People with chronic fatigue syndrome (CFS) may suffer from a dysfunctional cell receptor in their immune cells, a study in Clinical and Experimental Immunology has reported. The finding confirms earlier research that CFS is a biological condition, not a psychological one, and opens lines of inquiry for potential treatment options.
The transient receptor potential melastatin subfamily 3 (TRPM3) is one of the most primitive receptors in the body, Professor Sonya Marshall-Gradisnik told IFLScience. It's activated by a wide variety of agents, from bacteria and viruses to temperature and environmental factors such as perfumes. This diversity made it a logical suspect for a condition like CFS that has so many different triggers in different people.
Marshall-Gradisnik compared TRPM3 receptors in natural killer cells in blood taken from 15 people with CFS and 25 healthy controls, finding that TRPM3 levels were much lower in those with CFS. TRPM3 is an ion channel, controlling the way calcium ions are transmitted between cells and carrying instructions in the process. In some circumstances, CFS patients' cells showed much higher calcium ion flux, providing a possible explanation for CFS symptoms.
CFS patients have suffered a triple burden. In addition to the incapacitating nature of the disease itself, both the lack of clear tests and the difficulties of diagnosis have led to the condition being widely labeled “all in the mind”, or even fake. Moreover, with such diverse symptoms and so little known about the cause, treatments are hard to produce. Desperate patients sometimes turn to remedies co-author Professor Don Staines of Griffith University described to IFLScience as “lacking experimental evidence.”
Last year, Marshall-Gradisnik and Staines published work showing that the blood of people with CFS carry distinct biomakers. They are hoping to turn these into a reliable and affordable test for the condition, which will help those who suffer from it rebut those who disbelieve them and make it easier to test whether treatments are working.
Meanwhile, the identification of TRPM3's role offers opportunities to test treatment options in the lab. Staines told IFLScience that if it was shown that expensive drugs touted for use against CFS don't work even in vitro, it could help people stop wasting money on things that provide no benefit. Moreover, with many drugs already existing that affect the functioning of different ion channels, TRPM3 receptors give researchers a place to start in the search for something that is effective, which could then be tested in human trials.
Staines added that many potential treatments for malfunctioning channels “are already being used for other conditions.” Consequently, “we have good safety data on them, know how well they are tolerated, so if they are found to work in the lab, clinical trials should be smoother sailing.”