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超细碳颗粒聚集体会损害人类肺泡巨噬细胞的吞噬功能。

Human alveolar macrophage phagocytic function is impaired by aggregates of ultrafine carbon particles.

作者信息

Lundborg M, Johard U, Låstbom L, Gerde P, Camner P

机构信息

Division of Inhalation Toxicology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Environ Res. 2001 Jul;86(3):244-53. doi: 10.1006/enrs.2001.4269.

Abstract

Alveolar macrophages (AM) were collected by bronchoalveolar lavage from healthy volunteers. The AM were loaded with small masses (0.03-3 microg/10(6) AM) of ultrafine carbon particle aggregates. The phagocytic activity of the cells was studied 20 h after the loading. Fluorescein-labeled silica particles (3 microm) were used as test particles and the attachment and ingestion processes were studied separately. In some experiments, AM were incubated with interferon-gamma (IFN-gamma) for 20 h before and during the test of phagocytic activity and during measurement of oxidative metabolism. The ingested carbon particles induced a dose-related impairment of both the attachment and the ingestion processes with a marked impairment down to a carbon particle dose around 0.2 microg/10(6) AM. Such levels should reasonably occur after inhalation of existing concentrations of urban air particles, which to a considerable extent consist of aggregates of ultrafine particles with a carbon skeleton. Incubation with IFN-gamma (12.5 U/ml) also induced significant impairments in both the attachment and the ingestion processes. Loading with carbon further aggravated the effect of IFN-gamma. In contrast to earlier studies in rat AM, IFN-gamma did not impair the oxidative metabolism at rest in these human AM; instead the oxidative metabolism was increased. This difference was due to a difference between rat and human AM and not between rat and human IFN-gamma. Our results suggest that ingested environmental particles in AM, e.g., after an episode of high particle concentration, may impair phagocytic capacity of the cells, especially after infections that induce an increased production of IFN-gamma. Consequently, there might be a risk for additional infections. Moreover, inhaled particles not phagocytized by AM might damage the lung tissue.

摘要

通过支气管肺泡灌洗从健康志愿者中收集肺泡巨噬细胞(AM)。将AM用小剂量(0.03 - 3微克/10⁶个AM)的超细碳颗粒聚集体进行负载。在负载后20小时研究细胞的吞噬活性。使用荧光素标记的二氧化硅颗粒(3微米)作为测试颗粒,分别研究附着和摄取过程。在一些实验中,在吞噬活性测试以及氧化代谢测量之前和期间,将AM与干扰素 - γ(IFN - γ)孵育20小时。摄取的碳颗粒导致附着和摄取过程均出现剂量相关的损伤,在碳颗粒剂量约为0.2微克/10⁶个AM时损伤明显。吸入现有浓度的城市空气颗粒后,这种水平很可能会出现,这些颗粒在很大程度上由具有碳骨架的超细颗粒聚集体组成。用IFN - γ(12.5 U/ml)孵育也会导致附着和摄取过程出现显著损伤。用碳负载进一步加剧了IFN - γ的作用。与早期对大鼠AM的研究不同,IFN - γ在这些人AM中并未损害静息状态下的氧化代谢;相反,氧化代谢增加。这种差异是由于大鼠和人AM之间的差异,而非大鼠和人IFN - γ之间的差异。我们的结果表明,AM摄取的环境颗粒,例如在高颗粒浓度事件之后,可能会损害细胞的吞噬能力,尤其是在诱导IFN - γ产生增加的感染之后。因此,可能存在额外感染的风险。此外,未被AM吞噬的吸入颗粒可能会损害肺组织。

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