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大肠杆菌肺炎会增强粒细胞生成以及骨髓祖细胞向体循环的动员。

Escherichia coli pneumonia enhances granulopoiesis and the mobilization of myeloid progenitor cells into the systemic circulation.

作者信息

Shahbazian Lotfollah M, Quinton Lee J, Bagby Gregory J, Nelson Steve, Wang Guansong, Zhang Ping

机构信息

Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.

出版信息

Crit Care Med. 2004 Aug;32(8):1740-6. doi: 10.1097/01.ccm.0000132900.84627.90.

DOI:10.1097/01.ccm.0000132900.84627.90
PMID:15286552
Abstract

OBJECTIVE

The process by which hematopoietic tissues respond to a pulmonary infection remains poorly understood. This study investigated the potential role of lung-derived granulopoietic cytokines in facilitating this response.

DESIGN

Laboratory investigation.

SETTING

University laboratory.

SUBJECTS

Male Balb/c mice.

INTERVENTIONS

Mice were challenged with intratracheal Escherichia coli or granulocyte colony-stimulating factor (G-CSF). Bone marrow cells were isolated from normal mice and treated in vitro with G-CSF.

MEASUREMENTS AND MAIN RESULTS

Bronchoalveolar lavage fluid concentrations of G-CSF, macrophage inflammatory protein-2, and keratinocyte-derived chemokine were elevated 3 and 6 hrs after intratracheal E. coli. The increases in intrapulmonary G-CSF and keratinocyte-derived chemokine were associated with increases of their concentrations in the plasma. The numbers of granulocyte-macrophage colony forming units in bone marrow, spleen, and blood were increased 48 hrs after intratracheal E. coli or G-CSF. In addition, plasma G-CSF and the number of progenitor cells (lin-ckit+Sca-1(-)) in the blood were increased at 30 mins and 48 hrs, respectively, following intratracheal G-CSF. Signal transducer and activator of transcription-3 in bone marrow cells was activated following intratracheal E. coli or G-CSF in addition to activation by in vitro G-CSF stimulation.

CONCLUSIONS

During pulmonary infection, locally produced cytokines enter the circulation and may play an important role in initiating a granulopoietic response.

摘要

目的

造血组织对肺部感染作出反应的过程仍未得到充分了解。本研究调查了肺源性粒细胞生成细胞因子在促进这种反应中的潜在作用。

设计

实验室研究。

地点

大学实验室。

研究对象

雄性Balb/c小鼠。

干预措施

小鼠经气管内注射大肠杆菌或粒细胞集落刺激因子(G-CSF)进行攻击。从正常小鼠中分离骨髓细胞,并在体外使用G-CSF进行处理。

测量指标及主要结果

气管内注射大肠杆菌后3小时和6小时,支气管肺泡灌洗液中G-CSF、巨噬细胞炎性蛋白-2和角质形成细胞衍生趋化因子的浓度升高。肺内G-CSF和角质形成细胞衍生趋化因子的增加与它们在血浆中的浓度增加相关。气管内注射大肠杆菌或G-CSF后48小时,骨髓、脾脏和血液中粒细胞-巨噬细胞集落形成单位的数量增加。此外,气管内注射G-CSF后30分钟和48小时,血浆G-CSF和血液中祖细胞(lin-ckit+Sca-1(-))的数量分别增加。气管内注射大肠杆菌或G-CSF后,骨髓细胞中的信号转导和转录激活因子3被激活,体外G-CSF刺激也可激活该因子。

结论

在肺部感染期间,局部产生的细胞因子进入循环系统,并可能在启动粒细胞生成反应中发挥重要作用。

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