AIM: It is possible that macrophages may be effective for cancer treatment because once activated, lung macrophages have enhanced contact with lung tumor cells and have a cytotoxic effect. In this paper, we report that nitric oxide (NO) produced by lung macrophages activated with lipopolysaccharide (LPS) suppressed cell growth of human lung adenocarcinoma cells. MATERIALS AND METHODS: A549, a lung adenocarcinoma cell line, was cultured with NR8383, a rat alveolar macrophage cell line, in the presence and absence of LPS. The effect of LPS on the growth rate of A549 cells was examined as a function of NO production under cell-to-cell contact conditions. RESULTS: NR8383 cells showed potent cytostatic and cytocidal effects on A549 cells when both cells were co-cultured in the presence of LPS. These effects were mainly due to the production of NO, but another possible mechanism, such as cell-to-cell contact, may also be involved. CONCLUSION: Activation of alveolar macrophages by LPS suppresses the growth of lung carcinoma cells via NO production under cell-to-cell contact conditions.
AIM: It is possible that macrophages may be effective for cancer treatment because once activated, lung macrophages have enhanced contact with lung tumor cells and have a cytotoxic effect. In this paper, we report that nitric oxide (NO) produced by lung macrophages activated with lipopolysaccharide (LPS) suppressed cell growth of humanlung adenocarcinoma cells. MATERIALS AND METHODS: A549, a lung adenocarcinoma cell line, was cultured with NR8383, a rat alveolar macrophage cell line, in the presence and absence of LPS. The effect of LPS on the growth rate of A549 cells was examined as a function of NO production under cell-to-cell contact conditions. RESULTS: NR8383 cells showed potent cytostatic and cytocidal effects on A549 cells when both cells were co-cultured in the presence of LPS. These effects were mainly due to the production of NO, but another possible mechanism, such as cell-to-cell contact, may also be involved. CONCLUSION: Activation of alveolar macrophages by LPS suppresses the growth of lung carcinoma cells via NO production under cell-to-cell contact conditions.