Modulation of the PI3K/Akt/mTOR signaling pathway by probiotics as a fruitful target for orchestrating the immune response

Gut Microbes. 2021 Jan-Dec;13(1):1-17. doi: 10.1080/19490976.2021.1886844.

Abstract

The mammalian target of rapamycin (mTOR) and the phosphatidylinositol-3-kinase (PI3K)/protein kinase B or Akt (PKB/Akt) signaling pathways are considered as two but somewhat interconnected significant immune pathways which play complex roles in a variety of physiological processes as well as pathological conditions. Aberrant activation of PI3K/Akt/mTOR signaling pathways has been reported to be associated in a wide variety of human diseases. Over the past few years, growing evidence in in vitro and in vivo models suggest that this sophisticated and subtle cascade mediates the orchestration of the immune response in health and disease through exposure to probiotics. An expanding body of literature has highlighted the contribution of probiotics and PI3K/Akt/mTOR signaling pathways in gastrointestinal disorders, metabolic syndrome, skin diseases, allergy, salmonella infection, and aging. However, longitudinal human studies are possibly required to verify more conclusively whether the investigational tools used to understand the regulation of these pathways might provide effective approaches in the prevention and treatment of various disorders. In this Review, we summarize the experimental evidence from recent peer-reviewed studies and provide a brief overview of the causal relationship between the effects of probiotics and their metabolites on the components of PI3K/Akt/mTOR signaling pathways and human disease.

Keywords: bifidobacterium; lactobacillus; PI3K; akt; mTOR; probiotics.

Publication types

  • Review

MeSH terms

  • Animals
  • Gastrointestinal Diseases / diet therapy
  • Gastrointestinal Diseases / metabolism
  • Humans
  • Immunity*
  • Metabolic Syndrome / diet therapy
  • Metabolic Syndrome / metabolism
  • Neoplasms / diet therapy
  • Neoplasms / immunology
  • Non-alcoholic Fatty Liver Disease / diet therapy
  • Non-alcoholic Fatty Liver Disease / metabolism
  • Phosphatidylinositol 3-Kinase / metabolism*
  • Probiotics*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases

Grants and funding

The authors have no funding to report.