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埃立克体病:一个重要的“同一健康”机遇。

Ehrlichioses: An Important One Health Opportunity.

作者信息

Saito Tais B, Walker David H

机构信息

Department of Pathology, University of Texas Medical Branch at Galveston, Galveston, TX 77555, USA.

出版信息

Vet Sci. 2016 Aug 31;3(3):20. doi: 10.3390/vetsci3030020.

DOI:10.3390/vetsci3030020
PMID:29056728
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5606584/
Abstract

Ehrlichioses are caused by obligately intracellular bacteria that are maintained subclinically in a persistently infected vertebrate host and a tick vector. The most severe life-threatening illnesses, such as human monocytotropic ehrlichiosis and heartwater, occur in incidental hosts. have a developmental cycle involving an infectious, nonreplicating, dense core cell and a noninfectious, replicating reticulate cell. Ehrlichiae secrete proteins that bind to host cytoplasmic proteins and nuclear chromatin, manipulating the host cell environment to their advantage. Severe disease in immunocompetent hosts is mediated in large part by immunologic and inflammatory mechanisms, including overproduction of tumor necrosis factor α (TNF-α), which is produced by CD8 T lymphocytes, and interleukin-10 (IL-10). Immune components that contribute to control of ehrlichial infection include CD4 and CD8 T cells, natural killer (NK) cells, interferon-γ (IFN-γ), IL-12, and antibodies. Some immune components, such as TNF-α, perforin, and CD8 T cells, play both pathogenic and protective roles. In contrast with the immunocompetent host, which may die with few detectable organisms owing to the overly strong immune response, immunodeficient hosts die with overwhelming infection and large quantities of organisms in the tissues. Vaccine development is challenging because of antigenic diversity of , the necessity of avoiding an immunopathologic response, and incomplete knowledge of the protective antigens.

摘要

埃立克体病由专性细胞内细菌引起,这些细菌在持续感染的脊椎动物宿主和蜱传播媒介中处于亚临床状态。最严重的危及生命的疾病,如人单核细胞埃立克体病和心水病,发生在偶然宿主中。有一个发育周期,涉及传染性、非复制性、致密核心细胞和非传染性、复制性网状细胞。埃立克体分泌与宿主细胞质蛋白和核染色质结合的蛋白质,以利于操纵宿主细胞环境。免疫功能正常宿主中的严重疾病在很大程度上由免疫和炎症机制介导,包括肿瘤坏死因子α(TNF-α)的过度产生,TNF-α由CD8 T淋巴细胞产生,以及白细胞介素-10(IL-10)。有助于控制埃立克体感染的免疫成分包括CD4和CD8 T细胞、自然杀伤(NK)细胞、干扰素-γ(IFN-γ)、IL-12和抗体。一些免疫成分,如TNF-α、穿孔素和CD8 T细胞,发挥致病和保护双重作用。与免疫功能正常的宿主不同,免疫功能正常的宿主可能因免疫反应过强而在几乎检测不到病原体的情况下死亡,免疫缺陷宿主则死于严重感染且组织中有大量病原体。由于埃立克体具有抗原多样性、避免免疫病理反应的必要性以及对保护性抗原的了解不完整,疫苗开发具有挑战性。

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PLoS One. 2016 Apr 19;11(4):e0153223. doi: 10.1371/journal.pone.0153223. eCollection 2016.
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Inhibition of JAK2 attenuates the increase in inflammatory markers in microglia from APP/PS1 mice.抑制JAK2可减轻APP/PS1小鼠小胶质细胞中炎症标志物的增加。
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Ehrlichia chaffeensis infection in the reservoir host (white-tailed deer) and in an incidental host (dog) is impacted by its prior growth in macrophage and tick cell environments.查菲埃立克体在储存宿主(白尾鹿)和偶然宿主(狗)中的感染受到其先前在巨噬细胞和蜱细胞环境中生长情况的影响。
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