The leaky gut and the gut microbiome in sepsis - targets in research and treatment
Issued Date
2023-04-26
Resource Type
eISSN
14708736
Scopus ID
2-s2.0-85153421647
Pubmed ID
37083032
Journal Title
Clinical science (London, England : 1979)
Volume
137
Issue
8
Start Page
645
End Page
662
Rights Holder(s)
SCOPUS
Bibliographic Citation
Clinical science (London, England : 1979) Vol.137 No.8 (2023) , 645-662
Suggested Citation
Chancharoenthana W., Kamolratanakul S., Schultz M.J., Leelahavanichkul A. The leaky gut and the gut microbiome in sepsis - targets in research and treatment. Clinical science (London, England : 1979) Vol.137 No.8 (2023) , 645-662. 662. doi:10.1042/CS20220777 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/82069
Title
The leaky gut and the gut microbiome in sepsis - targets in research and treatment
Other Contributor(s)
Abstract
Both a leaky gut (a barrier defect of the intestinal surface) and gut dysbiosis (a change in the intestinal microbial population) are intrinsic to sepsis. While sepsis itself can cause dysbiosis, dysbiosis can worsen sepsis. The leaky gut syndrome refers to a status with which there is an increased intestinal permeability allowing the translocation of microbial molecules from the gut into the blood circulation. It is not just a symptom of gastrointestinal involvement, but also an underlying cause that develops independently, and its presence could be recognized by the detection, in blood, of lipopolysaccharides and (1→3)-β-D-glucan (major components of gut microbiota). Gut-dysbiosis is the consequence of a reduction in some bacterial species in the gut microbiome, as a consequence of intestinal mucosal immunity defect, caused by intestinal hypoperfusion, immune cell apoptosis, and a variety of enteric neuro-humoral-immunity responses. A reduction in bacteria that produce short-chain fatty acids could change the intestinal barriers, leading to the translocation of pathogen molecules, into the circulation where it causes systemic inflammation. Even gut fungi might be increased in human patients with sepsis, even though this has not been consistently observed in murine models of sepsis, probably because of the longer duration of sepsis and also antibiotic use in patients. The gut virobiome that partly consists of bacteriophages is also detectable in gut contents that might be different between sepsis and normal hosts. These alterations of gut dysbiosis altogether could be an interesting target for sepsis adjuvant therapies, e.g., by faecal transplantation or probiotic therapy. Here, current information on leaky gut and gut dysbiosis along with the potential biomarkers, new treatment strategies, and future research topics are mentioned.