Liu Q, Hamblin M R
Wellman Center for Photomedicine, Massachusetts General Hospital, Boston, MA 02114, USA.
Int J Immunopathol Pharmacol. 2005 Jul-Sep;18(3):391-402. doi: 10.1177/039463200501800301.
Macrophage-targeted photodynamic therapy (PDT) may have applications in the selective killing of cells involved in atherosclerosis, inflammation and tumor. We have previously shown that a conjugate between the photosensitizer chlorin(e6) (ce6) and maleylated bovine serum albumin (BSA-mal) gives highly selective targeting to macrophages. In this report we examine the effect of macrophage activation and scavenger receptor class A (SRA) expression on this targeting in two murine macrophage tumor cell lines (RAW264.7 and P388D1) and a control murine mammary sarcoma cell line (EMT-6). Cells were pretreated with interferon gamma (IFNgamma) and/or lipopolysaccharide (LPS) followed byBSA-ce6-mal addition, and SRA expression, tumor necrosis factor alpha (TNFalpha) release, conjugate uptake and PDT killing were measured. Both macrophage cell lines expressed SRA and took up conjugate specifically in an SRA-dependent manner, but differences were observed in their response to activation. RAW264.7 expressed increasingly more SRA and took up increasingly more BSA-ce6-mal in response to IFNgamma, LPS, and IFNgamma+LPS, respectively. The PDT killing did not follow the same pattern as the uptake of the photosensitizer. The increase in uptake in the IFNgamma treated cells did not lead to an increase in PDT killing, while stimulation with LPS or IFNgamma + LPS resulted in a significant protection against PDT, despite a significant increase in photosensitizer uptake. P388D1 was responsive to neither IFNgamma, nor to LPS, or to IFNgamma +LPS with respect to SRA expression, conjugate uptake, and PDT killing. These data may have implications for the use of PDT to target physiologically undesirable macrophage subtypes implicated in disease, and on how manipulation of the activation status of the macrophage will influence the PDT effect.
巨噬细胞靶向光动力疗法(PDT)可能在选择性杀死参与动脉粥样硬化、炎症和肿瘤的细胞方面具有应用价值。我们之前已经表明,光敏剂二氢卟吩(e6)(ce6)与马来酰化牛血清白蛋白(BSA-mal)之间的共轭物对巨噬细胞具有高度选择性靶向作用。在本报告中,我们研究了巨噬细胞激活和A类清道夫受体(SRA)表达对两种小鼠巨噬细胞肿瘤细胞系(RAW264.7和P388D1)以及一种对照小鼠乳腺肉瘤细胞系(EMT-6)中这种靶向作用的影响。细胞先用干扰素γ(IFNγ)和/或脂多糖(LPS)预处理,然后加入BSA-ce6-mal,测量SRA表达、肿瘤坏死因子α(TNFα)释放、共轭物摄取和PDT杀伤作用。两种巨噬细胞系均表达SRA,并以SRA依赖的方式特异性摄取共轭物,但在它们对激活的反应中观察到差异。RAW264.7分别对IFNγ、LPS和IFNγ+LPS反应时,表达越来越多的SRA,并摄取越来越多的BSA-ce6-mal。PDT杀伤作用与光敏剂摄取模式不同。IFNγ处理的细胞摄取增加并未导致PDT杀伤作用增加,而LPS或IFNγ+LPS刺激导致对PDT有显著保护作用,尽管光敏剂摄取显著增加。P388D1在SRA表达、共轭物摄取和PDT杀伤方面对IFNγ、LPS或IFNγ+LPS均无反应。这些数据可能对使用PDT靶向与疾病相关的生理上不良的巨噬细胞亚型以及巨噬细胞激活状态的操纵如何影响PDT效果具有启示意义。