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Gut Microbiota Variations between Henoch-Schonlein Purpura and Henoch-Schonlein Purpura Nephritis
Fang Zhou1, Qimin Shao1, Lihong Jia1
1Department of Rheumatoid Immune Nephrology, Hangzhou Children's Hospital, Hangzhou, 310014 Zhejiang, China.
Insights
Children with Henoch-Schonlein purpura (HSP) and HSP nephritis (HSPN) show altered gut microbiota compared to healthy children. This suggests potential for microbe-based therapies to improve outcomes for these conditions.
Area of Science:
- Microbiology
- Pediatrics
- Gastroenterology
Background:
- Gut microbiota differences between children with Henoch-Schonlein purpura (HSP) and HSP nephritis (HSPN) are not well understood in China.
- HSP is an autoimmune disease causing inflammation in small blood vessels, often affecting the skin, joints, and kidneys.
Purpose of the Study:
- To investigate and compare the gut microbiota composition in children diagnosed with HSP, HSPN, and healthy controls.
- To identify potential microbial biomarkers associated with HSP and HSPN in pediatric populations.
Main Methods:
- Recruited three groups of 25 children: HSP, HSPN, and healthy controls.
- Analyzed fecal samples using 16S rRNA gene sequencing (V3-V4 region).
- Compared gut microbial diversity and abundance between the groups.
Main Results:
- Significant differences in gut microbial diversity were observed between the three groups (P = 0.0224).
- Children with HSP exhibited lower Bifidobacterium abundance compared to healthy children and those with HSPN.
- HSPN patients showed reduced Akkermansia and increased Alistipes abundance relative to HSP patients.
Conclusions:
- The study indicates gut microbiota dysbiosis in children with HSP and HSPN.
- Findings suggest that gut microbiota alterations may play a role in the pathogenesis of HSP and HSPN.
- Results support the potential development of microbiome-targeted therapies for managing or preventing pediatric HSP and HSPN.
Background:
In China, little is known regarding the differences between children with Henoch-Schonlein purpura (HSP) and Henoch-Schonlein purpura nephritis (HSPN) concerning their gut microbiota.
Methods:
We recruited 25 children with HSP, 25 children with HSPN, and 25 healthy children to investigate the differences. Fecal samples were collected and analyzed by sequencing the V3-V4 region of the 16S rRNA gene. The diversity of the fecal gut microbiota was compared between the patient groups.
Results:
Rarefaction curves showed that the gut microbial diversity between the three groups differed significantly (P = 0.0224). The top five most abundant gut microbial genera were Bacteroides, Faecalibacterium, Prevotella, Ruminococcaceae, and Megamonas in children with HSP; Bacteroides, Faecalibacterium, Prevotella, Bifidobacterium, and Ruminococcaceae in children with HSPN; and Bacteroides, Prevotella, Faecalibacterium, Ruminococcaceae, and Bifidobacterium in healthy children. Children with HSP had the lowest Bifidobacterium abundance among the three groups (P < 0.05). Children with HSPN had a lower abundance of Akkermansia than children with HSP (P < 0.05), whereas children with HSPN had a higher Alistipes abundance than children with HSP (P < 0.05). Fecal microbial community composition did not differ significantly between groups (ANOSIM, R = -0.002, P = 0.46). Despite the small sample size, our results indicate that children with HSP or HSPN displayed dysbiosis of the gut microbiota.
Conclusion:
This study provides valuable insights that will benefit the development of future microbe-based therapies to improve clinical outcomes or prevent the incidence of HSP or HSPN in children.
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