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吸烟会削弱接触惰性粉尘后肺泡巨噬细胞的激活。

Smoking impairs alveolar macrophage activation after inert dust exposure.

作者信息

Möller W, Barth W, Pohlit W, Rust M, Siekmeier R, Stahlhofen W, Heyder J

机构信息

GSF-Institut für Inhalationsbiologie, Oberschleissheim, Germany.

出版信息

Toxicol Lett. 1996 Nov;88(1-3):131-7. doi: 10.1016/0378-4274(96)03728-9.

Abstract

Magnetopneumography was applied to investigate intracellular phagosome motion in alveolar macrophage cells of healthy subjects (non-smokers and smokers). Ingested magnetic microparticles are inhaled and phagocytized by alveolar macrophages within hours. Thereby the particles are transferred into phagolysosomes. After magnetization the particles produce a macroscopic magnetic field of the lungs. Cellular motility causes a decay of the field (relaxation) by stochastic disorientation of the dipole particles (phagolysosomes) in the cells. Our studies have shown that the deposition of magnetite test particles induces a non-specific activation of the macrophage cells with a faster relaxation. This activation vanishes within the first day after particle deposition. This macrophage activation due to dust exposure was not present in smokers. It follows that cigarette smoking either causes a damage of the cellular defense or causes an adaptation of the macrophage cells to the permanent cigarette smoke inhalation.

摘要

应用磁肺造影术研究健康受试者(非吸烟者和吸烟者)肺泡巨噬细胞内吞噬体的运动。吸入的磁性微粒在数小时内被肺泡巨噬细胞吸入并吞噬。由此,微粒被转移到吞噬溶酶体中。磁化后,微粒会产生肺部的宏观磁场。细胞运动通过细胞内偶极微粒(吞噬溶酶体)的随机取向改变导致磁场衰减(弛豫)。我们的研究表明,磁铁矿测试微粒的沉积会诱导巨噬细胞的非特异性激活,弛豫加快。这种激活在微粒沉积后的第一天内消失。吸烟者不存在因接触灰尘导致的这种巨噬细胞激活。由此可见,吸烟要么会损害细胞防御,要么会使巨噬细胞适应长期吸入香烟烟雾的情况。

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