Inflammatory bowel diseases (IBD) are chronic inflammatory disorders that contain two major entities: Crohn’s disease (CD) and ulcerative colitis (UC), both of which may affect the entire gastrointestinal tract. Recent evidence indicates that IBD results from an inappropriate inflammatory response to intestinal microbes in a genetically susceptible host. IBD is a lifelong disease that leads to serious complications and disability if not optimally treated. The prevalence and incidence of IBD markedly increased while since the beginning of the 21st century, IBD has been considered as one of the most prevalent gastrointestinal diseases. Since this illness involved an abnormal response to the body’s immune system, Creative Biolabs puts effort into the field of IBD research and we are glad to share our accumulated experience about the IgA in the pathologies of IBD with our partners all over the world.
Clinical Presentation of Inflammatory Bowel Disease
Ulcerative colitis (UC) and Crohn’s disease (CD) are classified as chronic inflammatory bowel diseases (IBD) which have similar symptoms while leading to digestive disorders and inflammation in the digestive system. While UC occurs limited in the inner of the colon or rectum, CD involved any segment of the gastrointestinal tract.
The inflammation of the intestinal mucosa in IBD is characterized by episodes of abdominal pain, diarrhea, bloody stools, weight loss, and the influx of neutrophils and macrophages that produce cytokines, proteolytic enzymes, and free radicals that result in inflammation and ulceration. IBD is rarely fatal, but can greatly affect the life situation because of pain, vomiting, and diarrhea. Moreover, the risk of colorectal cancer is increased as a serious complication of IBD.
Fig.1 Normal colon (left) and histological lesion in CD (middle) and UC (right). (Lemmens, 2014)
Pathogenesis of Inflammatory Bowel Disease
IBD appears to result from abnormal host immune responses to the intestinal microbiota while the intestinal microbiota is the major environmental driver of IBD. The villi and intestinal glands, along with the lamina propria, associated gut-associated lymphoid tissue, and muscular mucosae, constitute the essential features of the small-intestinal mucosa. However, genetic and environmental factors induce the disruption of tight junctions, causing increased permeability of the intestinal epithelium and increased uptake of commensal bacteria and microbial products, which leads to immune cell activation and cytokine, various interleukins, IgA or IgG, and TNF-α production. If acute mucosal inflammation cannot be resolved by anti-inflammatory mechanisms, chronic IBD develops.
Fig.2 Pathophysiology of inflammatory bowel disease. (Nunes, 2018)
Treatment of Inflammatory Bowel Disease
Up to 2017, over 1 million residents in the US are estimated to have IBD, with substantial costs of about $6 billion for health care. The first step in treating IBD is pharmaceutical treatments. Physicians usually prescribe medication stage by stage. The corticosteroids, aminosalicylates, and antibiotics are used to treat early IBD. The initial stage of IBD remedy is by applying anti-inflammatory drugs, patients with refractory medical disease, who develop complications such as abscesses or malignancy, or do not tolerate medical therapy are candidates for surgery.
Investigation shows a rise in the number of people with IBD, reflecting a need for more research to cure the IBD. If you are interested in the research of IBD, or for more details in the research of the therapeutic molecular field, please feel free to contact us.
References
- Lemmens, B.; et al. Inflammatory Bowel Diseases. Elsevier. 2014, 1297-1304.
- Nunes, S.; et al. Resveratrol and inflammatory bowel disease: The evidence so far. Nutrition research reviews. 2018, 31(1), 85-97.
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