Abstract

The community structure and metabolic potential of gut microbiome is not well investigated, especially in chronically critically ill patients with prolonged dependence on support systems after severe brain disorders. Microbial phenolic metabolites can target the brain function by the direct and indirect modulation of inflammation. The aim of this study was to investigate the features of the gut microbiota and profile of certain metabolites in the progression and reversibility of neurological disorders in chronically critically ill patients. Fecal samples were collected in dynamics from such patients (n = 44) and analyzed using 16S rRNA sequencing. Serum microbial and mitochondrial metabolites were measured by GC-MS and compared with the biomarkers and clinical neurological scores. The identified associations between specific bacterial taxa in fecal samples, neurological status and serum levels of metabolites suggest that impacts on specific members of the gut microbiota and their metabolism might be a promising tool for regulating brain function in future.

Highlights

  • Over the past decades, advances in therapeutic techniques have substantially improved the survival of patients after acute events, and simultaneously expanded the population of patients with prolonged dependence on life support systems

  • We identified 75 bacterial taxa and 4 phenylcarboxylic acids (PhCAs) that were differentially abundant between the critical illness (CCI) patients and healthy subjects

  • Were higher in the CCI patients, while phenylpropionic acid (PhPA) concentration was higher in healthy controls (FDR < 0.05, Table 1, Figure 1c)

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Summary

Introduction

Advances in therapeutic techniques have substantially improved the survival of patients after acute events, and simultaneously expanded the population of patients with prolonged dependence on life support systems. This gave rise to the concept of chronic critical illness (CCI) [1]. Most surviving patients after severe brain injury meet CCI criteria They are compromised by the risk of the CCI-attributed neurological dysfunction aggravated by their condition. It may be caused by the functional or metabolic impairment mediated by pro- or noninflammatory factors, including microglia hyperactivation, blood brain barrier disruption and altered neurotransmission [3]

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