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首页> 外文期刊>Infection and immunity >Production of interleukin-8 (IL-8) by cultured endothelial cells in response to Borrelia burgdorferi occurs independently of secreted [corrected] IL-1 and tumor necrosis factor alpha and is required for subsequent transendothelial migration of neutrophils.
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Production of interleukin-8 (IL-8) by cultured endothelial cells in response to Borrelia burgdorferi occurs independently of secreted [corrected] IL-1 and tumor necrosis factor alpha and is required for subsequent transendothelial migration of neutrophils.

机译：培养的内皮细胞响应伯氏疏螺旋体产生白细胞介素8（IL-8），与分泌的[校正的] IL-1和肿瘤坏死因子α无关，这是嗜中性粒细胞随后跨内皮迁移所必需的。

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Previous studies have shown that Borrelia burgdorferi, the spirochetal agent of Lyme disease, promotes inflammation by stimulating endothelial cells to upregulate adhesion molecules for leukocytes and to produce a soluble agent that is chemotactic for neutrophils. We determined that interleukin-8 (IL-8) was the chemotactic agent for neutrophils present in conditioned media from cultured human umbilical vein endothelial cells stimulated with B. burgdorferi. As few as one spirochete per endothelial cell stimulated production of IL-8 within 8 h of coincubation. When 10 spirochetes per endothelial cell were added, IL-8 was detected after 4 h of coculture. Production of IL-8 continued in a linear fashion for at least 24 h. Neutralizing antibodies against IL-8 reduced migration of neutrophils across spirochete-stimulated endothelial monolayers by 93%. In contrast, pretreatment of neutrophils with antagonists of platelet-activating factor did not inhibit migration. Increases in production of IL-8 and expression of the adhesion molecule E-selectin by endothelial cells in response to B. burgdorferi were not inhibited by IL-1 receptor antagonist or a neutralizing monoclonal antibody directed against tumor necrosis factor alpha, used either alone or in combination. These results suggest that activation of endothelium by B. burgdorferi is not mediated through the autocrine action of secreted IL-1 or tumor necrosis factor alpha. Rather, it appears that B. burgdorferi must stimulate endothelium either by a direct signaling mechanism or by induction of a novel host-derived proinflammatory cytokine.
机译：先前的研究表明，莱姆病的螺旋体疏螺旋体伯氏疏螺旋体通过刺激内皮细胞上调白细胞的粘附分子并产生对嗜中性粒细胞趋化性的可溶性试剂来促进炎症。我们确定白介素8（IL-8）是嗜中性白细胞的趋化剂，该嗜中性白细胞存在于条件培养液中，该条件培养液由伯氏疏螺旋体刺激培养的人脐静脉内皮细胞。在共孵育的8小时内，每个内皮细胞只有少量螺旋体刺激了IL-8的产生。当每个内皮细胞添加10个螺旋体时，共培养4小时后检测到IL-8。 IL-8的产生以线性方式持续至少24小时。抗IL-8的中和抗体使嗜中性粒细胞的迁移跨螺旋体刺激的内皮单层减少了93％。相反，用血小板活化因子拮抗剂预处理中性粒细胞并不能抑制迁移。 IL-1受体拮抗剂或针对肿瘤坏死因子α的中和性单克隆抗体（单独使用或单独使用）均不会抑制IL-8产生的增加以及内皮细胞响应伯氏疏螺旋体的粘附分子E-选择素的表达。结合。这些结果表明，B。burgdorferi对内皮的激活不是通过分泌的IL-1或肿瘤坏死因子α的自分泌作用来介导的。而是，伯氏疏螺旋体似乎必须通过直接的信号传导机制或通过诱导新的宿主衍生的促炎细胞因子来刺激内皮。

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