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深度型膜过滤器中(1-->3)-β-D-葡聚糖的释放及其对促炎细胞因子产生的体外影响。

Release of (1-->3)-beta-D-glucan from depth-type membrane filters and their in vitro effects on proinflammatory cytokine production.

作者信息

Ohata Atsushi, Usami Makoto, Horiuchi Takashi, Nagasawa Koichi, Kinoshita Keiko

机构信息

Faculty of Health Sciences, Kobe University School of Medicine, Kobe, Japan.

出版信息

Artif Organs. 2003 Aug;27(8):728-35. doi: 10.1046/j.1525-1594.2003.07137.x.

Abstract

To clarify the origin of (1-->3)-beta-D-glucan in blood products and assess the biological activity of filter extracts, we evaluated (1-->3)-beta-D-glucan extraction from depth filters used to process blood products and their in vitro effects on proinflammatory cytokine production from macrophages. Cellulose or nylon filters were analyzed for (1-->3)-beta-D-glucan using the Fungitec G test. To evaluate the biological activity of the filter extracts, Mono Mac 6 cells (a human macrophage cell line) were cultured with filter extracts with or without lipopolysaccharide, and tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1beta) concentrations in the culture media were measured. (1-->3)-beta-D-Glucan was released from seven cellulose filters but the nylon filter level was undetectable. Proinflammatory cytokine production ranged from 74.3% to 119.0% of the control for TNF-alpha and 81.2% to 115.9% for IL-1beta. TNF-alpha and IL-1beta levels were low without lipopolysaccharide. The data indicate that (1-->3)-beta-D-glucan in blood products is contaminated with the depth filters and that these filter extracts modulate proinflammatory cytokine production from macrophages.

摘要

为了阐明血液制品中(1→3)-β-D-葡聚糖的来源并评估滤器提取物的生物活性,我们评估了用于处理血液制品的深层滤器中(1→3)-β-D-葡聚糖的提取情况及其对巨噬细胞促炎细胞因子产生的体外影响。使用Fungitec G试验分析纤维素或尼龙滤器中的(1→3)-β-D-葡聚糖。为了评估滤器提取物的生物活性,将Mono Mac 6细胞(一种人巨噬细胞系)与有或无脂多糖的滤器提取物一起培养,并测量培养基中肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的浓度。(1→3)-β-D-葡聚糖从七个纤维素滤器中释放出来,但尼龙滤器中的水平无法检测到。促炎细胞因子的产生范围为TNF-α的对照组的74.3%至119.0%,IL-1β的为81.2%至115.9%。无脂多糖时TNF-α和IL-1β水平较低。数据表明血液制品中的(1→3)-β-D-葡聚糖被深层滤器污染,并且这些滤器提取物调节巨噬细胞促炎细胞因子的产生。

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