Inflammation-associated nitrate facilitates ectopic colonization of oral bacterium Veillonella parvula in the

Daniel F Rojas-Tapias1,2,3, Eric M Brown1,2, Emily R Temple1

  • 1Broad Institute of MIT and Harvard, Cambridge, MA, USA.

Nature Microbiology
|September 22, 2022
PubMed

Insights

Inflammation enables oral bacteria Veillonella parvula to thrive in the gut. Nitrate metabolism allows this microbe to utilize new food sources and colonize effectively during gut inflammation.

Area of Science:

  • Microbiology
  • Gastroenterology
  • Metabolic pathways

Background:

  • Oral microbes can colonize the intestine, contributing to diseases like inflammatory bowel disease (IBD).
  • The mechanisms enabling oral bacteria, such as Veillonella parvula, to expand in the intestinal niche are poorly understood.
  • Veillonella parvula, an anaerobic oral bacterium, increases in the gut during IBD.

Purpose of the Study:

  • To investigate the metabolic mechanisms enabling Veillonella parvula intestinal colonization during inflammation.
  • To determine the role of nitrate metabolism in V. parvula's adaptation to the inflamed intestine.

Main Methods:

  • Analysis of V. parvula's metabolic response to nitrate.
  • Gene expression analysis of the narGHJI operon.
  • Assessment of V. parvula growth on various carbon sources.
  • In vivo colonization studies using a mouse model of colitis.

Main Results:

  • Nitrate allows V. parvula to switch from fermentation to anaerobic respiration via the narGHJI operon.
  • Nitrate respiration enhances V. parvula's growth on organic acids and enables utilization of amino acids and peptides.
  • This metabolic shift alters carbon metabolism and ATP production pathways.
  • A V. parvula narG deletion mutant showed significantly reduced colonization in a mouse colitis model compared to wild-type.

Conclusions:

  • Veillonella parvula utilizes inflammation-associated nitrate to adapt its metabolism for intestinal colonization.
  • Nitrate respiration is crucial for V. parvula's ability to colonize the inflamed gut.
  • This highlights a mechanism by which oral bacteria exploit inflammatory conditions to expand in the intestine.