THE ROLE OF MYCOPLASMA INFECTION IN CHRONIC INFLAMMATION AND CANCEROGENESIS
Many Mycoplasma species can cause pathological changes in the host organism, often complicated by immune disorders. Inflammatory diseases associated with mycoplasmal infection are known as atypical pneumonia, mastitis, urethritis, salpingitis, arthritis and bronchopulmonary dysplasia. Mycoplasma can have a direct effect on the metabolism and physiology of host cells, interfering with the process of nutrient intake, releasing reactive oxygen tipes, which causes genotoxic stress. DNA damage is usually controlled by the nuclear transcription factor, the p53 protein, the main tumor suppressor, also known as the «genome gard». However, in the case of mycoplasmal infection, the activity of the p53 factor is constantly decreasing, and simultaneously its physiological antagonist, the nuclear factor NF-кБ, which is the mediator of inflammatory reactions, is activated. The reaction to mycoplasmal infection in mammals includes several signaling systems that activate the mechanisms of congenital and acquired immunity and, consequently, the development of both acute and chronic inflammatory processes. Inflammation is associated with the action of immune mediators, which are released by epithelial cells and leukocytes in response to mycoplasma infection. The signaling cascade, caused by the recognition of the pathogen, induces the activation of NF-кБ, followed by the expression of pro-inflammatory cytokines and chemokines. The transcription factor NF-кБ causes chronic inflammation at the site of the pathogen invasion, which against the background of suppression of the activity of the nuclear factor p53, eventually forms foci that promote the formation of the tumor.