Inflammatory Bowel Disease and Industrialization Essay

Crohn’s Disease was named after an American gastroenterologist, Dr. Burrill Bernard Crohn, in 1932. He and his colleagues discovered an abnormal pathogen, Mycobacterium paratuberculosis while studying a related disease, ulcerative colitis, which belongs to a larger group if illnesses called Inflammatory Bowel Disease (IBD). The discovery was made while studying the effects of ulcerative colitis in cattle and noticing the similar characteristics in humans. The infections had an abnormal response with the body’s immune system in both the cattle and humans.

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.

Crohn 's disease is one of two conditions referred to by the term "Inflammatory Bowel Disease" (IBD). The other condition that is referred to as an IBD is called Ulcerative Colitis. Both Crohn’s and Ulcerative Colitis are conditions that cause recurring or persistent inflammation in one or more sections of the intestine. The literal definition of "inflammation" is "being set on fire". It is a protective reaction that happens when tissue is injured or destroyed. There are two types of inflammations. The first is acute inflammation, which is defined by heat, redness, pain and swelling. The

An inflammatory bowel disease is characterized by intermittent and recurrent abdominal pain associated with ulceration in bowel function. Inflammatory bowel disease is a group of chronic disorders that cause inflammation or ulceration in the small and large intestines. Most often, inflammatory bowel disease is classified as ulceration colitis or Crohn’s disease but may be referred to as colitis, enteritis, ileitis, or proctitis (Crohn's disease-website).

Crohn's disease, also known as inflammatory bowel disease (IBD) is simply an inflammation of the digestive tract, which includes your mouth, esophagus, stomach, small and large intestine, rectum and anus. Additionally, many individuals mainly encounter pain and/or irritation in the small intestine. Unlike other digestive health concerns, this disease affects some regions of the tract. Unfortunately, there is no cure for Crohn's disease, it is considered a chronic condition; long lasting. Medication is provided to help relieve pain and discomfort, oftentimes patients experience irregular symptoms. For instance, they may have no pain or they may have heavy pain.

The immune system responds by sending out cells throughout the blood stream to fight the bacteria. This causes inflammation, which is a normal reaction to this response. However, in a person with Crohn's, the inflammation is severe and very persistent. This inflammation stretches deeply into the bowels, thus causing major problems and deeply scarring all layers of the lining. It is the relentless inflammation that triggers the symptoms of Crohn's. The inflammation is most common in the ileum, or the lowermost portion of the small intestine (hence the original name Regional Ileitis). Although

Crohn’s disease (CD) involves the entire alimentary tract and is characterized by focal exacerbations, with intermittent activity throughout the patient’s life. The etiology of Crohn’s disease (CD) remains largely unexplained, but there have been major advances in recent years concerning the pathogenic mechanisms underlying intestinal inflammation. There is a multifactorial character of the disease, in which a genetic predisposition, the external environment, intestinal microbial flora, and the immune system are all involved. Systemic symptoms include unexplained fever, weight loss, and extraintestinal symptoms such as arthralgias and perianal abscess. Delays by the patient in seeking medical help and by the physician to identify the disease

Inflamed tissues from Ulcerative Colitis (UC) patients show increased oxidative and nitrosative damage, leading to accumulation of mutations and dysplastic progression27,28. Infiltrating leukocytes from these patients have increased ROS production in basal conditions and in response to different ligands29. Since TLR4 mediates ROS production in leukocytes22, it is easy to speculate that immune cells drive pro-tumorigenic effects of TLR4. However, bone marrow-transfer experiments in our lab demonstrate that non-immune TLR4 participates in development of neoplasia8. Furthermore, we have shown that epithelial TLR4 activation predisposes to colitis and CAC6. To understand the role of epithelial TLR4 in neoplasia, our research has focused on the

