免疫原性细胞死亡在抗癌治疗中发挥着重要作用，因为它将细胞死亡与损伤相关分子模式的出现结合起来，这些分子模式有可能激活抗癌免疫。主要研究了基于氨基乙酰丙酸的光动力疗法诱导的损伤相关分子模式对树突状细胞的影响。他们尚未对构成肿瘤微环境重要组成部分的巨噬细胞进行深入研究。本研究的目的是分析食管癌细胞死亡特征与损伤相关分子模式种类释放能力的关系，并测试相关细胞外环境改变对巨噬细胞的影响。食管 Kyse 450 癌细胞接受氨基乙酰丙酸-基于不同浓度氨基乙酰丙酸的光动力疗法。从单核细胞 THP-1 细胞系制备静息巨噬细胞、IFN/LPS 和 IL-4 巨噬细胞亚型。通过基于荧光的活细胞成像分析细胞死亡特征和巨噬细胞修饰。通过 ELISA 测定测定细胞培养基中的 ATP 和 HMGB1 水平。通过分光光度法检测硫代巴比妥酸反应物质来评估培养基中脂质过氧化产物的存在。基于氨基乙酰丙酸的光动力疗法诱导了Kyse 450细胞的多种死亡途径，包括凋亡、坏死和铁死亡的特征。经处理的 Kyse 450 细胞的细胞外环境中 ATP 量随着氨基乙酰丙酸浓度的增加而增加。通过 ELISA 检测培养基中的 HMGB1 水平，在治疗后有所下降。基于氨基乙酰丙酸的光动力疗法诱导细胞结构的脂质过氧化并增加细胞外脂质过氧化产物的水平。在经过基于氨基乙酰丙酸的光动力疗法处理的 Kyse 450 细胞的条件培养基中孵育静息巨噬细胞和 IL-4 巨噬细胞，诱导了巨噬细胞的形态变化，然而，来自未经处理的癌细胞的条件培养基也诱导了类似的变化。 基于氨基乙酰丙酸的光动力疗法导致局部细胞外损伤相关分子模式水平的改变，然而，需要进行全面的研究来发现它们是否可以导致巨噬细胞表型改变。

Immunogenic cell death plays an important role in anticancer treatment because it combines cell death with appearance of damage associated molecular patterns that have the potential to activate anticancer immunity. Effects of damage associated molecular patterns induced by aminolevulinic acid-based photodynamic therapy were studied mainly on dendritic cells. They have not been deeply studied on macrophages that constitute the essential component of the tumor microenvironment. The aim of this study was to analyze features of esophageal cancer cell death in relation to release capacity of damage associated molecular pattern species, and to test the effect of related extracellular environmental alterations on macrophages.Esophageal Kyse 450 carcinoma cells were subjected to aminolevulinic acid-based photodynamic therapy at different concentrations of aminolevulinic acid. Resting, IFN/LPS and IL-4 macrophage subtypes were prepared from monocytic THP-1 cell line. Cell death features and macrophage modifications were analyzed by fluorescence-based live cell imaging. ATP and HMGB1 levels in cell culture media were determined by ELISA assays. The presence of lipid peroxidation products in culture media was assessed by spectrophotometric detection of thiobarbituric acid reactive substances.Aminolevulinic acid-based photodynamic therapy induced various death pathways in Kyse 450 cells that included features of apoptosis, necrosis and ferroptosis. ATP amounts in extracellular environment of treated Kyse 450 cells increased with increasing aminolevulinic acid concentration. Levels of HMGB1, detectable by ELISA assay in culture media, were decreased after the treatment. Aminolevulinic acid-based photodynamic therapy induced lipid peroxidation of cellular structures and increased levels of extracellular lipid peroxidation products. Incubation of resting and IL-4 macrophages in conditioned medium from Kyse 450 cells treated by aminolevulinic acid-based photodynamic therapy induced morphological changes in macrophages, however, comparable alterations were induced also by conditioned medium from untreated cancer cells.Aminolevulinic acid-based photodynamic therapy leads to alterations in local extracellular levels of damage associated molecular patterns, however, comprehensive studies are needed to find whether they can be responsible for macrophage phenotype modifications.