SKIN exposure to ultraviolet (UV) light triggers kidney inflammation via neutrophil infiltration and migration in individuals with lupus, a new collaborative study has revealed. Lupus is a long-term, autoimmune disease, which causes inflammation to the kidneys, skin, and various other organs. Foregoing research reports that 80% of patients experience local skin inflammation and systemic flares on exposure to sunlight; however, prior to this study little has been understood regarding the underlying mechanisms.
Researchers at the Geisel School of Medicine at Dartmouth College, Hanover, New Hampshire, USA, and the University of Washington, Seattle, Washington, USA, investigated the role of neutrophils in UV-induced kidney inflammation, due to the white blood cell’s role as a first responder to any kind of body inflammation. The study looked for markers of inflammation and injury in the skin, blood, and kidney of mice at different time points following exposure to UV light. Their findings not only revealed neutrophil infiltration to the UV light-exposed skin, but also neutrophil dispersion throughout the blood and migration to the kidneys. In reference to the neutrophil migration, Dr Sladjana Skopelja-Gardner, Assistant Professor of Medicine, commented how it was “a bit unusual; we normally think of neutrophils as short-lived cells that sort of zoom to where the inflammation is and then die off there.”
The findings additionally revealed how a single exposure of skin to UV light in healthy mice resulted in inflammation and injury to the kidneys, including transient proteinuria. In comparison to the type of kidney disease that is seen in patients with lupus, healthy mice will experience only subclinical injury to the kidney, where the inflammation and injury is not visible through pathology or by looking at the tissue itself and the mice will fully recover. “However, this subclinical injury may lead to pathologic consequences in the vulnerable setting of pre-existing inflammation in lupus patients, and lead to kidney disease flare after exposure to sunlight,” explained Dr Skopelja-Gardner.
Notably, the markers of inflammation and injury identified in the UV light exposed mice were very similar to the renal injury markers seen in patients with lupus with severe kidney damage. Additionally, the UV exposure triggered a Type 1 interferon immune response, which is often expressed in individuals with lupus.
Looking forward, these findings present new options for the management of lupus and novel therapeutic opportunities to be explored for the prevention and treatment of any associated kidney damage.
