Effects of mycoplasma infection on the host organism response via p53/NF-κB signaling

J Cell Physiol. 2018 Jan;234(1):171-180. doi: 10.1002/jcp.26781. Epub 2018 Aug 26.

Abstract

Mycoplasmas are bacteria lacking the cell wall, which is the major characteristic of this taxonomic class (Mollicutes). Among bacteria, mycoplasmas possess the smallest genome known for free-living organisms. This feature limits the autonomy of bacteria and makes them increasingly susceptible to changes in the host organism. Many mycoplasmas themselves cause pathological changes in the host organism, often complicated by immune disorders. Infection with certain strains of mycoplasma results in the activation of the nuclear factor kappa-light-chain-enhancer of activated B cells, which is the major mediator of the inflammatory response. Furthermore, mycoplasmas can inhibit p53-mediated checkpoint control of cell cycle and apoptosis. Collectively, these properties indicate that mycoplasmas might act as cancer-promoting factors. In this review, we summarize the information known to date on the role of mycoplasmas in the regulation of the host immune response and their functional interactions with p53.

Keywords: inflammation; mycoplasma; nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); p53; posttranslational modifications.

Publication types

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

MeSH terms

  • Apoptosis / genetics
  • Apoptosis / immunology
  • Cell Division / genetics
  • Host-Pathogen Interactions / genetics
  • Host-Pathogen Interactions / immunology
  • Humans
  • Lymphocyte Activation / genetics
  • Lymphocyte Activation / immunology
  • Mycoplasma / genetics
  • Mycoplasma / immunology
  • Mycoplasma / pathogenicity*
  • Mycoplasma Infections / genetics*
  • Mycoplasma Infections / immunology
  • Mycoplasma Infections / microbiology
  • NF-kappa B / genetics*
  • Signal Transduction
  • Transcription Factor RelA / genetics
  • Transcription Factor RelA / immunology
  • Tumor Suppressor Protein p53 / genetics*

Substances

  • NF-kappa B
  • RELA protein, human
  • TP53 protein, human
  • Transcription Factor RelA
  • Tumor Suppressor Protein p53