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Summary
Tissues that are stressed by injury or by invading pathogens elicit signals for the recruitment of inflammatory immune cells such as macrophages and neutrophils, which consequently release reactive oxygen and nitrogen species (RONS) as part of the innate immune response (1). This flood of RONS is important for directly attacking invading pathogens and for warding off infection of damaged tissue. But the efficiency of RONS in inactivating invading cells and viruses creates an Achilles heel of the innate immune response, namely that RONS are also able to kill and mutate cells in healthy tissues. Although inflammatory responses are usually counterbalanced over time by an opposing anti-inflammatory response, achieving the optimal balance with minimal collateral tissue damage is difficult even in healthy individuals, and virtually impossible in individuals with certain disease conditions such as ulcerative colitis and rheumatoid arthritis (2). Therefore, the development of anti-inflammatory drugs, targeting inflammation from a variety of different angles, has flourished in recent decades. On page 834 of this issue, Visnes et al. (3) present an entirely new approach to suppressing the inflammatory response. Counter-intuitively, this approach involves the inhibition of the 8-oxoguanine DNA glycosylase 1 (OGG1) DNA repair enzyme that recognizes and initiates the base excision repair of 7,8-dihydro-8-oxoguanine (8-oxoG), one of the major types of DNA base damage induced by RONS.
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