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• W3029420556 abstract "Abstract The gut microbiome regulates a number of homeostatic mechanisms in the healthy host including immune function and gut barrier protection. Loss of normal gut microbial structure and function has been associated with diseases as diverse as Clostridioides difficile infection, asthma, and epilepsy. Recent evidence has also demonstrated a link between the gut microbiome and sepsis. In this review, we focus on three key areas of the interaction between the gut microbiome and sepsis. First, prior to sepsis onset, gut microbiome alteration increases sepsis susceptibility through several mechanisms, including (a) allowing for expansion of pathogenic intestinal bacteria, (b) priming the immune system for a robust pro-inflammatory response, and (c) decreasing production of beneficial microbial products such as short-chain fatty acids. Second, once sepsis is established, gut microbiome disruption worsens and increases susceptibility to end-organ dysfunction. Third, there is limited evidence that microbiome-based therapeutics, including probiotics and selective digestive decontamination, may decrease sepsis risk and improve sepsis outcomes in select patient populations, but concerns about safety have limited uptake. Case reports of a different microbiome-based therapy, fecal microbiota transplantation, have shown correlation with gut microbial structure restoration and decreased inflammatory response, but these results require further validation. While much of the evidence linking the gut microbiome and sepsis has been established in pre-clinical studies, clinical evidence is lacking in many areas. To address this, we outline a potential research agenda for further investigating the interaction between the gut microbiome and sepsis." @default.
• W3029420556 created "2020-06-05" @default.
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• W3029420556 date "2020-06-01" @default.
• W3029420556 modified "2023-10-17" @default.
• W3029420556 title "The gut microbiome’s role in the development, maintenance, and outcomes of sepsis" @default.
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• W3029420556 doi "https://doi.org/10.1186/s13054-020-02989-1" @default.
• W3029420556 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7266132" @default.
• W3029420556 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32487252" @default.
• W3029420556 hasPublicationYear "2020" @default.
• W3029420556 type Work @default.
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• W3029420556 citedByCount "124" @default.

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