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用强毒立氏立克次体感染内皮细胞会增加白细胞的迁移。

Infection of endothelial cells with virulent Rickettsia prowazekii increases the transmigration of leukocytes.

作者信息

Bechah Yassina, Capo Christian, Raoult Didier, Mege Jean-Louis

机构信息

Unité des Rickettsies, Centre National de la Recherche Scientifique, Unité Mixte de Recherche, Université de la Méditerranée, Institut Fédératif de Recherche, Faculté de Médecine, Marseille, France.

出版信息

J Infect Dis. 2008 Jan 1;197(1):142-7. doi: 10.1086/523649.

DOI:10.1086/523649
PMID:18171297
Abstract

Rickettsia prowazekii, the etiologic agent of epidemic typhus, infects vascular endothelium, leading to vasculitis and tissue infiltration of leukocytes. Murine and human endothelial cells (ECs) were infected with R. prowazekii, including the virulent Breinl strain and the attenuated Madrid E strain. The transendothelial migration (TM) of murine and human peripheral blood mononuclear cells (PBMCs) across ECs infected with Breinl organisms was significantly increased compared with that for uninfected ECs or for ECs infected with attenuated organisms, demonstrating that increased TM was related to R. prowazekii virulence. Increased TM was associated with a specific inflammatory pattern. Indeed, only Breinl organisms induced the expression of transcripts for inflammatory cytokines and chemokines by ECs. Murine PBMCs that had transmigrated across ECs infected with Breinl organisms overexpressed inflammatory cytokines and chemokines as well as tissue factor, whereas interleukin-10 expression was down-regulated. The impact of R. prowazekii infection on the TM of PBMCs may play a prominent role in the development of lesions in epidemic typhus.

摘要

普氏立克次体是流行性斑疹伤寒的病原体,可感染血管内皮细胞,导致血管炎和白细胞的组织浸润。用普氏立克次体感染小鼠和人的内皮细胞(ECs),包括强毒株布雷因尔株和减毒株马德里E株。与未感染的内皮细胞或感染减毒株的内皮细胞相比,布雷因尔株感染的内皮细胞上小鼠和人外周血单个核细胞(PBMCs)的跨内皮迁移(TM)显著增加,表明TM增加与普氏立克次体毒力有关。TM增加与特定的炎症模式相关。实际上,只有布雷因尔株能诱导内皮细胞表达炎性细胞因子和趋化因子的转录本。穿过布雷因尔株感染的内皮细胞的小鼠PBMCs过度表达炎性细胞因子、趋化因子以及组织因子,而白细胞介素-10的表达下调。普氏立克次体感染对PBMCs跨内皮迁移的影响可能在流行性斑疹伤寒病变发展中起重要作用。

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J Infect Dis. 2008 Jan 1;197(1):142-7. doi: 10.1086/523649.
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