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UV light selectively inhibits spinal cord inflammation and demyelination in experimental autoimmune encephalomyelitis
Yanping Wang1, Steven J Marling1, Emily F Beaver1
1Department of Biochemistry, University of Wisconsin-Madison, 433 Babcock Drive, Madison, WI 53706, United States.
Abstract:
Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system (CNS). The incidence of MS is inversely related to sun light exposure or ultraviolet radiation (UVR). UVR was found to suppress experimental autoimmune encephalomyelitis (EAE), an animal model of MS, independent of vitamin D production. The mechanism of this suppression remains to be elucidated. To this end, several elements of an immune response in the spinal cord, spleen and skin during development of EAE were studied. As expected, UVR (10kJ/m(2)) inhibits inflammation and demyelination of the spinal cord. Most significant, UVR dramatically reduced spinal cord chemokine CCL5 mRNA and protein levels. UVR also suppressed IL-10 in skin and spleen but not the spinal cord. As expected from the UVR action on skin, macrophage population and IFN-γ levels are increased in that organ. UVR had no effect on lymphocyte proliferation and IFN-γ in spleen. From these measurements, we suggest that UVR suppression of EAE prevents the migration of inflammatory cells into the CNS by a focal inhibition of chemokine CCL-5 in the CNS and a systemic elevation of immunosuppressive IL-10.
Insights
Ultraviolet radiation (UVR) suppresses experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis (MS). UVR inhibits CNS inflammation and demyelination by reducing chemokine CCL5 and increasing IL-10.
Area of Science:
- Neuroimmunology
- Dermatology
- Immunology
Background:
- Multiple sclerosis (MS) is a chronic central nervous system (CNS) demyelinating disease.
- MS incidence correlates inversely with sunlight exposure or ultraviolet radiation (UVR).
- UVR suppresses experimental autoimmune encephalomyelitis (EAE), an MS animal model, independent of vitamin D.
Purpose of the Study:
- To elucidate the mechanism by which UVR suppresses EAE.
- To investigate the effects of UVR on immune responses in the spinal cord, spleen, and skin during EAE development.
Main Methods:
- Induction of EAE in a suitable animal model.
- Exposure to ultraviolet radiation (UVR) at a specific dose (10 kJ/m²).
- Analysis of immune markers including chemokine CCL5 mRNA and protein, IL-10, macrophage populations, IFN-γ, and lymphocyte proliferation in CNS, spleen, and skin.
Main Results:
- UVR significantly inhibited spinal cord inflammation and demyelination in EAE.
- UVR markedly reduced spinal cord chemokine CCL5 mRNA and protein levels.
- UVR suppressed IL-10 in skin and spleen, but not in the spinal cord, while increasing skin macrophages and IFN-γ.
Conclusions:
- UVR suppression of EAE may involve preventing inflammatory cell migration into the CNS.
- This prevention is potentially mediated by focal inhibition of CNS chemokine CCL5.
- Systemic elevation of immunosuppressive IL-10 may also contribute to UVR's protective effects in EAE.
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