Bacteria and Sepsis: Microbiome to the Rescue?

Kang, Hansol; Thomas, Ryan M.

doi:10.3390/jcm10163578

Cited by 7 publications

(8 citation statements)

References 62 publications

(78 reference statements)

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“…The microbiome has recently become a topic of interest among several mechanisms of the host response to sepsis [ 40 ]. Microbiome diversity decreases in both male and female mice after cecal ligation and puncture.…”

Section: Animal Modelsmentioning

confidence: 99%

Interactions between Gender and Sepsis—Implications for the Future

et al. 2023

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Sex and gender dimorphisms are found in a large variety of diseases, including sepsis and septic shock which are more prevalent in men than in women. Animal models show that the host response to pathogens differs in females and males. This difference is partially explained by sex polarization of the intracellular pathways responding to pathogen–cell receptor interactions. Sex hormones seem to be responsible for this polarization, although other factors, such as chromosomal effects, have yet to be investigated. In brief, females are less susceptible to sepsis and seem to recover more effectively than males. Clinical observations produce more nuanced findings, but men consistently have a higher incidence of sepsis, and some reports also claim higher mortality rates. However, variables other than hormonal differences complicate the interaction between sex and sepsis, including comorbidities as well as social and cultural differences between men and women. Conflicting data have also been reported regarding sepsis-attributable mortality rates among pregnant women, compared with non-pregnant females. We believe that unraveling sex differences in the host response to sepsis and its treatment could be the first step in personalized, phenotype-based management of patients with sepsis and septic shock.

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Section: Animal Modelsmentioning

confidence: 99%

Interactions between Gender and Sepsis—Implications for the Future

et al. 2023

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“…In this respect, bile duct ligated mice in which BA-FXR physiology is restored via the administration of a semisynthetic BA and FXR ligand, display a restored gut barrier integrity and Akkermansia muciniphila enrichment [ 96 ]. Loss of barrier caused by pathogenic bacteria disrupting epithelial integrity can lead to sepsis by triggering systemic inflammation (reviewed in [ 98 ]), and, in turn, sepsis increases the risk of liver damage [ 99 ]. Intriguingly, these studies suggest that sepsis-induced liver damage could potentially be prevented by harnessing the GM in ICU septic patients.…”

Section: The Gut Microbiota and The Hostmentioning

confidence: 99%

The central role of the gut in intensive care

et al. 2022

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Critically ill patients undergo early impairment of their gut microbiota (GM) due to routine antibiotic therapies and other environmental factors leading to intestinal dysbiosis. The GM establishes connections with the rest of the human body along several axes representing critical inter-organ crosstalks that, once disrupted, play a major role in the pathophysiology of numerous diseases and their complications. Key players in this communication are GM metabolites such as short-chain fatty acids and bile acids, neurotransmitters, hormones, interleukins, and toxins. Intensivists juggle at the crossroad of multiple connections between the intestine and the rest of the body. Harnessing the GM in ICU could improve the management of several challenges, such as infections, traumatic brain injury, heart failure, kidney injury, and liver dysfunction. The study of molecular pathways affected by the GM in different clinical conditions is still at an early stage, and evidence in critically ill patients is lacking. This review aims to describe dysbiosis in critical illness and provide intensivists with a perspective on the potential as adjuvant strategies (e.g., nutrition, probiotics, prebiotics and synbiotics supplementation, adsorbent charcoal, beta-lactamase, and fecal microbiota transplantation) to modulate the GM in ICU patients and attempt to restore eubiosis.

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“…One key aspect to septic outcomes is the host microbiome. 12 , 13 The microbiota is the collection of trillions of microorganisms that form a symbiont and pathobiont relationship with its host. Its role in various human diseases, including posttrauma recovery, has gained much traction recently given its interaction with the immune system and host metabolic processes.…”

mentioning

confidence: 99%

“…Critical illness has been shown to disturb the host microbiome, 12 and evidence exists demonstrating that a host dysbiome worsens outcomes after sepsis. 13 Importantly, it is not simply the changes in host microbiome that contributes to its pathology but the ability (or inability) of the microbiome to recover from perturbations, known as microbiota resilience, that can determine host morbidity and mortality. 18 Furthermore, sex is considered one the most important factors affecting the gut microbiota.…”

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confidence: 99%

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Sex differences associate with late microbiome alterations after murine surgical sepsis

Efron

Darden

et al. 2022

J Trauma Acute Care Surg

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BACKGROUND: Sepsis-induced gut microbiome alterations contribute to sepsis-related morbidity and mortality. Given evidence for improved postsepsis outcomes in females compared with males, we hypothesized that female mice maintain microbiota resilience versus males. METHODS:Mixed-sex C57BL/6 mice underwent cecal ligation and puncture (CLP) with antibiotics, saline resuscitation, and daily chronic stress and were compared with naive (nonsepsis/no antibiotics) controls. For this work, the results of young (3-5 months) and old (18-22 months) adult mice were analyzed by sex, independent and dependent of age. Mice were sacrificed at days 7 and 14, and 16S rRNA gene sequencing was performed on fecal bacterial DNA. α and β diversity were determined by Shannon index and Bray-Curtis with principal coordinate analysis, respectively. False discovery rate (FDR) correction was implemented to account for potential housing effect. RESULTS:In control mice, there was no difference in α or β diversity between male and female mice (FDR, 0.76 and 0.99, respectively). However, male mice that underwent CLP with daily chronic stress had a decrease in microbiota α diversity at 7 days post-CLP (Shannon FDR, 0.005), which was sustained at 14 days post-CLP (Shannon FDR, 0.001), compared with baseline. In addition, male mice maintained differences in β diversity even at day 14 compared with controls (FDR, <0.0001). In contrast, female mice had a decreased microbiota α diversity (Shannon FDR, 0.03) and β diversity (FDR, 0.02) 7 days post-CLP but recovered their α and β diversity by post-CLP day 14 (Shannon FDR, 0.5, and FDR, 0.02, respectively). Further analysis of females revealed that only young female mice were not different (β diversity) post-CLP day 14 to controls. CONCLUSION: Although sepsis-induced perturbations of the intestinal microbiota occur initially in both male and female C57BL/6 mice, females demonstrate different microbiota by day 14. This may be seen primarily in younger females. This difference in recovery may play a role in outcome differences between sexes after sepsis.

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Bacteria and Sepsis: Microbiome to the Rescue?

Cited by 7 publications

References 62 publications

Interactions between Gender and Sepsis—Implications for the Future

Interactions between Gender and Sepsis—Implications for the Future

The central role of the gut in intensive care

Sex differences associate with late microbiome alterations after murine surgical sepsis

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