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Porphyromonas gingivalis lipopolysaccharide induces tumor necrosis factor-α and interleukin-6 (IL-6) secretion and CCL25 gene expression in mouse primary gingival cell lines: IL-6-driven activation of CCL2

机译:牙龈卟啉单胞菌脂多糖诱导小鼠原发性牙龈细胞系中的肿瘤坏死因子-α和白细胞介素6(IL-6)分泌及CCL25基因表达:IL-6驱动的CCL2活化

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摘要

Background and ObjectivePorphyromonas gingivalis infection is strongly associated with periodontitis. Although P. gingivalis is known to elicit a strong inflammatory response, details of that remain fragmentary. To understand the local response to P. gingivalis, primary cell lines derived from mouse gingival tissues were exposed to P. gingivalis or E. coli lipopolysaccharide (LPS), and cytokine production for interleukin-6 (IL-6) and tumor necrosis factor-α (TNFα were measured. CCL25 gene expression was measured by real-time PCR. Cells stimulated with combinations of IL-6, soluble IL-6 receptor (sIL-6R), and/or soluble gp130 (sgp130) were assayed for CCL2 and TNFα secretion.
机译:背景与目的牙龈卟啉单胞菌感染与牙周炎密切相关。尽管已知牙龈卟啉单胞菌会引起强烈的炎症反应,但有关细节仍不完整。为了解对牙龈卟啉单胞菌的局部反应,将源自小鼠牙龈组织的原代细胞系暴露于牙龈卟啉单胞菌或大肠杆菌脂多糖(LPS),并分泌白介素6(IL-6)和肿瘤坏死因子-的细胞因子。测定α(TNFα。通过实时PCR测定CCL25基因表达。测定结合IL-6,可溶性IL-6受体(sIL-6R)和/或可溶性gp130(sgp130)刺激的细胞的CCL2和TNFα分泌。

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