[The relevance of cytokines in the radiation-induced lung reaction. Experimental basis and clinical significance].

BACKGROUND: The radiosensitivity of the lung tissue limits the dose of radiation which can be delivered to tumors in the thoracic region. Radiation-induced lung damage implies the induction of numerous cytokines which form the basis for the multicellular interactions of the inflammatory and fibrogenic processes associated with radiation injury. It is of special clinical significance, how far local radiation induced cytokine production in the lung tissue may be reflected in increased cytokine blood levels in patients during radiotherapy and may predict the later development of radiation-induced lung damage. Another potential cause of increased cytokine levels in the blood of oncologic patients is the secretion of cytokines in the blood circulation by tumor specimens.
METHODS: Published data on radiation-induced cytokine expression from experimental and clinical studies are reviewed. 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.