Biological material on inhaled coarse fraction particulate matter activates airway phagocytes in vivo in healthy volunteers
Biological material on inhaled coarse fraction particulate matter activates airway phagocytes in vivo in healthy volunteers
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DOI：
10.1016/j.jaci.2006.02.030
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发表时间：
2006-06-01
影响因子：
14.2
通讯作者：
Becker, S
中科院分区：
文献类型：
--
作者：
Alexis, NE;Lay, JC;Becker, S
背景：在体外，粗粒颗粒物 (PM2.5-10) 上的内毒素占 PM2.5-10 诱导肺泡巨噬细胞细胞因子反应能力的大部分。目的：我们在体内检查了从当地环境空气中吸入的 PM2.5-10 是否会引起健康人气道的炎症和免疫反应，以及 PM2.5-10 上的生物物质是否会造成这些影响。方法：在 3 次单独访视中，9 名健康受试者吸入雾化盐水（0.9%，对照）、从当地环境空气中收集的 PM2.5-10（经加热灭活生物物质 (PM2.5-10-)），或非加热 PM (PM2.5-10+)- PM2.5-10 沉积（类似于 0.65 毫克/受试者）靶向支气管气道（通过使用放射性标记气溶胶证实），吸入后 2 至 3 小时获得诱导痰，用于分析炎症和先天免疫功能的细胞和生化标记物。结果：吸入 PM2.5-10+ 诱导炎症升高（% PMNs、巨噬细胞）与生理盐水相比，mRNA TNF-α）、嗜酸细胞趋化因子增加、巨噬细胞免疫表面表型上调（mCD14、CD11b、HLA-DR）以及吞噬作用（单核细胞）增加（P < .05）。 PM2.5-10 (PM2.5-10-) 的生物灭活对中性粒细胞没有影响，但显着 (P < .05) 减弱 mRNA TNF-α、嗜酸细胞活化趋化因子水平、细胞表面标志物反应和吞噬作用。 结论：PM2.5-10 的生物成分对于诱导中性粒细胞反应不是必需的，但对于介导巨噬细胞反应至关重要。 PM2.5-10 能够激活单核细胞，并通过提高嗜酸细胞活化趋化因子水平，潜在地使气道偏向过敏表型，这可能会增强过敏个体对过敏原或细菌的反应。临床意义：PM2.5-10 可能会增强对空气细菌过敏的个体的反应。
Background: In vitro, endotoxin on coarse fraction particulate matter (PM2.5-10) accounts for the majority of the ability of PM2.5-10 to induce cytokine responses from alveolar macrophages. Objective: We examined in vivo whether inhaled PM2.5-10 from local ambient air induce inflammatory and immune responses in the airways of healthy human beings and whether biologic material on PM2.5-10 accounts for these effects.Methods: On 3 separate visits, 9 healthy subjects inhaled nebulized saline (0.9%, control), PM2.5-10 collected from local ambient air that was heated to inactivate biological material (PM2.5-10-), or nonheated PM (PM2.5-10+)- PM2.5-10 deposition (similar to 0.65 mg/subject) targeted the bronchial airways (confirmed by using radiolabeled aerosol), and induced sputum was obtained 2 to 3 hours postinhalation for analysis of cellular and biochemical markers of inflammation and innate immune function.Results: Inhaled PM2.5-10+ induced elevated inflammation (% PMNs, macrophage mRNA TNF-alpha), increased eotaxin, upregulated immune surface phenotypes on macrophages (mCD14, CD11b, HLA-DR), and increased phagocytosis (monocytes) versus saline (P < .05). Biological inactivation of PM2.5-10 (PM2.5-10-) had no effect on neutrophilia but significantly (P < .05) attenuated mRNA TNF-alpha, eotaxin levels, cell surface marker responses, and phagocytosis.Conclusion: Biological components of PM2.5-10 are not necessary to induce neutrophil responses but are essential in mediating macrophage responses. The ability Of PM2.5-10 to activate monocytic cells and potentially skew the airways toward an allergic phenotype by enhancing eotaxin levels may enhance responses to allergens or bacteria in individuals with allergy. Clinical implications: PM2.5-10 might enhance the response of individuals with allergy to airborne bacteria.