Mycoplasma infection with M. Arginini results in NF-κB constitutive activation and inhibition of apoptosis in cells expressing toll-like receptors TLR2/6

Transcription factor NF-κB is one of the main determinants of cell survival under different stress conditions. It is known that different mycoplasma species and their structural elements activate this transcription factor upon interacting with specific combinations of Toll-like receptors on the surface of the host cell. We supposed that activation of NF-κB in response to mycoplasma infection resulted in an increased resistance of the infected cell cultures to proapoptotic factors. In the present study, we demonstrated that the infection of cells that expressed Toll-like receptors 2/6 with mycoplasma M. arginini resulted in the activation of transcription factor NF-κB and inhibited apoptosis induced by different chemotherapeutical drugs such as cisplatin, 5-fluoruracyl, taxol.