Dual-directional regulation of spinal cord injury and the gut microbiota

There is increasing evidence that the gut microbiota affects the incidence and progression of central nervous system diseases via the brain-gut axis.The spinal cord is a vital important part of the central nervous system;however,the underlying association between spinal cord injury and gut interactions remains unknown.Recent studies suggest that patients with spinal cord injury frequently experience intestinal dysfunction and gut dysbiosis.Alterations in the gut microbiota can cause disruption in the intestinal barrier and trigger neurogenic inflammatory responses which may impede recovery after spinal cord injury.This review summarizes existing clinical and basic research on the relationship between the gut microbiota and spinal cord injury.Our research identified three key points.First,the gut microbiota in patients with spinal cord injury presents a key characteristic and gut dysbiosis may profoundly influence multiple organs and systems in patients with spinal cord injury.Second,following spinal cord injury,weakened intestinal peristalsis,prolonged intestinal transport time,and immune dysfunction of the intestine caused by abnormal autonomic nerve function,as well as frequent antibiotic treatment,may induce gut dysbiosis.Third,the gut microbiota and associated metabolites may act on central neurons and affect recovery after spinal cord injury;cytokines and the Toll-like receptor ligand pathways have been identified as crucial mechanisms in the communication between the gut microbiota and central nervous system.Fecal microbiota transplantation,probiotics,dietary interventions,and other therapies have been shown to serve a neuroprotective role in spinal cord injury by modulating the gut microbiota.Therapies targeting the gut microbiota or associated metabolites are a promising approach to promote functional recovery and improve the complications of spinal cord injury.

Insights into the mechanism of shortened developmental duration and accelerated weight gain associated with Wolbachia infection in Hylyphantes graminicola

Wolbachia infection is known to affect host reproduction and development.To date,however,the underlying mechanism related to the effects of Wolbachia on host development has not yet been reported.Here,we compared the developmental duration and body weight in different instars of Wolbachia-positive(W+)and Wolbachia-negative(W−)spiders(Hylyphantes graminicola)and detected the relative expression levels of 6 insulin-related genes and 3 ecdysone-related genes using reverse transcription qPCR.Results showed that the developmental duration was significantly shortened in W+spiders compared with W−spiders.Furthermore,W+spiders were significantly heavier thanW−spiders at the 3rd and 4th instars,although no significant differences in body weight were observed after maturity.We also found that the expression levels of insulin-like growth factor-2 mRNA-binding protein-1,insulin-degrading enzyme,and ecdysone-inducible protein-1 genes were significantly down-regulated in W+spiders compared with W−spiders,whereas the expression levels of insulin-like growth factor-binding protein-1,insulin-like peptide receptor,insulin receptor substrate 2-B,insulin-like,ecdysone-induced protein-2,and ecdysone receptor genes were significantly up-regulated inW+spiders.Our results suggest thatWolbachia may influence host development by affecting insulin and ecdysone signaling pathways.