Gut dysbiosis: Ecological causes and causative effects on human disease

The gut microbiota plays a role in many human diseases, but high-throughput sequence analysis does not provide a straightforward path for defining healthy microbial communities. Therefore, understanding mechanisms that drive compositional changes during disease (gut dysbiosis) continues to be a cent...

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Published inProceedings of the National Academy of Sciences - PNAS Vol. 120; no. 50; p. e2316579120
Main Authors Winter, Sebastian E, Bäumler, Andreas J
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 12.12.2023
Subjects
Availability
Community composition
Dysbacteriosis
Dysbiosis
Ecological effects
Gastrointestinal Microbiome
Homeostasis
Humans
Intestinal microflora
Microbial activity
Microbiomes
Microbiota
Microorganisms
Pathogenesis
Resource availability
Sequence analysis
Signs and symptoms
microbiota
colitis
colorectal cancer
dysbiosis
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Summary:The gut microbiota plays a role in many human diseases, but high-throughput sequence analysis does not provide a straightforward path for defining healthy microbial communities. Therefore, understanding mechanisms that drive compositional changes during disease (gut dysbiosis) continues to be a central goal in microbiome research. Insights from the microbial pathogenesis field show that an ecological cause for gut dysbiosis is an increased availability of host-derived respiratory electron acceptors, which are dominant drivers of microbial community composition. Similar changes in the host environment also drive gut dysbiosis in several chronic human illnesses, and a better understanding of the underlying mechanisms informs approaches to causatively link compositional changes in the gut microbiota to an exacerbation of symptoms. The emerging picture suggests that homeostasis is maintained by host functions that control the availability of resources governing microbial growth. Defining dysbiosis as a weakening of these host functions directs attention to the underlying cause and identifies potential targets for therapeutic intervention.
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ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.2316579120