The study was large in scale, drawing upon data from 50 research centers, led by Queensland University in Australia and QUT and Christian-Albrechts-University, Kiel, Germany. The basis of the study was to determine if serious inflammatory diseases are the product of environment or genetics (or a combination of the two). The outcome comes firmly down on a genetic connection.
Inflammation is a response by the human body to harmful stimuli, such as bacterial pathogens, damaged cells, or irritants. It is a complex and protective response, utilizing immune cells, blood vessels, and molecular mediators. Sometimes the body over-reacts and chronic inflammation occurs. This can lead to a host of diseases, including rheumatoid arthritis. The focus of the new study was with a set of serious autoimmune diseases.
The study drew connections between hundreds of genes and the following inflammatory disease: ankylosing spondylitis (a type of spinal arthritis), Crohn’s Disease and ulcerative colitis (both forms of inflammatory bowel disease), psoriasis, and primary sclerosing cholangitis. These diseases collectively affected around 3 percent of the global population.
The research data has shown the conditions occur because those affected share similar genetic backgrounds, based on a review of 86,000 people living in 26 countries. Those who had one of the inflammatory diseases were linked to one of 244 genetic variants. This means there are different diseases sharing genetic risk factors. The study trebled the number of genes thought to be involved (as identified from past research).
It is thought the genetic variants influence the bacteria present in the gut, leading to inflammation in joints, the liver or the gut. It is hoped the findings will form the basis of research into new treatments for the associate diseases and the development of therapeutic agents.
The research is published in the journal Nature Genetics. The research paper is titled “Analysis of five chronic inflammatory diseases identifies 27 new associations and highlights disease-specific patterns at shared loci.”
