A recent study has revealed a groundbreaking discovery, the presence of M cells in the lining of the gut that can aid in protecting the body against prion infections.
Recent medical investigations into the various conditions that impair and damage the brain have provided insightful explanations as to why certain individuals and animals are a greater risk for developing certain brain conditions.
This new study reports the entire process of how prion diseases first contaminate the meat, and also, how the disease begins to infect the gut when this contaminated meat is consumed. There are various kinds of prion diseases, of which bovine spongiform encephalopathy (BSE) is prevalent amongst cows, and Creutzfeldt-Jakob disease (vCJD).
Researchers conducted a study on mice that revealed that M cells, which are specialized cells lining the gut, can aid in determining whether the infection can take hold on the gut or not. Research reveals the interplay of certain factors that tend to affect the presence of M cells in the lining of the gut. These factors include ageing, inflammation and infection, and they tend to increase an individual’s risk of developing prion diseases after eating contaminated meat.
M cells are present in the lining of the gut and they are one of the defense that your body utilizes to combat against infections and bacteria. M cells play a pivotal role of taking material throughout the lining of the gut when all the other cells in the immune system are awaiting a response. The researchers discovered that prions utilize M cells in order to attack the body and spread the infection within the gut. Since mice do not have M cells lining their gut, their bodies are entirely resistant to prion infections.
The research further reveals that individuals who tend to have a greater number of M cells present in the lining of their gut tend to have a ten times greater risk of contracting prion diseases. The results provide ample evidence to support the claim that in the majority of prion infection cases found in youngsters are caused by the fact that young individuals tend to have a greater quantity of M cells lining their gut as compared to old and elderly individuals.
Prion proteins spread the infection with the help of M cells, which aid the infection in crossing the lining of the gut, and causing the infection to spread all over the gut. The research further claims that if there are other infections in the gut, for instance Salmonella, its presence increases the risk of the development of the infection caused by prion proteins.
Prion diseases, which have also been the medical term of Transmissible spongiform encephalopathies (TSEs), are basically infections that impair and damage the brain, and these diseases tend to affect both animals and people. This infection is caused by bizarrely shaped proteins that enter the body when an individual consumes contaminated meat.
Earlier researches that attempted to study the prion diseases concluded that in order for the prion infection to spread to the brain, the infectious proteins first need to accumulate inside the M cells present in the lining of the small intestine, also known as Peyer’s patches.
Prion diseases include, BSE amongst cows, vCJD amongst humans, chronic wasting disease amongst deer and scrapie amongst sheep. They all are responsible for causing serious neurological damage, such as personality changes, problems in moving body parts, and memory dysfunctions, along with severe and extensive nerve damage.
The research has been conducted by Professor Neil Mabbott at the Roslin Institute, a medical research department at the University of Edinburgh. The aim of this research is to understand and examine how the infectious prion proteins manipulate and use the M cells and succeed in spreading the infection within the small intestine.
If medical science can succeed in creating a treatment or medication that can prevent this influence exerted by the prions upon the M cells, it can lead to the discovery of a preventive method for curing prion diseases amongst humans and animals.