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大鼠肺泡巨噬细胞释放过氧化氢:与血液中性粒细胞的比较。

Hydrogen peroxide release by rat alveolar macrophages: comparison with blood neutrophils.

作者信息

Biggar W D, Sturgess J M

出版信息

Infect Immun. 1978 Feb;19(2):621-9. doi: 10.1128/iai.19.2.621-629.1978.

DOI:10.1128/iai.19.2.621-629.1978
PMID:564878
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC414128/
Abstract

Hydrogen peroxide release was examined using biochemical and cytochemical techniques in rat alveolar macrophages, at rest and during phagocytosis, and compared with rat blood neutrophils. Using biochemical techniques, alveolar macrophages released small amounts of hydrogen peroxide at rest, and no increase was observed after challenge with opsonized and nonopsonized zymosan particles at several particle-cell ratios (1:1 to 1:1,000). Neutrophils released similar quantities of hydrogen peroxide at rest but showed a 12-fold increase in hydrogen peroxide release following exposure to opsonized zymosan particles. Using cytochemical techniques to localize sites of hydrogen peroxide release, resting neutrophils showed little deposition of reaction product at the cell surface and occasional deposits in endocytotic vesicles. After exposure to latex particles, a dense reaction product was observed between the particle and the cell membrane, indicating significant increases in hydrogen peroxide release at the sites of particle contact with the neutrophil. The resting macrophage displayed a light, uniform precipitation of cerium over the cell surface and lining intracellular channels and endocytotic vesicles and vacuoles. Following particle exposure, there was no significant difference in the density or distribution of reaction product. These findings, together with previous studies of oxidative metabolism, suggest that alveolar macrophages do not release increased quantities of hydrogen peroxide during phagocytosis. In contrast to neutrophils, oxidative-dependent metabolic pathways may not be of primary importance for microbial killing by alveolar macrophages.

摘要

采用生化和细胞化学技术,对处于静息状态和吞噬过程中的大鼠肺泡巨噬细胞的过氧化氢释放情况进行了检测,并与大鼠血液中的中性粒细胞进行了比较。运用生化技术,静息状态下的肺泡巨噬细胞释放少量过氧化氢,在用不同颗粒 - 细胞比例(1:1至1:1000)的调理和未调理酵母聚糖颗粒刺激后,未观察到过氧化氢释放量增加。中性粒细胞在静息时释放的过氧化氢量与之相似,但在接触调理酵母聚糖颗粒后,过氧化氢释放量增加了12倍。利用细胞化学技术定位过氧化氢释放位点,静息中性粒细胞在细胞表面几乎没有反应产物沉积,仅在胞吞小泡中有偶尔的沉积。接触乳胶颗粒后,在颗粒与细胞膜之间观察到密集的反应产物,表明在颗粒与中性粒细胞接触部位过氧化氢释放显著增加。静息巨噬细胞在细胞表面、内衬细胞内通道以及胞吞小泡和液泡上呈现出轻度、均匀的铈沉淀。颗粒暴露后,反应产物的密度或分布没有显著差异。这些发现与先前关于氧化代谢的研究一起表明,肺泡巨噬细胞在吞噬过程中不会释放增加量的过氧化氢。与中性粒细胞不同,氧化依赖性代谢途径可能对肺泡巨噬细胞杀灭微生物并非至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/0e4804113f40/iai00194-0282-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/b9eee8389865/iai00194-0277-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/36433261083e/iai00194-0278-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/878e5e3c19f0/iai00194-0279-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/082405d7e716/iai00194-0279-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/662371f4ea69/iai00194-0279-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/27e2a6481fdf/iai00194-0280-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/78d78ef616f3/iai00194-0281-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/e91bfdfd1675/iai00194-0282-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/0e4804113f40/iai00194-0282-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/b9eee8389865/iai00194-0277-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/36433261083e/iai00194-0278-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/878e5e3c19f0/iai00194-0279-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/082405d7e716/iai00194-0279-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/662371f4ea69/iai00194-0279-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/27e2a6481fdf/iai00194-0280-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/78d78ef616f3/iai00194-0281-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/e91bfdfd1675/iai00194-0282-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e6b/414128/0e4804113f40/iai00194-0282-b.jpg

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引用本文的文献

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本文引用的文献

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Singlet oxygen: a unique microbicidal agent in cells.单线态氧:细胞内一种独特的杀菌因子。
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Biological defense mechanisms. The effect of bacteria and serum on superoxide production by granulocytes.生物防御机制。细菌和血清对粒细胞产生超氧化物的影响。
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Defective superoxide production by granulocytes from patients with chronic granulomatous disease.慢性肉芽肿病患者的粒细胞超氧化物生成缺陷。
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Biological defense mechanisms. The production by leukocytes of superoxide, a potential bactericidal agent.生物防御机制。白细胞产生超氧化物,一种潜在的杀菌剂。
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The superoxide anion and singlet molecular oxygen: their role in the microbicidal activity of the polymorphonuclear leukocyte.超氧阴离子与单线态分子氧:它们在多形核白细胞杀菌活性中的作用。
Biochem Biophys Res Commun. 1974 Oct 8;60(3):909-17. doi: 10.1016/0006-291x(74)90401-x.