The immune system is the one that causes the inflammation in response to what is happening to the persons body. Having this inflammation would cause flare ups depending on what food you eat, leaving you with very frequent trips to the bathroom and severe abdonminal pain. Also, constantly having diarrhea can cause dehydration and make your appetite decrease as well. Crohn's disease does have some genetic link. According to the case study in class, antibiotics can sometimes trigger this response in the persons GI tract because it throws off the bacteria in our digestive system and we need that

Inflammatory bowel disease (IBD) can be defined as the chronic condition (it is persistent/ long-standing disease) resulting from inappropriate mucosal immune activation. Inflammatory bowel disease (IBD) can start at any age. However, it is frequently seen among teenagers And also among young adults in their early twenties, both genders can be affected by this disease. There are two conditions that traditionally comprise inflammatory bowel disease (IBD): Ulcerative colitis and crohns disease. Comparison between Ulcerative colitis and crohns disease are clinically useful, because distinguishing between the two conditions allow specialists to choose the right management way. Comparison between Ulcerative colitis and crohns disease are

A UC can be easily induced in animals by administering either the chemicals or bacterial infection. [46]. An ideal experimental model should mimic human UC quite closely, simple to induce, cheap and highly reproducible. Unfortunately, human UC is so complex that there is no single model that fully imitates it [46] but every model of colitis contributes valuable observations into one or another major aspect of the disease, and together they have provoked the formation of now a generally accepted set of the principle of human UC pathogenesis [59]. Amongst that different causes of induced or genetically based inflammation give rise to a limited number of common pathways of immunopathogenesis; normal resident gut microbiota can lead to an intestinal inflammation; loss of oral tolerance and alteration of the epithelial barrier contribute to the development of intestinal inflammation; and polarized T helper cell responses, as well as defects in innate immunity, mediate disease [12].

Schenk, Bouchon, Seibold, and Mueller hypothesized that patients with active irritable bowel diseases have upregulated TREM-1 expression on intestinal macrophages, which could contribute to excessive inflammation and tissue destruction. Through analysis of mice induced with IBD, they found that there was a five-fold increase in frequency of TREM-1 expressing macrophages. Expanding on the idea of TREM-1’s association with pathology, Schenk, et al, explored the extent of TREM-1 expression in relation to the severity of IBD. While IBD remained in remission, TREM-1 mRNA was “nearly undetectable” through PCR, but 3-5 days after inducing the pathology, the mRNA was highly upregulated. This proves that the TREM-1 expression is directly correlated with the increase of inflammatory responses.

The term Inflammatory Bowel Disease (IBD) is a general name given to a few disorders that all fall under the category of inflamed intestines (they become red and swollen.) This is usually due to a reaction the body causes against its own intestinal tissue. The two most common types of Inflammatory Bowel Disease are Ulcerative Colitis (UC) and Crohn’s Disease (CD). Crohn’s disease can affect any part of the gastrointestinal tract; however, it more commonly affects the small intestine or colon.

In patients with IBD (European Journal of Immunology 2012 & Human Immunology paper) and in experimental murine T cell transfer models of colitis ( American Journal of immunology), environmental stimulants to the cells of the mucosal immune system (such as commensal microorganisms) have been shown to elicit pro-inflammatory and anti-inflammatory cytokine production. The figure below effectively shows the crucial transcription factors and cytokines generated by the T helper cell subsets in IBD-affected mucosa, also portraying significance of individual cell response pathways. Inflammation in IBD is caused by the loss of homeostasis between CD4+ CD25+ Foxp3+ regulatory cells (Treg) and proinflammatory effector Th17 cell, therefore the role

Inflammatory bowel disease (IBD) is a group of chronic inflammatory diseases of the intestine, including ulcerative colitis (UC) and Crohn’s disease (CD), which is caused by a combination of mucosal barrier disruption, immune system activation and dysbiosis of the intestinal microbiota. Greater than 66 animal models have been used to study IBD and can be classified into chemically-induced, cell transfer, mutant and genetically engineered models1. Each model induces IBD through specific mechanisms involving the immune system, physiological and pathological processes that lead to chronic intestinal inflammation. These