囊性胶质母细胞瘤是侵袭性的原发性脑肿瘤,随着其生长,可能会破坏和移位周围的脑组织。这些肿瘤破坏作用的潜在机制可能包括脑组织暴露于肿瘤衍生的细胞因子,但缺乏细胞因子的定量数据。这里,我们提供了21例囊性胶质母细胞瘤囊肿液中白细胞标记和细胞因子的定量数据,我们将其与13例脑脓肿脓液样本中的值进行比较。胶质母细胞瘤囊液中巨噬细胞/小胶质细胞标志物sCD163和MCP-1的浓度高于脑脓肿脓液;囊液和脓液中淋巴细胞标志物sCD25相似,而中性粒细胞标志物髓过氧化物酶在脓液中更高。胶质母细胞瘤囊液中细胞因子的中位数高(pg/mL):TNF-α:32,IL-6:1064,IL-8:23585,组织因子:28,趋化因子CXCL1:639。这些值与脓液中的值没有显着差异,指向高度促炎的胶质母细胞瘤环境。相比之下,IFN-γ水平,IL-1β,脓液中IL-2,IL-4,IL-10,IL-12和IL-13高于胶质母细胞瘤囊肿液中。根据定量数据,我们首次证明胶质母细胞瘤囊液中细胞因子的浓度与血白细胞水平相关,提示胶质母细胞瘤和循环之间的重要相互作用。囊性胶质母细胞瘤的术前MRI证实了脑组织的破坏和移位,但没有一个细胞因子水平与脑组织移位或肿瘤周围水肿的程度相关,可以通过MRI评估。我们得出的结论是,囊性胶质母细胞瘤是与循环相互作用的高度促炎环境,并且它们既取代又破坏脑组织。这些观察表明,在胶质母细胞瘤治疗中需要神经保护策略,其中可能包括抗炎方法。
Cystic glioblastomas are aggressive primary brain tumors that may both destroy and displace the surrounding brain tissue as they grow. The mechanisms underlying these tumors\' destructive effect could include exposure of brain tissue to tumor-derived cytokines, but quantitative cytokine data are lacking. Here, we provide quantitative data on leukocyte markers and cytokines in the cyst fluid from 21 cystic glioblastomas, which we compare to values in 13 brain abscess
pus samples. The concentration of macrophage/microglia markers sCD163 and MCP-1 was higher in glioblastoma cyst fluid than in brain abscess
pus; lymphocyte marker sCD25 was similar in cyst fluid and
pus, whereas neutrophil marker myeloperoxidase was higher in
pus. Median cytokine levels in glioblastoma cyst fluid were high (pg/mL): TNF-α: 32, IL-6: 1064, IL-8: 23585, tissue factor: 28, the chemokine CXCL1: 639. These values were not significantly different from values in
pus, pointing to a highly pro-inflammatory glioblastoma environment. In contrast, levels of IFN-γ, IL-1β, IL-2, IL-4, IL-10, IL-12, and IL-13 were higher in pus than in glioblastoma cyst fluid. Based on the quantitative data, we show for the first time that the concentrations of cytokines in glioblastoma cyst fluid correlate with blood leukocyte levels, suggesting an important interaction between glioblastomas and the circulation. Preoperative MRI of the cystic glioblastomas confirmed both destruction and displacement of brain tissue, but none of the cytokine levels correlated with degree of brain tissue displacement or peri-tumoral edema, as could be assessed by MRI. We conclude that cystic glioblastomas are highly pro-inflammatory environments that interact with the circulation and that they both displace and destroy brain tissue. These observations point to the need for neuroprotective strategies in glioblastoma therapy, which could include an anti-inflammatory approach.