Lupus, also known as Systemic Lupus Erythematosus, is a disease that affects 5 million people worldwide. More than 16,000 new cases of Lupus are registered around the country every year. The latest report from the Lupus Foundation of America states that around 1.5 million Americans are affected by this disease.
It is a chronic autoimmune disease that can affect any part of the body including skin, joints and organs. This leads to spreading of inflammation throughout the body. Lupus can be severe and may cause permanent damage to organs.
Even in this modern age, medical science is still struggling to find the “ultimate cure” for lupus. Due to its erratic nature, medical management of systemic lupus has been less than promising until now.
[ohd_ad_one]A study published in Science Translational Medicine states that the researchers from the University of Florida, Gainesville have found that it is possible to fight lupus in mice by preventing certain metabolic pathways in immune cells.
Understanding lupus
Here is a simple explanation about the pathophysiology of Lupus:
People suffering from lupus usually have hyper activated T cells, a component of our immune system responsible for combating foreign invaders. These hyperactive T cells tend to attack the body’s own cells causing damage and swelling. Such event leads to widespread inflammation in the body and later causes a lot of damage to it.
A glimmer of hope
According to a recent research involving mice, scientists say the damage brought about by lupus can be reversed by using a combination of two drugs that already exist.Though researchers have already tried using each of the drugs individually, only the combination of these two drugs seem to work.
It was necessary to use the combination of the two metabolic inhibitors to reverse the disease – which was indeed a shocking result from this study, said by Laurence Morel, Ph.D., director of experimental pathology and a professor of pathology, immunology and laboratory medicine in the University of Florida College of Medicine in an email to onlinehealthdigest.
Blocking metabolic pathways is the key
T cell metabolism is also related to mitochondrial metabolism, energy production in the cell, and glycolysis, which is the conversion of glucose into energy, and thus, researchers decided to study glycolysis and mitochondrial metabolism.
According to Morel, these two processes control the hyper-activated immune cells and are responsible for activating and sustaining lupus. He also added, “Our study is the first to show a detailed study of these cellular metabolic pathways in lupus.”
Researchers used the two drugs, which are metformin (FDA – approved) and 2DG (under development) to prevent mitochondrial metabolism and glycolysis —the processes involved in lupus. With the help of these two drugs, researchers successfully reversed lupus in mice.
These researchers also showed that the human T cells with increased glycolysis and mitochondrial metabolism, when exposed to metformin, saw slower cellular metabolism. However, T cells of a healthy mice were not affected by these two drugs. The scientists say, these drugs are available at a modest cost and can be safely used.
Researchers prove that the cellular metabolism normalizes by infusing low doses of these drugs in the hyper-activated immune cells of infected mice. Without blocking cellular metabolic activity completely, they diminished it.
Morel added, “this study may prove to be helpful for other metabolic pathways as well.”
This drug combination may be more beneficial to lupus infected patients in comparison to the traditional approach in treating this disease that completely rely on immunosuppressive drugs.
Prior to moving these drugs to clinical trials, it is necessary to compare the effects of these drugs on humans before it can be approved. The tests on mice are not yet over. There are still many tests to be done including the one that determines whether it is safe for humans to use the drug combo with the other lupus drugs or not.
Stay tune for more developments about this research.
