All of us are likely to know someone who suffers from persistent pain -- it is a very common condition, which can be caused by sports injuries, various diseases and the process of ageing. Treatment options are limited and doctors are often unable to offer anything more than partial relief with painkillers, leaving their patients resigned to suffering.
While chronic pain can have many different causes, the outcome is often the same: an overly sensitive nervous system which responds much more than it normally would. However, a question still remains as to why the nervous system should remain in this sensitive state over long periods of time, especially in instances where the underlying injury or disease has gone.
Researchers from King's sought to answer this question by examining immune cells in the nervous system of mice, which are known to be important for the generation of persistent pain.
In the study, published today in Cell Reports, they found that nerve damage changes epigenetic marks on some of the genes in these immune cells. Epigenetics is the process that determines which gene is expressed and where. Some epigenetic signals have direct functional consequences, while others are just primers: flags that indicate a potential to act or be modified.
Comment: The human genome is astonishingly complex and dynamic, with genes constantly turning on or off, depending on what biochemical signals they receive from the body. When genes are turned on, they express proteins that prompt physiological responses elsewhere in the body. Epigenetic modifiers have the ability to alter gene activity simply by blocking or not blocking the genetic code as it's being copied, meaning that our genes are not set in stone. The expression of specific genes is not just determined by our DNA, but also by our lifestyle and thus exercise, improving diet and decreasing stress can help regulate our genetic expression.