Analysis of the characteristics of intestinal microbiota in patients with different severity of obstructive sleep apnea.

Intestinal microbiota imbalance plays an important role in the progression of obstructive sleep apnea (OSA), and is considered to be the main mediator that triggers metabolic comorbidities. Here, we analyzed the changes in intestinal microbiota in patients with different severities of OSA based on apnea hypopnea index (AHI) classification, and explored the role of intestinal microbiota in the severity of OSA. This study included 19 healthy volunteers and 45 patients with OSA [5 ≤ AHI < 15 (n = 14), 15 ≤ AHI < 30 (n = 13), AHI ≥ 30 (n = 18)]. Relevant sleep monitoring data and medical history data were collected, and microbial composition was analyzed using 16S rRNA high-throughput sequencing technology. The diversity analysis of intestinal microbiota among different groups of people was conducted, including alpha diversity, beta diversity, species diversity, and marker species as well as differential functional metabolic pathway prediction analysis. With the increase of AHI classification, the alpha diversity in patients with OSA significantly decreased. The results revealed that the severity of OSA is associated with differences in the structure and composition of the intestinal microbiota. The abundance of bacteria producing short-chain fatty acids (such as Bacteroides, Ruminococcacea, and Faecalibacterium) in severe OSA is significantly reduced and a higher ratio of Firmicutes to Bacteroidetes. Random forest analysis showed that Parabacteroides was a biomarker genus with important discriminatory significance. The differential metabolic pathway prediction function shows that the main function of maintaining intestinal microbiota homeostasis is biosynthetic function. Our results show that the differences in the composition of intestinal microbiota in patients with different severities of OSA are mainly related to short-chain fatty acid-producing bacteria. These changes may play a pathological role in OSA combined with metabolic comorbidities.