The Interplay Between Inflammatory Signaling and Nuclear Structure and Function

Inflammation is an adaptive response that is triggered by noxious stimuli such as infection and tissue injury. Beside immune cells representing the main source of pro-inflammatory cytokines other, mainly damaged cells, contribute to production of these cytokines. For many of the pro-inflammatory cytokines were described that their prolonged exposure activates free radicals in normal and tumor cells which results in DNA damage, changes in nuclear structure and gene expression, activation of cell cycle checkpoints and cell cycle arrest. Failure of cell proliferation may help to stop the progression of premalignant and tumor cells, but changes in gene expression in these arrested cells (tumor and normal) are often accompanied with increased production of pro-inflammatory cytokines. If these arrested cells are not eliminated from organism they pose a threat to propagation of inflammation and development of degenerative diseases, cancer and aging.