Tissue distribution of migration inhibitory factor and inducible nitric oxide synthase in falciparum malaria and sepsis in African children.

Tissue distribution of migration inhibitory factor and inducible nitric oxide synthase in falciparum malaria and sepsis in African children.
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恶性疟疾和非洲儿童败血症中迁移抑制因子和诱导型一氧化氮合酶的组织分布。

DOI:
10.1186/1475-2875-2-6
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发表时间:
2003-04-08
期刊:
影响因子:
3
通讯作者:
Taylor, TE
Taylor, TE
中科院分区:
医学3区
文献类型:
--
作者:
Clark, IA;Awburn, MM;Whitten, RO;Harper, CG;Liomba, NG;Molyneux, ME;Taylor, TE

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恶性疟疾的炎症性质已被承认,因为增加的循环水平的肿瘤坏死因子(TNF)首次测量,但确切地说,从这个原型炎症介质下游的介质产生尚未调查。在这里,我们报告的细胞分布,免疫组织化学,迁移抑制因子(MIF)和诱导型一氧化氮合酶(iNOS)在这种疾病,并在败血症。我们对马拉维布兰太尔44例儿童尸检中收集的组织进行了MIF和iNOS染色。其中包括42名急性昏迷病人,其中32人经临床诊断为脑型疟疾,另外10人为非疟疾疾病。另外2例为非疟疾、非昏迷死亡。其他对照组织来自澳大利亚成年人。在32例临床诊断的脑型疟疾病例中,11例脑组织学变化可忽略不计,无或仅有少量寄生红细胞的血管内隔离,另外7例脑组织学变化无,但存在隔离的寄生红细胞(通常密集),其余14例脑显示微出血和血管内单核细胞积聚,加上隔离的寄生红细胞。后一组血管壁的iNOS染色最强烈。血管壁iNOS染色通常是低强度的第二组(7个大脑),几乎是不存在的10个昏迷患者的脑血管壁没有疟疾,也从对照组的大脑。选择胸壁作为典型的非脑部位,包括一系列感兴趣的组织。在所有组中,约50%的儿童血管壁和骨骼肌中存在明显的iNOS染色,包括脓毒性脑膜炎,无论脑血管壁的染色程度如何。在所有胸壁切片中,寄生虫或疟疾色素罕见或不存在。而MIF常见于胸壁血管中,通常与iNOS相关,脑血管中不存在。这些结果与以下观点一致,即非洲儿童临床诊断的脑型疟疾是通过不同器官系统发挥作用的重叠综合征的集合,具有几种机制,不一定与脑血管炎症和损伤相关,结合起来导致死亡。
The inflammatory nature of falciparum malaria has been acknowledged since increased circulating levels of tumour necrosis factor (TNF) were first measured, but precisely where the mediators downstream from this prototype inflammatory mediator are generated has not been investigated. Here we report on the cellular distribution, by immunohistochemistry, of migration inhibitory factor (MIF) and inducible nitric oxide synthase (iNOS) in this disease, and in sepsis. We stained for MIF and iNOS in tissues collected during 44 paediatric autopsies in Blantyre, Malawi. These comprised 42 acutely ill comatose patients, 32 of whom were diagnosed clinically as cerebral malaria and the other 10 as non-malarial diseases. Another 2 were non-malarial, non-comatose deaths. Other control tissues were from Australian adults. Of the 32 clinically diagnosed cerebral malaria cases, 11 had negligible histological change in the brain, and no or scanty intravascular sequestration of parasitised erythrocytes, another 7 had no histological changes in the brain, but sequestered parasitised erythrocytes were present (usually dense), and the remaining 14 brains showed micro-haemorrhages and intravascular mononuclear cell accumulations, plus sequestered parasitised erythrocytes. The vascular walls of the latter group stained most strongly for iNOS. Vascular wall iNOS staining was usually of low intensity in the second group (7 brains) and was virtually absent from the cerebral vascular walls of 8 of the 10 comatose patients without malaria, and also from control brains. The chest wall was chosen as a typical non-cerebral site encompassing a range of tissues of interest. Here pronounced iNOS staining in vascular wall and skeletal muscle was present in some 50% of the children in all groups, including septic meningitis, irrespective of the degree of staining in cerebral vascular walls. Parasites or malarial pigment were rare to absent in all chest wall sections. While MIF was common in chest wall vessels, usually in association with iNOS, it was absent in brain vessels. These results agree with the view that clinically diagnosed cerebral malaria in African children is a collection of overlapping syndromes acting through different organ systems, with several mechanisms, not necessarily associated with cerebral vascular inflammation and damage, combining to cause death.
DOI: 10.1016/s0035-9203(97)90083-3
发表时间: 1997-05-01
影响因子: 2.2
作者:
Agbenyega, T;Angus, B;Krishna, S
通讯作者: Krishna, S
DOI: 10.1172/jci9900
发表时间: 2000-11-01
影响因子: 15.9
作者:
Benigni, F;Atsumi, T;Bucala, R
通讯作者: Bucala, R
DOI: 10.1038/72262
发表时间: 2000-02-01
期刊: NATURE MEDICINE
影响因子: 82.9
作者:
Calandra, T;Echtenacher, B;Glauser, MP
通讯作者: Glauser, MP
DOI: 10.1073/pnas.56.1.72
发表时间: 1966-01-01
影响因子: 11.1
作者:
DAVID, JR
通讯作者: DAVID, JR
巨噬细胞是巨噬细胞迁移抑制因子的重要且以前未被认可的来源。
DOI: 10.1084/jem.179.6.1895
发表时间: 1994-06-01
影响因子: 15.3
作者:
Calandra, Thierry;Bernhagen, Juergen;Mitchell, Robert A.;Bucala, Richard
通讯作者: Bucala, Richard