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Inhalation of PM2.5 does not modulate host defense or immune parameters in blood or lung of normal human subjects.

机译:吸入PM2.5不会调节正常人血液或肺中的宿主防御或免疫参数。

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摘要

We tested the hypothesis that exposure of healthy volunteers to concentrated ambient air particles (CAPS) between 0.1 and 2.5 microm in diameter is associated with modulation of human alveolar macrophage (AM) function, cytokine production, and immune phenotype in both blood and lung. Thirty-eight volunteers were exposed to either filtered air or CAPS from the immediate environment of the U.S. Environmental Protection Agency human studies facility in Chapel Hill, North Carolina, USA. Particle concentrations in the chamber during the exposures ranged from 23.1 to 311.1 microg/m3. No symptoms were noted by volunteers after the exposure. Eighteen hours after exposure, analysis of cells obtained by bronchoalveolar lavage (BAL) showed a mild increase in neutrophils in both the bronchial (8.4 +/- 2%) and alveolar fractions (4.2 +/- 1.7%) in subjects exposed to the highest concentration of CAPS compared to neutrophils in the fluids of those exposed to filtered air (bronchial fraction 2.7 +/- 0.6%; alveolar fraction 0.8 +/- 0.3%). There was no change in the percentage of lymphocytes or AMs recovered in the lavage after inhalation of the highest particle levels (mean 207 microg/m3). There was also no change in the proportion of lymphocytes in the BAL expressing CD3, CD4, CD8, CD19, nor activation markers CD25 or CD69. Particle inhalation did not affect the expression of CD11b, CD64, CD16, CD14, CD71 on AM, nor was there an effect on phagocytosis or oxidant generation following stimulation with zymosan A. IL-6 and IL-8 levels detected by enzyme-linked immunoabsorbent assay in the BAL were unrelated to inhaled particle levels. The distribution of lymphocyte subsets in blood obtained 18 hr after exposure to CAPS did not differ from that found before exposure. We conclude that ambient air particles are capable of inducing a mild inflammation in the lower respiratory tract but have no effect on immune phenotype or macrophage function under the conditions tested.
机译:我们测试了以下假设:健康志愿者暴露于直径在0.1到2.5微米之间的浓缩环境空气颗粒(CAPS)中,这与人类肺泡巨噬细胞(AM)功能,细胞因子产生以及血液和肺部免疫表型的调节有关。 38名志愿者从位于美国北卡罗来纳州教堂山的美国环境保护署人类研究设施的直接环境中暴露于过滤空气或CAPS中。暴露过程中室内的颗粒浓度范围为23.1至311.1 microg / m3。暴露后志愿者没有发现任何症状。暴露后十八小时,对通过支气管肺泡灌洗(BAL)获得的细胞进行的分析显示,在暴露于最高剂量的受试者中,支气管(8.4 +/- 2%)和肺泡分数(4.2 +/- 1.7%)中的中性粒细胞轻度增加暴露于经过滤空气的患者的液体中CAPS的浓度与嗜中性粒细胞相比(支气管分数2.7 +/- 0.6%;肺泡分数0.8 +/- 0.3%)。吸入最高颗粒水平(平均207微克/立方米)后,灌洗液中回收的淋巴细胞或AM的百分比没有变化。在表达CD3,CD4,CD8,CD19或激活标记CD25或CD69的BAL中,淋巴细胞的比例也没有变化。吸入颗粒物不会影响AM上CD11b,CD64,CD16,CD14,CD71的表达,也不会影响经酵母聚糖A刺激后的吞噬作用或氧化剂的产生。酶联免疫吸附剂检测到IL-6和IL-8水平BAL中的血浆分析与吸入颗粒水平无关。暴露于CAPS后18小时获得的血液中淋巴细胞亚群的分布与暴露前无差异。我们得出结论,在所测试的条件下,环境空气颗粒能够在下呼吸道中引起轻度炎症,但对免疫表型或巨噬细胞功能没有影响。

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