Analysis of fecal microbiome in Chinese patients with non-severe aplastic anemia

By analyzing the fecal microbiome data of patients with non-severe aplastic anemia (NSAA), this study aims to explore the potential role of dysbiosis in the immune-mediated pathogenesis of NSAA. This study included 21 newly diagnosed NSAA patients from the Affiliated Hospital of Nanjing University of Chinese Medicine between July 2018 and June 2021, along with 24 healthy controls who underwent routine health checkups. Fecal samples were collected for DNA extraction. At the species level of phylum, class, order, family, genus and species, the intestinal microbial community of NSAA patients was significantly different from that of healthy controls. Alpha diversity analysis showed that the Chao and Observed species indices were significantly lower in the NSAA group compared to the control group ( P < 0.05 ), indicating that the gut microbiota diversity in NSAA patients was lower than that in normal individuals. Further multivariate statistical analysis revealed that the relative abundance of the following gut microbiota was higher in the NSAA group: Actinobacteriota, Coriobacteriia, Bifidobacteriales, Coriobacteriales, Pasteurellales, Prevotellaceae, Muribaculaceae, Bifidobacteriaceae, Coriobacteriaceae, Pasteurellaceae, Prevotella spp., Muribaculum spp., Barnesiella spp., Bifidobacterium spp., Mitsuokella spp., Collinsella spp., Alloprevotella spp. Meanwhile, the abundance of Lachnospirales spp. in the gut microbiota of NSAA patients was found to be lower than that of healthy controls. Correlation and model prediction analyses of the dominant microbial species in both the NSAA and control groups revealed a strong competitive relationship between Bacteroides spp. and Prevotella spp. NSAA patients exhibit a decrease in the abundance of Lachnospirales spp. and an increase in the abundance of Prevotella spp., which may be closely related to immune dysfunction mediated by NSAA Treg/Th17 imbalance, which, in turn, may contribute to the development of hematopoietic failure.