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大肠杆菌诱导家兔急性炎症的动力学。II. 超免疫、补体耗竭和白细胞耗竭的影响。

Kinetics of acute inflammation induced by Escherichia coli in rabbits. II. The effect of hyperimmunization, complement depletion, and depletion of leukocytes.

作者信息

Kopaniak M M, Movat H Z

出版信息

Am J Pathol. 1983 Jan;110(1):13-29.

PMID:6336905
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1916122/
Abstract

The inflammatory response to Escherichia coli was quantitated in the skin of normal rabbits and the kinetics established as described previously. Hyperemia, measured with radiolabeled microspheres; vascular permeability, estimated with 125 I-albumin; and leukocyte infiltration, quantitated with 51Cr-labeled autologous leukocytes, reached maximal values 3 hours after the injection of bacteria and subsided almost completely by 6 hours. Hemorrhage, measured with homologous 59Fe-erythrocytes, continued to increase between 1 and 6 hours after injection and then reached plateau levels. The lesions were studied up to 8 hours, since in the previous study no changes were observed beyond that time. In the study described in this paper, the host mediation systems were manipulated in various groups of rabbits in order to elucidate the mechanisms underlying the development of the inflammatory reaction. One group of animals was hyperimmunized with the E coli organisms, another was partially depleted of hemolytic complement with cobra venom factor, and yet another was rendered leukopenic with nitrogen mustard. In hyperimmunized animals hyperemia in the dermal lesions induced by the microorganisms was significantly more intense than in normal rabbits. Vascular permeability increase occurred earlier in hyperimmunized rabbits and at 1 hour was significantly greater than in normals. Decomplemented rabbits had significantly less vascular permeability than normal animals, whereas in leukopenic rabbits no increase in vascular permeability could be elicited. Leukocyte accumulation was increased over the normal animals in the lesions of hyperimmunized rabbits. Hemorrhage was significantly decreased in leukopenic rabbits. Histologic examination of the lesions revealed that whereas in normal animals the infiltrating neutrophils ingested most of the bacteria and formed definite abscesses by 6-8 hours, these abscesses were absent in leukopenic animals, and free-lying bacteria were demonstrable in lesions. Histologically more neutrophils were present in the hyperimmunized than in the normal rabbits, but this difference was striking when normal animals were compared with leukopenic animals, in some of which only very occasional small accumulations of neutrophils were present.

摘要

在正常兔的皮肤中对大肠杆菌的炎症反应进行了定量,并按照先前描述的方法确定了动力学。用放射性标记的微球测量充血;用125I-白蛋白估计血管通透性;用51Cr标记的自体白细胞对白细胞浸润进行定量,在注射细菌后3小时达到最大值,并在6小时时几乎完全消退。用同源的59Fe-红细胞测量出血情况,在注射后1至6小时之间持续增加,然后达到平台期水平。对病变进行了长达8小时的研究,因为在先前的研究中在此时间之后未观察到变化。在本文所述的研究中,对不同组的兔进行宿主介导系统的操作,以阐明炎症反应发生发展的潜在机制。一组动物用大肠杆菌进行超免疫,另一组用眼镜蛇毒因子部分消耗溶血补体,还有一组用氮芥使白细胞减少。在超免疫动物中,由微生物诱导的皮肤病变中的充血明显比正常兔更强烈。超免疫兔的血管通透性增加出现得更早,在1小时时明显高于正常兔。补体缺乏的兔的血管通透性明显低于正常动物,而在白细胞减少的兔中,未引起血管通透性增加。超免疫兔病变中的白细胞积聚比正常动物增加。白细胞减少的兔中的出血明显减少。病变的组织学检查显示,在正常动物中,浸润的中性粒细胞摄取了大部分细菌,并在6至8小时形成明确的脓肿,而在白细胞减少的动物中没有这些脓肿,并且在病变中可发现游离的细菌。组织学上,超免疫兔中的中性粒细胞比正常兔更多,但当将正常动物与白细胞减少的动物进行比较时,这种差异很明显,在一些白细胞减少的动物中,仅偶尔有少量中性粒细胞聚集。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/80e8c782ecb4/amjpathol00196-0031-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/f5ff2f37c855/amjpathol00196-0029-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/474c5061d936/amjpathol00196-0029-b.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/78df7a51bb76/amjpathol00196-0030-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/d53a3b62bcec/amjpathol00196-0031-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/80e8c782ecb4/amjpathol00196-0031-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/f5ff2f37c855/amjpathol00196-0029-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/474c5061d936/amjpathol00196-0029-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/ab7f7734e7b4/amjpathol00196-0030-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/78df7a51bb76/amjpathol00196-0030-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/d53a3b62bcec/amjpathol00196-0031-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f82/1916122/80e8c782ecb4/amjpathol00196-0031-b.jpg

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本文引用的文献

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