Effect of gut microbiota from Henoch-Schönlein Purpura patients on acid-sensitive ion channel 3 expression and intestinal motility in Germ-free rats

Abstract

Background It has been proven that intestinal microbiota alterations and acid-sensing ion channels are associated with the development of Henoch-Schönlein Purpura (HSP) and that the brain-gut axis, which involves the gut microbiota, plays important roles in many diseases. However, there have been no reports published on changes in ASIC3 expression caused by gut microbial composition and its impact on the development of HSP. This study was to investigate the impact of the intestinal microbiota in children with abdominal HSP on ASIC3 expression and interactions between the microbiota and ASIC3 expression on the development of HSP. Methods Feces collected from HSP children and healthy children at the First Affiliated Hospital of Anhui Medical University were made into fecal microbial solutions. Germ-free rats were randomly assigned to either the control or HSP groups. The HSP group of rats were administered the fecal microbiota solution of HSP children, while the control group rats were administered the fecal microbiota solution of healthy children. Abdominal withdrawal reflex (AWR) and intestinal propulsion rate of the rats were used to determine visceral sensitivity. Composition of the gut microbiota of HSP children was determined using 16S rRNA gene sequencing. ASIC3 expression in the dorsal root ganglion (DRG) was ascertained through real-time PCR as well as western blotting analysis. Results The results showed a reduction in the number of species and abundance in the intestinal microbiota of children with HSP. Visceral sensitivity and intestinal propulsion rate of HSP group rats increased significantly, compared with the control group. ASIC3 mRNA and protein levels in the DRG of the spinal cord of rats in the HSP group were found to be upregulated. Conclusions The microbiota dysbiosis of HSP patients could stimulate ASIC3 expression in the DRG of the spinal cord, which in turn affected intestinal motility. These results suggested that regulation of the brain-gut axis may show potential for the development of therapies that can prevent or treat HSP children, especially patients with severe gastrointestinal manifestations.