| First Author | Huehnchen P | Year | 2019 |
| Journal | Neurobiol Dis | Volume | 124 |
| Pages | 240-247 | PubMed ID | 30468863 |
| Mgi Jnum | J:274795 | Mgi Id | MGI:6295789 |
| Doi | 10.1016/j.nbd.2018.11.017 | Citation | Huehnchen P, et al. (2019) High salt diet ameliorates functional, electrophysiological and histological characteristics of murine spontaneous autoimmune polyneuropathy. Neurobiol Dis 124:240-247 |
| abstractText | BACKGROUND: It 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. METHODS: At 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 30weeks. RESULTS: Mice 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. CONCLUSIONS: We demonstrate beneficial effects of high salt diet regarding disease progression, functional, electrophysiological and histological parameters in a transgenic mouse model of spontaneous autoimmune neuropathy. |
