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首页> 外文期刊>Comparative Medicine >Influence of Genetic Background on Hematologic and Histopathologic Alterations during Acute Granulocytic Anaplasmosis in 129/SvEv and C57BL/6J Mice Lacking Type I and Type II Interferon Signaling
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Influence of Genetic Background on Hematologic and Histopathologic Alterations during Acute Granulocytic Anaplasmosis in 129/SvEv and C57BL/6J Mice Lacking Type I and Type II Interferon Signaling

机译：遗传背景对129 / SVEV和C57BL / 6J小鼠急性粒细胞胸腺细胞症期间血液学和组织病理改变的影响缺乏I型和II型干扰素信号

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The role of host type I IFN signaling and its interaction with other immune pathways during bacterial infections is incompletely understood. Type II IFN signaling plays a key role during numerous bacterial infections including granulocytic anaplasmosis (GA) caused by Anaplasma phagocytophilum infection. The function of combined type I and type II IFN signaling and their potential synergism during GA and similar tick -borne diseases is a topic of current research investigation. The goal of this study was to evaluate 2 mouse models of absent type I/type II IFN signaling in experimental A. phagocytophilum infection to determine the effects of background strain. Mice lacking both type I and type II IFN receptor signaling (IFNAR(-1-)/IFNGR(-/-)) on either the 129/SvEv or C57BL/6J genetic background were evaluated at days 0, 6, 8, and 12 of infection. Pathogen burden in multiple organs was largely similar between strains of infected mice, with few significant differences. Background strain influenced the immune response to infection. Mice of the 129/SvEv strain developed more severe hematologic abnormalities, particularly more severe leukocytosis with marked neutrophilia and lymphocytosis, throughout acute infection. Histopathologic changes occurred in infected mice of both strains and varied in severity by organ. 129/SvEv mice developed more severe pathologic changes in spleen and bone marrow, whereas C57BL/6J mice developed more severe renal pathology. This work highlights the importance of mouse background strain in dictating pathophysiologic response to infection and informs future work regarding the loss of type I and type II IFN signaling on the immune response during GA.
机译：宿主类型I IFN信号传导及其与细菌感染期间与其他免疫途径相互作用的作用被不完全理解。 II型IFN信号传导在许多细菌感染期间发挥关键作用，包括由Anplasma吞噬粒子感染引起的颗粒细胞瘤病（GA）。组合I型和II型IFN信号传导的功能及其在GA和类似蜱传票中的潜在协同作用是当前研究调查的主题。本研究的目标是评估实验A.吞噬噬菌体感染的缺陷型I / II型IFN信号传导的2个小鼠模型，以确定背景应变的影响。缺乏I型和II型IFN受体信令（IFNAR（-1 - ）/ IFNGR / 6J遗传背景的小鼠在第0,6,8和12天评估了129 / SVEV或C57BL / 6J遗传背景感染。多个器官的病原体负担在很大程度上相似，感染小鼠的菌株几乎没有显着差异。背景应变影响免疫应答感染。 129 / SVEV菌株的小鼠产生了更严重的血液学异常，特别是严重的白细胞增多症，具有显着的中性粒细胞和淋巴细胞症，在整个急性感染中。在两种菌株的受感染小鼠中发生组织病理学变化，并通过器官的严重程度变化。 129 / SVEV小鼠在脾脏和骨髓中产生了更严重的病理变化，而C57BL / 6J小鼠产生了更严重的肾病理学。这项工作突出了小鼠背景应变在对感染的病理物理学反应方面的重要性，并告知未来的作用关于I型和II型IFN信号传导在GA期间免疫应答。

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