Mitochondria, the gut microbiome and ROS

Cell Signal. 2020 Nov:75:109737. doi: 10.1016/j.cellsig.2020.109737. Epub 2020 Aug 15.

Abstract

In this review, we discuss the connections between mitochondria and the gut microbiome provided by reactive oxygen species (ROS). We examine the mitochondrion as an endosymbiotic organelle that is a hub for energy production, signaling, and cell homeostasis. Maintaining a diverse gut microbiome is generally associated with organismal fitness, intestinal health and resistance to environmental stress. In contrast, gut microbiome imbalance, termed dysbiosis, is linked to a reduction in organismal well-being. ROS are essential signaling molecules but can be damaging when present in excess. Increasing ROS levels have been shown to influence human health, homeostasis of gut cells, and the gastrointestinal microbial community's biodiversity. Reciprocally, gut microbes can affect ROS levels, mitochondrial homeostasis, and host health. We propose that mechanistic understanding of the suite of bi-directional interactions between mitochondria and the gut microbiome will facilitate innovative interdisciplinary studies examining evolutionary divergence and provide novel treatments and therapeutics for disease. GLOSS: In this review, we focus on the nexus between mitochondria and the gut microbiome provided by reactive oxygen species (ROS). Mitochondria are a cell organelle that is derived from an ancestral alpha-proteobacteria. They generate around 80% of the adenosine triphosphate that an organism needs to function and release a range of signaling molecules essential for cellular homeostasis. The gut microbiome is a suite of microorganisms that are commensal, symbiotic and pathogenic to their host. ROS are one predominant group of essential signaling molecules that can be harmful in excess. We suggest that the mitochondria- microbiome nexus is a frontier of research that has cross-disciplinary benefits in understanding genetic divergence and human well-being.

Keywords: Hydrogen peroxide; Intestinal epithelium; Mitochondrial DNA; Mitonuclear incompatibility; Superoxide.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Line
  • Gastrointestinal Microbiome*
  • Homeostasis
  • Humans
  • Intestinal Mucosa* / metabolism
  • Intestinal Mucosa* / microbiology
  • Mitochondria / metabolism*
  • Reactive Oxygen Species / metabolism*
  • Symbiosis

Substances

  • Reactive Oxygen Species