Fig. 8

Schematic diagram of the protective effects of FMT administration on the rotenone-induced PD mouse model through the microbiota-gut-brain axis. Briefly, FMT treatment restores the gut microbiota dysbiosis induced by rotenone, which decreases the generation of pathogenic LPS in the gut and inhibits the intestinal inflammation by downregulating the TLR4 signaling pathway. Then, the reduced intestinal barrier permeability decreases the leakage of microbes, LPS, and pro-inflammatory cytokines (e.g., TNF-α, IL-1β, and IL-6) into the systemic circulation. As a consequence of reduced systemic inflammation, lower levels of LPS and pro-inflammatory cytokines get access to the SN across the BBB, which inhibits neuroinflammation (activated astrocytes and microglia) through suppressing LPS-TLR4 signaling pathway activation in the SN. Eventually, the dopaminergic neuronal death is attenuated in the SN. This diagram demonstrates that FMT treatment can correct the gut microbiota dysbiosis and ameliorate the rotenone-induced PD mouse model, in which suppression of the inflammation mediated by the LPS-TLR4 signaling pathway both in the gut and the brain possibly plays a significant role. Further, it is shown that microbiota dysbiosis is involved in the genesis of PD via the microbiota-gut-brain axis