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首页> 外文期刊>Infection and immunity >Host Resistance of CD18 Knockout Mice against Systemic Infection with Listeria monocytogenes
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Host Resistance of CD18 Knockout Mice against Systemic Infection with Listeria monocytogenes

机译：CD18基因敲除小鼠对单核细胞增生性李斯特菌全身感染的宿主抗性

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Mice with targeted mutations of CD18, the common β2 subunit of CD11/CD18 integrins, have leukocytosis, impaired transendothelial neutrophil emigration, and reduced host defense to Streptococcus pneumoniae, a gram-positive extracellular bacterium. Previous studies using blocking monoclonal antibodies suggested roles for CD18 and CD11b in hepatic neutrophil recruitment and host innate response to Listeria monocytogenes, a gram-positive intracellular bacterium. We induced systemic listeriosis in CD18 knockout (CD18-ko) and wild-type (WT) mice by tail vein injection with Listeria. By 14 days postinjection (dpi), 8 of 10 WT mice died, compared with 2 of 10 CD18-ko mice (P < 0.01). Quantitative organ culture showed that numbers of Listeria organisms in livers and spleens were similar in both groups at 20 min postinfection. By 3, 5, and 7 dpi, however, numbers of Listeria organisms were significantly lower in livers and spleens of CD18-ko mice than in WT mice. Histopathology showed that following Listeria infection, CD18-ko mice had milder inflammatory and necrotizing lesions in both spleens and livers than did WT mice. Cytokine assays indicated that baseline interleukin-1β and granulocyte colony-stimulating factor (G-CSF) levels were higher in CD18-ko mice than in WT mice and that CD18-ko splenocytes produced higher levels of interleukin-1β and G-CSF than WT splenocytes under the same amount of Listeria stimulation. These findings show that CD18 is not an absolute requirement for antilisterial innate immunity or hepatic neutrophil recruitment. We propose that the absence of CD18 in the mice results in the priming of innate immunity, as evidenced by elevated cytokine expression, and neutrophilic leukocytosis, which augments antilisterial defense.
机译：具有CD18（CD11 / CD18整合素的常见β2亚基）靶向突变的小鼠具有白细胞增多症，跨内皮细胞嗜中性粒细胞迁移受损，并且对革兰氏阳性细胞外细菌肺炎链球菌的宿主防御能力降低。以前使用封闭性单克隆抗体的研究表明，CD18和CD11b在肝中性粒细胞募集和宿主对革兰氏阳性细胞内细菌单核细胞增生李斯特菌的先天反应中起作用。我们通过 Listeria 的尾静脉注射诱导了CD18基因敲除（CD18-ko）和野生型（WT）小鼠的全身性李斯特菌病。注射后第14天（dpi），每10只WT小鼠中有8只死亡，而每10只CD18-ko小鼠中有2只（ P <0.01）。定量器官培养显示，感染后20分钟，两组肝脏和脾脏中的 Listeria 生物数量相似。但是，到3、5和7 dpi时，CD18-ko小鼠的肝脏和脾脏中的 Listeria 生物体的数量显着低于WT小鼠。组织病理学表明，在李斯特菌感染后，CD18-ko小鼠脾脏和肝脏的炎症和坏死性病变均比野生型小鼠轻。细胞因子检测表明，CD18-ko小鼠的基线白细胞介素-1β和粒细胞集落刺激因子（G-CSF）水平高于野生型小鼠，而CD18-ko脾细胞产生的白细胞介素-1β和G-CSF水平高于野生型相同数量的 Listeria 刺激下的脾细胞。这些发现表明，CD18并不是抗李斯特氏先天免疫或肝中性粒细胞募集的绝对必要条件。我们提出，小鼠体内CD18的缺乏导致先天免疫的启动，这可以通过细胞因子表达升高和嗜中性白细胞增多来证明，后者可增强抗弹力。

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