Other studies have linked specific strains ...

The exact cause of Crohn's disease remains unknown, although more and more details appear. The study clearly showed that the disease has a genetic component, it is inherited, and those of his brother with the disease 30 times more likely to develop than normal people. Some ethnic groups, especially Eastern European Jews, appears to be genetically

through genetic mutations in the gene CARD15 (also known as NOD2 gene). However, people who have mutations have a very low probability (approximately 1:200) getting the disease.

In earlier studies, only two genes were associated with Crohn's, and scientists believed that humans with mutations in these two genes, different pathogenic bacteria can directly cause disease. The disease manifests itself in now is much more complicated than that. In contrast to the classical view of Crohn's, like, in which the immune system goes into overdrive, other, more recent hypothesis about the origin of disease - based on the above facts - is that Crohn's patients are born with genetic mutations that, combined with a perfect storm of factors environment is actually the mechanism of the immune system down. Thus, this innate immune deficiency in which the body compensates for the decrease in immune system function through the development of adaptive immunity in the form of excessive cytokine responses, Th1. In some cases, the side effect that adaptive immunity is a chronic inflammation of the intestine. In particular, people with Crohn's disease, genetic mutations lead to a protective layer of mucus on the walls of the gastrointestinal tract, underdeveloped or abnormally thin and weak. Different organisms use their hosts weakened by multiplying the mucosa in large quantities, and, consequently, Crohn's patients have a hard time clearing bacteria from the intestinal wall and produce more cytokines to combat them, thereby causing inflammation of the intestine. Simply put, healthy people, there are millions of bacteria in the digestive system to help them process the food they eat. Their immune system to keep these helpful intestinal bacteria in check, not allowing them to spread to other parts of the body where they can cause more harm than good. Crohn's patients have the same intestinal bacteria, as healthy people, but their immune system is too weak to prevent these germs multiply in the gut until they cause chronic inflammation. The latest gene to be implicated in Crohn's disease is ATG16L1, which can cause autofahiyi and prevent suits ability to attack invasive bacteria. As a result, the bacteria multiply in the intestines and cause inflammation. More evidence for this hypothesis that Crohn's disease results not from overactive immune response, and in violation of secretion of cytokines by macrophages, resulting from mutations in ATG16L1. When the researchers combined the results of genetic data with direct patient assessment of immunity, they found that patients Crohn born with weak immune systems of higher than normal probability of failure. Scientists now believe that there are over thirty genes that play a role, or causing Crohn directly or acting as a mediator variable that increases the likelihood of other genes that cause disease. For example, anomalies in the XBP1 gene have recently been identified as a factor pointing to the role of proteins deployed by reaction of endoplasmic reticulum in lasix purchase inflammatory bowel disease. Other studies have shown that Mycobacterium paratuberculosis subspecies mycosis plays an important role in Crohn's disease, in particular, because it causes a similar disease, sickness Jones cattle. Mannose bearing antigens (mannins) of yeast can cause the immune response. Other studies have linked specific strains of enteroadherent E. coli to the disease. However, the relationship between certain types of bacteria and Crohn's disease remains unclear. One group of scientists found that some features common to Crohn's disease, ulcerative colitis and irritable bowel syndrome may have the same reason. All three groups of patients in the study were colon with abnormally high levels of serine protease, a chemical which, when injected into experimental mice results in mice experiencing the same painful symptoms associated with irritable bowel syndrome and colitis in humans. The authors of this study did not show why the additional protease was. Although the genetic link to Crohn's was found, genetic abnormalities do not cause disease themselves. Environmental factors are also important. For example, the relatively high prevalence of Crohn's disease in industrialized countries may be associated with a diet rich in protein and dairy products. Among patients Crohn's, smoking appears to increase the risk of outbreaks or recurrence of Crohn's symptoms after a period of remission. In the United States in the 1960s, after birth control pills and other hormone-based contraceptives have become common, there was a sharp increase in incidence of Crohn's disease. Do not scientists have not demonstrated a statistically significant link between the contraceptive pill and Crohn's, but many suspect, however, that these products violate the digestive system very similar to smoking. Another interesting statistical correlation between the advent of refrigeration in the United States and various parts of Europe and the growth of the disease. More recent studies have supported this hypothesis. .