Interleukin-1β Promotes Repair of the CNS

TLDR

Interleukin‑1β is a proinflammatory cytokine implicated in demyelinating disorders such as multiple sclerosis and CNS viral infections. Our study shows that IL‑1β promotes remyelination in the adult CNS, likely by inducing IGF‑1 production from microglia–macrophages and astrocytes, which facilitates oligodendrocyte precursor differentiation.

Abstract

Interleukin-1β (IL-1β) is a proinflammatory cytokine associated with the pathophysiology of demyelinating disorders such as multiple sclerosis and viral infections of the CNS. However, we demonstrate here that IL-1β appears to promote remyelination in the adult CNS. In<i>IL-1</i>β^−/− mice, acute demyelination progressed similarly to wild-type mice and showed parallel mature oligodendrocyte depletion, microglia–macrophage accumulation, and the appearance of oligodendrocyte precursors. In contrast,<i>IL-1</i>β^−/− mice failed to remyelinate properly, and this appeared to correlate with a lack of insulin-like growth factor-1 (IGF-1) production by microglia–macrophages and astrocytes and to a profound delay of precursors to differentiate into mature oligodendrocytes. Thus, IL-1β may be crucial to the repair of the CNS, presumably through the induction of astrocyte and microglia–macrophage-derived IGF-1.