Dysbiosis Disrupts Gut Immune Homeostasis and Promotes Gastric Diseases

Int J Mol Sci. 2019 May 16;20(10):2432. doi: 10.3390/ijms20102432.

Abstract

Perturbation in the microbial population/colony index has harmful consequences on human health. Both biological and social factors influence the composition of the gut microbiota and also promote gastric diseases. Changes in the gut microbiota manifest in disease progression owing to epigenetic modification in the host, which in turn influences differentiation and function of immune cells adversely. Uncontrolled use of antibiotics, chemotherapeutic drugs, and any change in the diet pattern usually contribute to the changes in the colony index of sensitive strains known to release microbial content in the tissue micromilieu. Ligands released from dying microbes induce Toll-like receptor (TLR) mimicry, skew hypoxia, and cause sterile inflammation, which further contributes to the severity of inflammatory, autoimmune, and tumorous diseases. The major aim and scope of this review is both to discuss various modalities/interventions across the globe and to utilize microbiota-based therapeutic approaches for mitigating the disease burden.

Keywords: TLR mimicry; gut microbiota; immune epigenetics; macrophages; metabolism; sterile inflammation.

Publication types

  • Review

MeSH terms

  • Animals
  • Anti-Bacterial Agents / adverse effects
  • Anti-Bacterial Agents / therapeutic use
  • Antineoplastic Agents / adverse effects
  • Antineoplastic Agents / therapeutic use
  • Autoimmune Diseases
  • Diet
  • Dysbiosis / immunology*
  • Dysbiosis / microbiology
  • Gastrointestinal Microbiome / drug effects
  • Gastrointestinal Microbiome / immunology*
  • Gastrointestinal Microbiome / physiology
  • Homeostasis*
  • Host Microbial Interactions / drug effects
  • Host Microbial Interactions / immunology*
  • Host Microbial Interactions / physiology
  • Humans
  • Hypoxia
  • Inflammation / immunology
  • Macrophages / immunology
  • Stomach Diseases / immunology*
  • Stomach Diseases / microbiology
  • Toll-Like Receptors / metabolism

Substances

  • Anti-Bacterial Agents
  • Antineoplastic Agents
  • Toll-Like Receptors