Dysbacteriosis induces abnormal neurogenesis via LPS in a pathway requiring NF-κB/IL-6

In this study, we identified elevated levels of LPS and suppressed neurogenesis in a successfully established mouse model of gut microbiota dysbiosis. We mimicked these phenotypes using mouse and chicken embryos exposed to LPS and found that dramatic variation in gene expression was due to changes in the dorsal-ventral patterning of the neural tube. Cell survival and excess ROS were also involved in this process. Antioxidant administration alleviated LPS-activated NF-kappa B signaling, while directly blocking NF-kappa B signaling altered the LPS-induced inhibition of neurogenesis. Furthermore, IL-6 was proven to play a vital role in the expression of crucial neurogenesis-related genes and NF-kappa B. In summary, we found that the suppression of neurogenesis induced by dysbacteriosis-derived LPS was significantly reversed in mice with fecal microbiota transplantation. This study reveals that gut dysbacteriosis-derived LPS impairs embryonic neurogenesis, and that the NF-kappa B/IL-6 pathway could be one of the main factors triggering the downstream signaling cascade.

Automated summary

The study identified that the suppression of neurogenesis induced by dysbacteriosis-derived LPS could be significantly reversed through fecal microbiota transplantation. This suggests that gut dysbacteriosis impairs embryonic neurogenesis. The NF-kappa B/IL-6 pathway may be one of the main factors triggering the downstream signaling cascade.