Alterations of the gut microbiome and plasma proteome in Chinese patients with adolescent idiopathic scoliosis.

Abstract

The etiology of adolescent idiopathic scoliosis (AIS), the most common rotational deformity of the spine, is still unclear. Emerging evidence suggests that gut microbiota dysbiosis influences musculoskeletal diseases such as arthritis and osteoporosis. However, the alterations of the fecal microbiome in AIS remain unknown. Thus, the current study was conducted to explore the gut microbiota compositions of Chinese AIS patients. Microbiota communities in the feces of 51 AIS patients and 34 age- and sex-matched healthy individuals were investigated using 16S rRNA sequencing. Meanwhile, the changes in the plasma proteome were detected using tandem mass tag (TMT) labeling coupled with liquid chromatography-mass spectrometry (LC-MS). The relationship between gut microbiota and AIS clinical characteristics as well as the correlation between gut microbiota and the changes in plasma proteins were analyzed. The structure of the gut microbiota differed between the AIS and healthy groups, however, the richness was similar. The genera Prevotella, Gelria, and Desulfovibrio were enriched in the feces of AIS patients. In contrast, the abundance of Parasutterella, Tyzzerella, and Phascolarctobacterium was decreased in the AIS group. More remarkably, a positive correlation between the abundance of the fecal genera Prevotella and the Cobb angles of the AIS patients was observed. Moreover, the major differential plasma proteins related to AIS were Fibronectin 1 (FN1), voltage-dependent anion channel 1 (VDAC1), Ras homolog family member A (RHOA), and AHNAK nucleoprotein (AHNAK). Additionally, the positive correlations between fecal Prevotella and the expression of host plasma FN1 as well as the negative relationships between fecal Prevotella and the expression of host VDAC1 and AHNAK were confirmed. Elucidating these differences in the gut microbiota will provide a foundation to improve our understanding of the pathogenesis of AIS and to support potential therapeutic options based on modifying the gut microbiota.