Multiple Sclerosis (MS) is an autoimmune inflammatory condition that affects the central nervous system. It is characterized by destruction of the insulating covers of nerve cells in the brain and spinal cord known as myelin sheaths.
To date, the etiology of MS remains unknown. Epidemiological research has shown that MS is inversely related to ultraviolet radiation (UVR). In mice, UVR has been shown to decrease inflammatory markers, and researchers are interested in determining if it has an effect on the disease activity of MS.
When studying the effects of UV radiation, particularly UVB radiation in mice, researchers use mice that have experimental autoimmune encephalomyelitis. Experimental autoimmune encephalomyelitis (EAE) is an animal model of a type of brain inflammation, the pathology of which resembles multiple sclerosis in humans and therefore serves as a model for multiple sclerosis. In a groundbreaking discovery, Professor Hector DeLuca’s groups at the University of Wisconsin-Madison have shown the UVB radiation suppresses EAE independent of vitamin D production but the mechanism is unknown.
In order to uncover this mechanism, researchers from the University of Wisconsin-Madison conducted an experiment in which they exposed mice with EAE to UVB radiation, and then measured levels of immune and inflammatory markers.
They maintained the mice in a sterile environment. Every mouse was fed the same, standard rodent diet. Half of the mice had their backs shaved and were exposed to UVB radiation (280 – 320 nm) and the other half were not exposed to UVB radiation. A week later, all of the mice were injected with a concoction of inflammatory proteins and pertussis toxin to induce EAE. The mice originally exposed to UVB radiation were then exposed to UVB radiation for another 30 days.
The researchers then measured levels of key immune and inflammatory cells and molecules in the spinal cord central nervous system (CNS), and the spleen and skin peripheral nervous system (PNS).
How did the mice in the control group differ from the mice exposed to UVB radiation? Here is what they found:
- Four out of 10 of the mice exposed to UVB did not develop EAE, whereas all 12 of the mice who weren’t exposed developed the disease.
- UV radiation significantly decreased various markers of inflammation in the CNS by day 30 (p < 0.05) as well as significantly decreased overall disease severity.
- Unlike its outcome within the CNS, UVB did not suppress immune response or decrease inflammation in the PNS.
The researchers concluded,
“Taken together, UVB did not suppress immune response in the PNS, but selectively inhibited the inflammation of the CNS and EAE.”
They went on to add,
“If the immune response is intact in the PNS, but selectively inhibited in the CNS after UVB irradiation, it suggests that the migration of T cells or reactivation of Tcells might be diminished by UVB irradiation.”
This study adds to the growing amount of evidence suggesting that sunlight provides benefits above and beyond from stimulation vitamin D production. It’s important to remember that because the study was performed in mice, we can’t be certain that the findings would directly relate to humans.