Abstract

IntroductionIntermittent hypoxia and sleep fragmentation are critical pathophysiological processes involved in obstructive sleep apnea‐hypopnea syndrome (OSAHS). Those manifestations independently affect similar brain regions and contribute to OSAHS‐related comorbidities that are known to be related to the host gut alteration microbiota. We hypothesized that gut microbiota disruption may cross talk the brain function via the microbiota–gut–brain axis. Thus, we aim to survey enterotypes and polysomnographic data of patients with OSAHS.MethodsSubjects were diagnosed by polysomnography, from whom fecal samples were obtained and analyzed for the microbiome composition by variable regions 3–4 of 16S rRNA pyrosequencing and bioinformatic analyses. We examined the fasting levels of interleukin‐6 and tumor necrosis factor‐alpha of all subjects.ResultsThree enterotypes Bacteroides, Ruminococcus, and Prevotella were identified in patients with OSAHS. Arousal‐related parameters or sleep stages are significantly disrupted in apnea‐hypopnea index (AHI) ≥15 patients with Prevotella enterotype; further analysis this enterotype subjects, obstructive, central, and mixed apnea indices, and mean heart rate are also significantly elevated in AHI ≥15 patients. However, blood cytokines levels of all subjects were not significantly different.ConclusionsThis study indicates the possibility of pathophysiological interplay between enterotypes and sleeps structure disruption in sleep apnea through a microbiota–gut–brain axis and offers some new insight toward the pathogenesis of OSAHS.

Highlights

  • Intermittent hypoxia and sleep fragmentation are critical pathophysi‐ ological processes involved in obstructive sleep apnea‐hypopnea syndrome (OSAHS)

  • We examined whether impaired sleep architecture is associated with gut microbiota alteration by investigating sleep parameters of polysomnography (PSG) data and pro‐inflammatory cytokines in various enterotypes of OSAHS subjects

  • The Intermittent hypoxia (IH) mechanism alone is insufficient to inter‐ pret the complete pathogenesis of OSAHS because OSAHS is affected by several other aspects, including the central nervous system (CNS) causing neu‐ ropsychiatric and neurodegenerative disorders (Farré et al, 2018; Gaspar et al, 2017; Lavie, 2015; Rosenzweig et al, 2014)

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Summary

| INTRODUCTION

Intermittent hypoxia (IH) and sleep fragmentation (SF) are the hall‐ marks of obstructive sleep apnea‐hypopnea syndrome (OSAHS) (Moreno‐Indias et al, 2015, 2016; Poroyko et al, 2016). Emerging evidence suggests that the gut microbiota plays a crucial role in modulating the risk of several chronic diseases and maintaining intestinal immunity and whole body homeostasis. These effects have important implications for diseases such as obesity, car‐ diometabolic abnormalities, inflammatory bowel disease (IBD), and mental illness (Singh et al, 2017). Gut microbiomes can respond to the brain via the microbiota–gut–brain axis, as has been declared in psychiatric disorders (Sherwin, Sandhu, Dinan, & Cryan, 2016) This hypothesis has not been verified for OSAHS. We examined whether impaired sleep architecture is associated with gut microbiota alteration by investigating sleep parameters of polysomnography (PSG) data and pro‐inflammatory cytokines in various enterotypes of OSAHS subjects

| MATERIALS AND METHODS
Findings
| DISCUSSION

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