Borrelia burgdorferi and interleukin-1 promote the transendothelial migration of monocytes in vitro by different mechanisms
Borrelia burgdorferi and interleukin-1 promote the transendothelial migration of monocytes in vitro by different mechanisms
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DOI：
10.1128/iai.66.10.4875-4883.1998
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发表时间：
1998-10-01
影响因子：
3.1
通讯作者：
Furie, MB
中科院分区：
文献类型：
--
作者：
Burns, MJ;Furie, MB
莱姆病的一个突出特征是单核白细胞在血管周围的积聚。将在羊膜组织上培养的人脐静脉内皮细胞（HUVEC）与白细胞介素-1（IL-1）或莱姆病的螺旋体病原体伯氏疏螺旋体（Borrelia burgdorferi）孵育，增加了人单核细胞迁移穿过内皮单层的速率。极晚期抗原4（VLA-4）和CD 11/CD 18整联蛋白介导单核细胞迁移穿过暴露于B的HUVEC。burgdorferi或IL-1。趋化因子单核细胞趋化蛋白1（MCP-1）的中和抗体抑制单核细胞穿过未刺激的、IL-1处理的或B的迁移。分别降低91% +/-3%、65% +/-2%或25% +/-22%。用B刺激HUVEC。伯氏疏螺旋体还促进人CD 4（+）T淋巴细胞迁移增加6倍+/- 2倍。尽管MCP-1在单核细胞迁移通过B、伯氏螺旋体处理的HUVEC中仅发挥有限的作用，但暴露于螺旋体的CD 4（+）T淋巴细胞迁移通过HUVEC高度依赖于这种趋化因子。抗炎细胞因子IL-10降低单核细胞迁移和响应于B的内皮细胞产生MCP-1。然而，当用IL-1刺激HUVEC时，IL-10既不抑制MCP-1的迁移也不抑制MCP-1的分泌。我们的研究结果表明，B。莱姆病相关的慢性炎性浸润的形成。由伯氏B介导的单核细胞的跨内皮迁移对MCP-1的依赖性明显低于IL-1介导的迁移。IL-10的选择性抑制进一步表明B. Burgdorferi和IL 1采用不同的机制来激活内皮细胞。
A prominent feature of Lyme disease is the perivascular accumulation of mononuclear leukocytes, Incubation of human umbilical vein endothelial cells (HUVEC) cultured on amniotic tissue with either interleukin-l (IL-1) or Borrelia burgdorferi, the spirochetal agent of Lyme disease, increased the rate at which human monocytes migrated across the endothelial monolayers. Very late antigen 4 (VLA-4) and CD11/CD18 integrins mediated migration of monocytes across HUVEC exposed to either B. burgdorferi or IL-1 in similar manners. Neutralizing antibodies to the chemokine monocyte chemoattractant protein 1 (MCP-1) inhibited the migration of monocytes across unstimulated, IL-l-treated, or B. burgdorferi-stimulated HUVEC by 91% +/- 3%, 65% +/- 2%, or 25% +/- 22%, respectively. Stimulation of HUVEC with B. burgdorferi also promoted a 6 fold +/- 2-fold increase in the migration of human CD4(+) T lymphocytes. Although MCP-1 played only a limited role in the migration of monocytes across B, burgdorferi-treated HUVEC, migration of CD4(+) T lymphocytes across HUVEC exposed to spirochetes was highly dependent on this chemokine, The anti-inflammatory cytokine IL-10 reduced both migration of monocytes and endothelial production of MCP-1 in response to B. burgdorferi by approximately 50%, yet IL-10 inhibited neither migration nor secretion of MCP-1 when HUVEC were stimulated with IL-1. Our results suggest that activation of endothelium by B. burgdorferi may contribute to formation of the chronic inflammatory infiltrates associated with Lyme disease. The transendothelial migration of monocytes that is induced by B, burgdorferi is significantly less dependent on MCP-1 than is migration induced by IL 1. Selective inhibition by IL-IO further indicates that B. burgdorferi and IL 1 employ distinct mechanisms to activate endothelial cells.