Mapping Pesticide-Induced Metabolic Alterations in Human Gut Bacteria

Li Chen1,2, Hong Yan3,4, Shanshan Di5

  • 1Human Nutrition Program, Department of Human Sciences, The Ohio State University, Columbus, OH 43210, USA.

Insights

Pesticides alter gut microbiota (GM) composition and metabolism, even at low doses. This study reveals specific pesticide-gut bacteria interactions and their impact on host health via metabolic changes.

Area of Science:

  • Environmental Science
  • Microbiology
  • Toxicology

Background:

  • Pesticides are known to affect gut microbiota (GM) composition.
  • The precise mechanisms and consequences of these interactions remain largely unknown.

Purpose of the Study:

  • To investigate the specific effects of pesticides on GM growth, composition, and metabolism.
  • To establish a comprehensive network of pesticide-GM-metabolite (PMM) interactions.
  • To elucidate the molecular mechanisms by which pesticides impact host health through GM modulation.

Main Methods:

  • In vitro assessment of pesticide effects on GM species growth.
  • Generation of a PMM network to identify pesticide-sensitive bacteria and metabolic alterations.
  • In vivo validation using a mouse model to confirm PGP interactions and host inflammatory responses.

Main Results:

  • Pesticides inhibit or promote GM growth and can accumulate within the microbiota.
  • Significant alterations in gut bacterial metabolism were observed, with hundreds of metabolites affected.
  • A PMM network identified 306 pesticide-GM pairs (PGPs) and linked them to specific metabolic changes.
  • In vivo studies confirmed PGP interactions and demonstrated pesticide-induced inflammation via dysregulated microbial lipid metabolism.

Conclusions:

  • The study provides a PMM interactions atlas, detailing how pesticides affect GM and host metabolism.
  • Pesticides impact host health at a molecular level by modulating GM metabolism, particularly lipid metabolism.
  • Findings highlight the critical role of GM in mediating pesticide toxicity and host inflammatory responses.