Abstract

BackgroundIt was previously reported that high salt dietary conditions can drive autoimmunity and worsen severity and symptoms of autoimmune diseases. Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a common autoimmune condition of the peripheral nervous system which leads to progressive paralysis and sensory deficits due to a demyelination and secondary axonal loss of peripheral nerves. We used a previously described model with a knockout of CD86 in non-obese diabetic mice (CD86−/− NOD), which results in the spontaneous development of an autoimmune peripheral neuropathy similar to CIDP and investigated the influence of a high salt diet on functional impairment, electrophysiological parameters, demyelination and neuroinflammation in these mice. MethodsAt seven weeks of age, asymptomatic female CD86−/− NOD mice were randomly assigned to a normal or high salt diet containing 4% sodium chloride in food and 1% in water. The diet was continued for a total of 30 weeks. ResultsMice on the high salt diet showed a delayed onset of clinical symptoms and an ameliorated disease course with a reduced decline of locomotor function. Furthermore, electrophysiological parameters of neuropathy and demyelination were attenuated in mice on the high salt diet, which was confirmed with histological analysis. Additionally, we observed a reduced immune cell infiltration of sciatic nerves in mice which had received the high salt diet. ConclusionsWe demonstrate beneficial effects of high salt diet regarding disease progression, functional, electrophysiological and histological parameters in a transgenic mouse model of spontaneous autoimmune neuropathy.

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