Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba 278-8510, Japan.
Anticancer Res. 2010 Aug;30(8):3135-41.
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.
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.
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.
Activation of alveolar macrophages by LPS suppresses the growth of lung carcinoma cells via NO production under cell-to-cell contact conditions.
巨噬细胞可能对癌症治疗有效，因为一旦被激活，肺巨噬细胞就会增强与肺肿瘤细胞的接触，并具有细胞毒性作用。本文报告了脂多糖（LPS）激活的肺巨噬细胞产生的一氧化氮（NO）抑制了人肺腺癌细胞的生长。
用 NR8383（大鼠肺泡巨噬细胞系）培养 A549（肺腺癌细胞系），在存在和不存在 LPS 的情况下。在细胞接触条件下，考察 LPS 对 A549 细胞生长率的影响与 NO 产生的关系。
当两种细胞在 LPS 存在下共培养时，NR8383 细胞对 A549 细胞表现出强烈的细胞生长抑制和杀伤作用。这些作用主要归因于 NO 的产生，但也可能涉及其他机制，如细胞间接触。
LPS 激活肺泡巨噬细胞通过细胞接触条件下的 NO 产生抑制肺癌细胞的生长。
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