteroidetes and Firmicutes. Additionally, individual’s with CD were preassigned for antibiotics in between 2-5 years before diagnosed for CD rather than unaffected persons. Up to date, the medical treatment methods, which were using are immunosuppression medicals like prednisone, azathioprine,
There are currently two tumour necrosis factor alpha (TNFα) antagonist available on the PBS for treatment of IBD: infliximab and adalimumab.1 Another biological is vedolizumab which is a gut specific humanised monoclonal antibody that binds to and inhibits α4β7 integrin expressed on the surface of lymphocytes preventing their binding to mucosal addressin cell adhesion molecule-1 expressed on vascular endothelial cells within the GI tract.16 Blocking this binding prevents lymphocyte migration into intestinal tissue thus reduce inflammation.16 Lastly, the most recent approved biological agent by PBS is
For instance, Crohn’s disease(CD) is a chronic relapsing inflammatory bowel disease (IBDs), which affect the various areas of GI tract (from mouse to anus) and lead to abdominal cramps, weight loss, diarrhea, fever and the other symptom. According to the survey, Crohn’s disease was found to be more common in developed industrialized countries than less developed tropical countries because people who lived in developed areas have less chance of exposure to helminthes. Therefore, although the cause of Crohn’s disease is not fully understood, but it is consider to be related to environmental, genetic factor and autoimmune reaction. Medically speaking, Crohn’s disease is classified as an autoimmune disorder. Usually, there are many harmless and
IgA antibodies play a major role in maintaining homeostasis at mucosal surfaces including the gastrointestinal tract (Brandtzaeg, 2013; Gutzeit et al., 2014). Peyer’s patches (PP) are critical inductive sites in the mammalian small intestine where naïve B cells are initially activated by exogenous luminal antigens and then differentiate with T cell help into IgA plasmablasts that circulate in the blood before preferentially homing to the intestinal lamina propria to become resident IgA-secreting plasma cells (Cebra et al., 1998; Macpherson et al., 2008). High local concentrations of TGF-β and retinoic acid and the presence of IL-21-producing follicular helper T (Tfh) cells are all factors that promote IgA class switching in PP (Cao et al., 2015; Cerutti, 2008). Many of the dimeric SIgA antibodies produced by lamina propria IgA-secreting plasma cells are transcytosed across the epithelial layer and bind to commensal enteric bacteria after reaching the lumen (Benckert et al., 2011). SIgA directed against bacterial antigens has a variety of effects that help to shape gut microbial populations including immune exclusion from the inner mucus layer, inhibition of bacterial motility, impairment of bacterial fitness and neutralization of toxins (Cullender et al., 2013; Gutzeit et al., 2014; Peterson et al., 2007). A high level of bound IgA on gut resident bacteria may flag those commensal bacteria with a propensity to elicit a strong host immune response and induce