Microbial mechanisms of regulation of the activity of nuclear transcription factor NF-kB1

Zakharova Yu.V., Soboleva O.M., Otdushkina L.Yu., Levanova L.A.

Kemerovo State Medical University, Kemerovo

Nuclear transcription factor NF-kB1 is a regulator of the expression of immune response genes, apoptosis, inflammatory reactions and cell proliferation. Microorganisms are able to change the activity of the nuclear transcription factor, which allows them to modulate the immune response of the macroorganism and/or have a pathogenic effect on organs and tissues.
The aim of the study is to systematize data on microbial molecular factors regulating the transcription nuclear factor NFkB-1.
The review describes microbial molecules, the mechanisms of their action on the nuclear transcription factor NF-kB1. The A52R protein of the smallpox vaccine virus acts as a homologue of MyD88, the Yersinia YopP/J protein acetylates the IKKß subunit, thereby inhibiting kB kinase (IKK) and preventing the activation of the nuclear factor NFkB. The EBNA1 protein of the Epstein-Barr virus is a "stop signal" for the proteasome, so blocking proteolysis disrupts the presentation of virus antigens on MHC I and the overall immune response. The OspG protein of microorganisms of the genus Shigella prevents ubiquitination, and also inhibits the degradation of phosphorylated IKKß, which disrupts the activation of NFkB-1. Enteropathogenic Escherichia coli (EPEC) produces three effectors to inhibit the function of NFkB. Two of these effectors, NleB and NleE block signaling at the level of TGF-beta-activated kinase 1 or IKKß kinase, the third NleH protein binds to the RPS3 (ribosomal protein S3) cofactor of the NFkB factor and suppresses the transcription of many genes.
The components of bacterial cells – lipopolysaccharides of the cell walls of gram-negative bacteria, representatives of the Enterobacteriaceae family, participate in modulating the activity of the transcription factor. This polymer affects the presentation genes of MHC class I and II antigens, the death receptor, IL-6 signaling, IFN-γ signaling and the P38 signaling pathway.
Conclusion. Protein and non-protein substances of microorganisms, components of bacterial cell structures are molecules that have a multidirectional effect on the activity of proteasomes that regulate inflammatory and immune responses in the macroorganism.