Background : Radiation therapy plays an important role in the treatment of lung cancer. However, it also radiation therapy often induces serious complications such as radiation-induced pneumonitis and its underlying mechanism remains to be elucidated.
Objectives : The present study examined whether radiation might stimulate human lung fibroblasts (HLF) to release neutrophil and monocyte chemotactic activity (NCA and MCA).
Methods : HLF were exposed to varying doses of radiation (3-12 Gy) at varying incubation times (12-72 hr). The chemotaxis assays of NCA and MCA were performed by a 48-well microchemotaxis chamber method. The effect of polyclonal antibodies of various cytokines on NCA and MCA was evaluated. Furthermore, the protein and mRNA expression of these effective cytokines was assessed by ELISA and RT-PCR.
Results : HLF released NCA and MCA in response to irradiation in a dose- and time- dependent manner. NCA was significantly inhibited by anti-interleukin (IL)-8 antibody and MCA was significantly attenuated by antimonocyte chemoattractant protein (MCP)-1 antibody. The protein secretion of IL-8 and MCP-1 was significantly increased by irradiation, and mRNA expression of IL-8 and MCP-1 was upregulated by irradiation.
Conclusion : These findings suggest that HLF may, at least partly, participate in the development of radiationinduced pneumonitis.

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A 70-year-old man with a history of doing wiring work for 30 years was admitted to our hospital because of lower abdominal pain and ascites. Four months before admission he underwent cholecystectomy due to cholelithiasis and cholecystitis. At that time there were no macroscopic abnormal findings in the peritoneum, surface of the gall bladder, liver, stomach or intestine. We suspected peritonitis carcinomatosa, but ascetic fluid was light yellow and clear, and cytology showed no malignant cells. Computed tomography (CT) showed no malignant findings in visceral organs including the liver, pancreas, spleen, kidney and lung, but prominent ascites and thickening of the peritoneum and omentum were observed. After admission the ascites increased significantly and pleural effusion appeared. The patient died due to respiratory insufficiency two weeks from the onset of disease. Autopsy findings revealed sarcomatoid mesothelioma of the peritoneum, omentum and mesentery. Asbestos bodies were found in the lung, and the concentration of hyaluronic acid in ascites was very high. In conclusion, in cases with rapidly progressive and refractory ascites, asbestos-induced mesothelioma should be included in the differential diagnosis.

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