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首页> 外文期刊>Infection and immunity >Effect of endothelial cells on phagocyte-mediated anticryptococcal activity.
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Effect of endothelial cells on phagocyte-mediated anticryptococcal activity.

机译：内皮细胞对吞噬细胞介导的抗隐球菌活性的影响。

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The anticryptococcal activity of peripheral blood polymorphonuclear leukocytes (PMN) and monocytes was compared on plastic versus human umbilical vein endothelial cell surfaces. Various amounts of PMN and monocytes were incubated on plastic or endothelial surfaces and then challenged for 18 h with Cryptococcus neoformans. Both phagocyte populations exhibited significantly more anticryptococcal activity on an endothelial cell monolayer than on plastic. Prestimulating the endothelial cell monolayer with interleukin-1 augmented the antifungal activity of PMN but not that of monocytes. In the absence of phagocytes, endothelial cells lacked activity. Blocking antibodies directed against endothelial adhesion molecules ICAM-1 and ELAM-1 did not affect PMN-mediated inhibition of fungal growth. Recombinant interleukin-1 and interleukin-8 (two cytokines secreted by endothelial cells) activated neutrophils for modestly enhanced antifungal activity. However, supernatants derived from endothelial cells, as well as neutralizing antibodies directed against the endothelial cell-derived cytokines interleukin-8 and granulocyte-macrophage colony-stimulating factor failed to augment PMN antifungal activity. PMN viability after 18 h was diminished on plastic compared with endothelial surfaces. While the percentages of C. neoformans bound to neutrophils were similar on both surfaces, the patterns of binding were markedly different: on endothelial (but not plastic) surfaces, most cryptococci were surrounded by greater than five PMN. Thus, phagocyte-mediated inhibition of cryptococcal growth is enhanced on endothelial monolayers compared with plastic surfaces, possibly as a result of differences in phagocyte viability and patterns of binding. Bolstering the activity of circulating phagocytes by stimulating endothelial cells may be of relevance in the treatment of patients with or at risk for cryptococcemia.
机译：比较了外周血多形核白细胞（PMN）和单核细胞在塑料和人脐静脉内皮细胞表面的抗隐球菌活性。将各种数量的PMN和单核细胞在塑料或内皮表面孵育，然后用新隐球菌攻击18小时。两个吞噬细胞群体在内皮细胞单层上的抗隐球菌活性均显着高于塑料上的水平。用白介素-1刺激内皮细胞单层可增强PMN的抗真菌活性，但不能增强单核细胞的抗真菌活性。在没有吞噬细胞的情况下，内皮细胞缺乏活性。针对内皮粘附分子ICAM-1和ELAM-1的封闭抗体不会影响PMN介导的真菌生长抑制。重组白介素-1和白介素8（内皮细胞分泌的两种细胞因子）激活嗜中性粒细胞，以适度增强抗真菌活性。然而，源自内皮细胞的上清液以及针对内皮细胞衍生的细胞因子白细胞介素8和粒细胞巨噬细胞集落刺激因子的中和抗体未能增强PMN的抗真菌活性。与内皮表面相比，塑料在18 h后的PMN活力降低。虽然在两个表面上结合嗜中性粒细胞的新孢梭菌的百分比相似，但结合方式却明显不同：在内皮（而非塑料）表面上，大多数隐球菌被五个以上的PMN包围。因此，与塑料表面相比，吞噬细胞介导的隐球菌生长抑制作用在内皮单层上得到增强，这可能是吞噬细胞生存力和结合方式不同的结果。通过刺激内皮细胞增强循环吞噬细胞的活性可能与治疗隐球菌血症或有隐球菌血症风险的患者有关。

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