Exposure of the Host-Associated Microbiome to Nutrient-Rich Conditions May Lead to Dysbiosis and Disease Development-an Evolutionary Perspective

Inflammatory diseases, such as inflammatory bowel diseases, are dramatically increasing worldwide, but an understanding of the underlying factors is lacking. We here present an ecoevolutionary perspective on the emergence of inflammatory diseases. We propose that adaptation has led to fine-tuned hos...

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Bibliographic Details
Published in:mBio 2019-05, Vol.10 (3)
Main Authors: Lachnit, Tim, Bosch, Thomas C G, Deines, Peter
Format: Article
Language:English
Subjects:
Animals
Biological Evolution
Diet, Western - adverse effects
dysbiosis
Dysbiosis - etiology
fasting
Gastrointestinal Microbiome - drug effects
holobiont
Host-Microbe Biology
host-microbe homeostasis
Humans
Inflammation - etiology
Inflammatory Bowel Diseases - etiology
inflammatory disease
metaorganism
Mice
Nutrients - adverse effects
Nutrients - pharmacology
Opinion/Hypothesis
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Summary:Inflammatory diseases, such as inflammatory bowel diseases, are dramatically increasing worldwide, but an understanding of the underlying factors is lacking. We here present an ecoevolutionary perspective on the emergence of inflammatory diseases. We propose that adaptation has led to fine-tuned host-microbe interactions, which are maintained by secreted host metabolites nourishing the associated microbes. A constant elevation of nutrients in the gut environment leads to an increased activity and changed functionality of the microbiota, thus severely disturbing host-microbe interactions and leading to dysbiosis and disease development. In the past, starvation and pathogen infections, causing diarrhea, were common incidences that reset the gut bacterial community to its "human-specific-baseline." However, these natural clearing mechanisms have been virtually eradicated in developed countries, allowing a constant uncontrolled growth of bacteria. This leads to an increase of bacterial products that stimulate the immune system and ultimately might initiate inflammatory reactions.
ISSN:2161-2129
2150-7511
DOI:10.1128/mBio.00355-19