Department of Pediatrics, First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China.
Department of Medical Technology, Anhui Medical College, Hefei, 230026, China.
BMC Pediatr. 2021 Dec 1;21(1):536. doi: 10.1186/s12887-021-03013-3.
It has been proven that gut microbiota alterations are involved in the development of Henoch-Schönlein Purpura (HSP). However, the pathogenesis of HSP hasn't been eluciated. This study was to investigate the impact of gut microbiota from HSP on ASIC3 expression and interactions between microbiota and ASIC3 expression in the development of HSP.
Feces collected from HSP 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 colon was ascertained through qRT-PCR as well as western blotting analysis.
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. Colon ASIC3 mRNA and protein levels in the HSP group were found to be upregulated. The microbiota dysbiosis of HSP patients could stimulate ASIC3 expression in the colon of Germ-free rats, which in turn affected intestinal motility.
These results suggested that HSP children had intestinal microbiota disorder, which might affect gut motility by down-regulating colon ASIC3 expression in rats.
已有研究证明肠道微生物群的改变与过敏性紫癜（HSP）的发生发展有关，但 HSP 的发病机制尚未阐明。本研究旨在探讨 HSP 患儿肠道微生物群对 ASIC3 表达的影响，以及微生物群与 ASIC3 表达在 HSP 发病中的相互作用。
收集安徽医科大学第一附属医院 HSP 患儿和健康儿童的粪便，制成粪便微生物溶液。无菌大鼠随机分为对照组和 HSP 组。HSP 组大鼠给予 HSP 患儿粪便微生物溶液，对照组大鼠给予健康儿童粪便微生物溶液。采用腹壁退缩反射（AWR）和肠道推进率来评估大鼠内脏敏感性。采用 16S rRNA 基因测序技术检测 HSP 患儿肠道微生物群的组成。通过 qRT-PCR 和 Western blot 分析检测结肠中 ASIC3 的表达。
结果显示，HSP 患儿肠道微生物种类和丰度减少。与对照组相比，HSP 组大鼠的内脏敏感性和肠道推进率明显增加。HSP 组大鼠结肠 ASIC3 mRNA 和蛋白水平上调。HSP 患者的肠道微生物失调可刺激无菌大鼠结肠中 ASIC3 的表达，进而影响肠道运动。
这些结果提示 HSP 患儿存在肠道微生物群紊乱，可能通过下调大鼠结肠 ASIC3 表达来影响肠道动力。
