4.7 Article

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

Journal

MBIO
Volume 10, Issue 3, Pages -

Publisher

AMER SOC MICROBIOLOGY
DOI: 10.1128/mBio.00355-19

Keywords

dysbiosis; fasting; holobiont; host-microbe homeostasis; inflammatory disease; metaorganism; microbiome; overfeeding; starvation

Categories

Funding

  1. Deutsche Forschungsgemeinschaft (DFG)
  2. Collaborative Research Center (CRC) 1182 (Origin and Function of Metaorganisms)
  3. DFG Cluster of Excellence program Inflammation at Interfaces
  4. Volkswagen Foundation (funding program Experiment!-In search of bold research ideas)
  5. European Union's Framework Program for Research and Innovation Horizon 2020 (2014-2020) under the Marie Sklodowska-Curie grant [655914]
  6. Deutscher Akademischer Austausch Dienst (DAAD)
  7. Marie Curie Actions (MSCA) [655914] Funding Source: Marie Curie Actions (MSCA)

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available