Murine Lyme disease: no evidence for active immune down-regulation in resolving or subclinical infection.
Murine Lyme disease: no evidence for active immune down-regulation in resolving or subclinical infection.
复制标题
鼠莱姆病：没有证据表明主动免疫下调可以解决或亚临床感染。
DOI：
10.1086/320703
复制
发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Malawista,SE
中科院分区：
文献类型：
--
作者：
Montgomery,RR;Wang,XM;Malawista,SE
巨噬细胞在体外迅速吞噬并杀死伯氏疏螺旋体，而体内的一些螺旋体可能在宿主体内存活并导致莱姆病的并发症。这种生存的一种策略可能是下调免疫系统。为了测试这一点，我们通过检查对照和B小鼠巨噬细胞中的细胞因子表达来评估活动性疾病部位（心脏）中巨噬细胞的活化程度。感染伯氏疏螺旋体的动物。使用原位双标记免疫荧光染色，我们发现受感染心脏中的浸润巨噬细胞会产生白细胞介素 (IL)–1。通过半定量逆转录聚合酶链反应分析，在疾病高峰期和消退期间，检测到促炎细胞因子 IL-1、肿瘤坏死因子-α 和 IL-12 mRNA 水平增加。未检测到抗炎细胞因子 IL-10 和转化生长因子-β 增加。在没有活动性疾病的感染部位——腹膜腔——局部巨噬细胞中未检测到促炎或抗炎细胞因子水平增加。因此，没有证据表明测试区域存在下调炎症活动的压力
Macrophages in vitro rapidly ingest and killBorrelia burgdorferiyet some spirochetes in vivo may survive in the host and lead to complications of Lyme disease. One strategy for such survival may be the down-regulation of the immune system. To test this, we evaluated the degree of macrophage activation in a site of active disease—the heart—by examining cytokine expression in murine macrophages from control andB. burgdorferi–infected animals. Using double-label immunofluorescent staining in situ, we showed that infiltrating macrophages in infected hearts produce interleukin (IL)–1. By semiquantitative reverse transcription–polymerase chain reaction analysis, increased levels of mRNA were measured for the proinflammatory cytokines IL-1, tumor necrosis factor–α, and IL-12 during peak and resolving disease. No increases in the anti-inflammatory cytokines IL-10 and transforming growth factor–β were detected. In an infected site without active disease—the peritoneal cavity—no increases in levels of proinflammatory or anti-inflammatory cytokines were detected in local macrophages. Thus, there is no evidence of pressure toward the down-regulation of inflammatory activity in the regions tested