Radiation-induced inflammatory response

Radiation-induced inflammatory responses arise when ionizing radiation causes DNA damage directly or indirectly via reactive oxygen species generation. This triggers cellular stress pathways including activation of ataxia telangiectasia mutated protein kinase (ATM), tumor suppressor p53, and nuclear factor kappa B (NF-kB). These transcription factors regulate expression of numerous pro-inflammatory cytokines such as tumor necrosis factor alpha (TNFα), interleukins IL1β and IL6, chemokines like CCL2/3/8/20 along with adhesion molecules that promote leukocyte recruitment. Macrophages exposed to low-dose irradiation adopt diverse phenotypes ranging from pro-inflammatory states promoting anti-tumor immunity through inducible nitric oxide synthase upregulation to immunosuppressive profiles depending on tumor microenvironment cues. This plasticity influences cancer progression or regression following radiotherapy. Overall, the "radiation-induced inflammatory response" represents an orchestrated network linking DNA damage sensing with innate immunity activation that impacts both therapeutic outcomes in cancer treatment and normal tissue side effects[1][2][3][4].

Other names

Radiation-triggered inflammationRadiation-induced immune activationIonizing radiation-induced inflammatory signaling

Drugs targeting components involved in this process act by: Inhibiting pro-inflammatory cytokine production or action (e.g., TNF-alpha blockers); Modulating transcription factor activity such as NF-kB or p53 pathways; Scavenging reactive oxygen species to reduce oxidative stress