Effects of mycoplasma infection on the host organism response via p53/NF-κB signaling.
Sergey N BorchseniusAlexandra DaksOlga FedorovaOlga ChernovaNickolai A BarlevPublished in: Journal of cellular physiology (2018)
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.
Keyphrases
- nuclear factor
- cell cycle
- toll like receptor
- inflammatory response
- immune response
- cell wall
- cell proliferation
- oxidative stress
- lps induced
- escherichia coli
- dna damage
- machine learning
- squamous cell carcinoma
- cell death
- healthcare
- signaling pathway
- lipopolysaccharide induced
- papillary thyroid
- young adults
- dna methylation
- binding protein
- childhood cancer