The Black Death and the Modern Link to Autoimmune Diseases

Drain C.

Genetics, Stockton University

https://www.bbc.com/news/health-63316538 

During the 1300s, the deadliest plague was raging across Europe, killing approximately 200 million people in its path. Medicine was merely a thought and there was really no true way of fighting off this deadly disease. But somehow people managed to survive. For those who have managed to survive the plague, studies have found a mutation on the endoplasmic reticulum aminopeptidase 2 gene.  Not saying that everyone who had this mutation survived, but those who had the mutation were 40% more likely to survive. That's great! 

But, in modern day health and science studies have found that same exact gene mutation is causing an increase in autoimmune diseases such as Crohn's disease. The same mutation that basically eliminated the deadliest plague, is now the cause of other silent diseases. While causing an overabundance in the enzymes that destroy the unhealthy cells, the enzymes attack the healthy cells too. ERAP2 does not have an off function, so it will continue to produce enzymes that negatively affect the body. Treatments for specific auto immune diseases include an increase of ERAP2 inhibitors. 

 

Auto-immune diseases are often categorized as the infected immune cells targeting and attacking the healthy cells or organs. Initially auto immune diseases were thought to be inked to stress, but with recent studies there have been additional linkages to genetics and an outside surrounding environment. Your body is supposed to remove the infected cells, but to an auto-immune disease there is no differentiation of what a healthy cell and an unhealthy cell looks like. Unfortunately, everything is caught in the cross-fire and every cell is attacked. This article is saying that although genes are a factor to an auto-immune disease, that is not the final be all. There can be people in your family that do not have the linked gene but you could, or vise versa. Having an auto-immune disease may not be entirely inheritable. Scientists and researchers are still looking into the causes and effects of autoimmune diseases.  

https://www.hopkinsmedicine.org/health/wellness-and-prevention/autoimmune-disease-why-is-my-immune-system-attacking-itself

New inflammation inhibitor discovered

Researchers at Karolinska Institute in Sweden have developed a new type of drug molecule that inhibits inflammation. The drug acts on a protein that is believed to be the cause for how inflammation arises in cells. This discovery was a result of Dr. Thomas Helleday's work on how DNA is repaired by the body. His initial objective during his research was to fight cancer by targeting damage to the tumor cells DNA. When developing a molecule for inhibiting the enzyme that repairs oxygen damage to DNA, the researchers found out that it also lowered inflammation. They discovered that the enzyme OGG1 triggers inflammation. Thus, the inhibitor they had developed blocks the release of inflammatory proteins, such as TNF alpha. In preliminary trials on mice with pulmonary disease, the researchers identified a decrease in inflammation. They are now developing a specific inhibitor for OGG1 and examining whether it can lead to new treatments for inflammatory diseases such as Crohn's Disease.

First, this shows that you should interpret and examine all of your data because you never know when you will discover something new by accident! On another note, one of my best friends suffers from Crohn's disease daily, so it is nice to hear they are developing different types of drugs that could potentially be effective in treating Crohn's. He currently takes a Humira shot every week to help treat his disease but it often leaves him feeling sick for a few days. It would be interesting to see if this new treatment has any side effects that are similar to Humira and to see if it could possible be a once of year kind of treatment. It could also be possible that it is a possible cure because if the inhibitor never degrades, then it would just continuously inhibit the inflammatory proteins.

Crohn's genes make cells deaf to messages from beneficial gut bacteria

Crohn's disease is an inflammatory bowel disease that affects the gastrointestinal tract.  Crohn's mainly affects the ileum of bowel and the start of the colon.  In addition, Crohn's disease can impact any part of the gastrointestinal tract.  An individual with Crohn's disease typically suffers an enlarged intestinal tract.  Currently, Crohn's disease is thought to be a genetic disease that is affected by environmental factors like stress and diet.  It tends to affect people with European backgrounds.

Recent studies suggest that beneficial bacteria might have no effect in patients with Crohn's.  Defective genes block microbial messages to immune cells that would normally prohibit damage to the intestinal tract.  Patients with Crohn's disease actually experience an increased immune response, causing chronic inflammation.  The inflammation is linked to approximately 200 genes, including ATG16L1 and NOD2.  Mice with these defective genes are unable to effectively utilize good bacteria to reduce gastrointestinal inflammation.  Luckily, some genes are responsible for killing bad bacteria also work to suppress the immune system when necessary.  So, this prevents Crohn's disease from going out of control.

Crohn's disease is clearly a detrimental disease, but research does offer some silver linings.  If there are genes that can suppress the immune system efficiently, it seems as though there are potential ways to reduce Crohn's effects.  It is also possible that the same genes could be used for other gastrointestinal diseases like ulcers.

Genetic Links to Gastrointesitinal Disorders

A recent study on Crohns disease and colitis, both autoimmune disorders of the gut, found that the diseases were genetically linked. Crohn's disease and colitis are both contributors to Inflammatory Bowel Disease, where colitis only effects the colon and Crohns may effect any of the gastrointestinal regions. Dr. Ramnik Xavier, one of the authors in this study stated that, “We used genome-wide association studies in combination with fine mapping tools ... to identify genetic factors that either increase or decrease the risk for developing these diseases".



These diseases have been heavily studied and only a couple of genes had previously been linked to these diseases. As of recently though, about 163 loci have been related to these diseases, with close to 71 of these loci being contributed from this study alone. With data from his own lab and team, Xavier was able to identify several pathways in which these genes were associated with these diseases and thanks to the help of different labs the specific genes linked to these conditions were identified. An observation that the researchers made was the the genes associated with IBD diseases also contributed to risk of type-1 diabetes and psoriasis. It is in hope that through the results of this study, further measures can be taken to help identify specific clues to understanding disease pathogenesis.

Article:      http://www.thecrimson.com/article/2012/11/9/gut-diseases-genetics/

Sub-Article:       http://www.news-medical.net/news/2007/04/17/23647.aspx