RESULTS AND CONCLUSION: The major pro-inflammatory cytokines in the radiation
response of the lung include tumor necrosis factor-alpha (TNF-alpha),
interleukin-1 (IL-1), and interleukin-6 (IL-6). Transforming growth factor-beta
(TGF-beta) appears to be of particular importance in the development of lung
fibrosis. First approaches with radioprotective agents and gene therapy to modify
radiation-induced cytokine expression have been investigated for prevention of
late effects of irradiation lung damage in animal experiments. Preliminary data
of clinical studies suggest that elevated plasma TGF-beta-levels during
radiotherapy may predict the development of symptomatic radiation pneumonitis.
The biological impacts of endogenous radiation-induced cytokine production by
tumor cells in respect of tumor behavior, potential damage to normal tissue, and
clinical status of the host still need to be determined more precisely.