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恶性疟原虫色素诱导单核细胞释放高水平的肿瘤坏死因子-α和白细胞介素-1β。

Plasmodium falciparum pigment induces monocytes to release high levels of tumor necrosis factor-alpha and interleukin-1 beta.

作者信息

Pichyangkul S, Saengkrai P, Webster H K

机构信息

Department of Immunology and Parasitology, U.S. Army Medical Component, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand.

出版信息

Am J Trop Med Hyg. 1994 Oct;51(4):430-5.

PMID:7943569
Abstract

We show that high levels of tumor necrosis factor-alpha (TNF-alpha) activity were consistently detected when monocytes were cocultured with Plasmodium falciparum schizont stage-parasitized erythrocytes that subsequently ruptured. Isolated pigment recovered from ruptured schizonts was found to specifically induce monocyte release of high levels of TNF-alpha and interleukin-1 beta (IL-1 beta). Particulate free-culture supernatant that contained various soluble parasite macromolecules induced relatively low levels of TNF-alpha and IL-1 beta. When isolated pigment was treated with protease, the monokine inducing-activity was abolished. Isolated pigment prepared from different natural isolates of P. falciparum stimulated variable levels of monokine production. We propose that in vivo, malaria pigment from parasites sequestered in the host microvasculature is a physiologically relevant moiety that interacts with monocytes and stimulates the release of TNF-alpha and IL-1 beta. These observations suggest that malaria pigment may be a virulence factor in the monokine-mediated induction of organ-specific and systemic pathophysiology in falciparum malaria.

摘要

我们发现,当单核细胞与随后破裂的恶性疟原虫裂殖体期寄生红细胞共培养时,可持续检测到高水平的肿瘤坏死因子-α(TNF-α)活性。从破裂的裂殖体中分离出的色素被发现能特异性诱导单核细胞释放高水平的TNF-α和白细胞介素-1β(IL-1β)。含有各种可溶性寄生虫大分子的无颗粒培养上清液诱导产生的TNF-α和IL-1β水平相对较低。当分离出的色素用蛋白酶处理时,单核因子诱导活性被消除。从不同的恶性疟原虫天然分离株制备的分离色素刺激产生的单核因子水平各不相同。我们提出,在体内,宿主微血管中隔离的寄生虫产生的疟色素是一种生理相关成分,它与单核细胞相互作用并刺激TNF-α和IL-1β的释放。这些观察结果表明,疟色素可能是恶性疟疾中单核因子介导的器官特异性和全身病理生理诱导的毒力因子。

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