STAT3 activation in macrophages following infection with Salmonella
STAT3 activation in macrophages following infection with Salmonella
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DOI：
10.1016/j.bbrc.2004.07.039
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发表时间：
2004-09-03
影响因子：
3.1
通讯作者：
Bost, KL
中科院分区：
文献类型：
--
作者：
Lin, T;Bost, KL
巨噬细胞中信号转导和转录激活因子（STAT）的诱导是细胞活化所必需的，我们研究了沙门氏菌感染后这些细胞中STAT 3的活化。与对照小鼠相比，在感染后6小时和24小时，在肠系膜淋巴结和脾脏中观察到STAT 3活化增加。从感染小鼠的肠系膜淋巴结分离的CD 11b（+）细胞在感染后6小时就表现出增加的STAT 3活化。用沙门氏菌培养骨髓源性巨噬细胞导致STAT 3易位到细胞核和STAT 3磷酸化，早在暴露后30分钟。在感染后IL-6或IL-10产生缺陷的小鼠的淋巴器官或巨噬细胞中也观察到STAT 3活化增加。总之，这些研究清楚地证明了在用野生型沙门氏菌感染后体内和体外STAT 3活化的早期增加。(C)2004年爱思唯尔公司All rights reserved.
The induction of signal transducer and activators of transcription (STATs) in macrophages is necessary for cellular activation, and we investigated the activation of STAT3 in these cells following infection with Salmonella. Increased activation of STAT3 was observed at 6 and 24 h post-infection in the mesenteric lymph nodes and spleens when compared to control mice. CD11b(+) cells isolated from the mesenteric lymph nodes of infected mice demonstrated increased STAT3 activation as early as 6 h following infection. Culturing bone marrow-derived macrophages with Salmonella resulted in translocation of STAT3 to the nucleus and STAT3 phosphorylation as early as 30min post-exposure. Increased STAT3 activation was also observed in the lymphoid organs or in macrophages from mice deficient for IL-6 or IL-10 production following infection. Taken together, these studies clearly demonstrate an early increase in the activation of STAT3 in vivo and in vitro following infection with wild type Salmonella. (C) 2004 Elsevier Inc. All rights reserved.