Aβ Induces Neuroinflammation and Microglial M1 Polarization via cGAS-STING-IFITM3 Signaling Pathway in BV-2 Cells

Microglia, innate immune cells of the brain, constantly monitor the dynamic changes of the brain microenvironment under physiological conditions and respond in time. Growing evidence suggests that microglia-mediated neuroinflammation plays an important role in the pathogenesis of Alzheimer's disease. In this study, we investigated that the expression of IFITM3 was significantly upregulated in microglia under the A beta treatment, and knockdown of IFITM3 in vitro suppressed the M1-like polarization of microglia. Moreover, IFITM3 was regulated by cGAS-STING signaling in activated microglia, and inhibition of cGAS-STING signaling reduces IFITM3 expression. Taken together, our findings suggested that the cGAS-STING-IFITM3 axis may be involved in A beta-induced neuroinflammation in microglia.

Automated summary

This study found that microglia-mediated neuroinflammation plays an important role in the pathogenesis of Alzheimer's disease. The expression of IFITM3 was significantly upregulated in microglia under the A beta treatment, and knockdown of IFITM3 in vitro suppressed the M1-like polarization of microglia. Moreover, IFITM3 was regulated by cGAS-STING signaling in activated microglia, and inhibition of cGAS-STING signaling reduces IFITM3 expression. In conclusion, the cGAS-STING-IFITM3 axis may be involved in A beta-induced neuroinflammation in microglia.