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牙龈卟啉单胞菌脂多糖对单核细胞和炎性巨噬细胞的菌株依赖性激活

Strain-dependent activation of monocytes and inflammatory macrophages by lipopolysaccharide of Porphyromonas gingivalis.

作者信息

Shapira L, Champagne C, Van Dyke T E, Amar S

机构信息

Department of Periodontology, Hebrew University-Hadassah School of Dental Medicine, Jerusalem, Israel.

出版信息

Infect Immun. 1998 Jun;66(6):2736-42. doi: 10.1128/IAI.66.6.2736-2742.1998.

DOI:10.1128/IAI.66.6.2736-2742.1998
PMID:9596741
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC108263/
Abstract

Porphyromonas gingivalis is one of the pathogens associated with periodontal diseases, and its lipopolysaccharide (LPS) has been suggested as a possible virulence factor, acting by stimulation of host cells to secrete proinflammatory mediators. However, recent studies have shown that P. gingivalis LPS inhibited some components of the inflammatory response. The present study was designed to test the hypothesis that there are strain-dependent variations in the ability of P. gingivalis LPS to elicit the host inflammatory response. By using LPS preparations from two strains of P. gingivalis, W50 and A7346, the responses of mouse macrophages and human monocytes were evaluated by measuring the secretion of nitric oxide (NO) and tumor necrosis factor alpha (TNF-alpha). Both direct and indirect (priming) effects were investigated. LPS from Salmonella typhosa was used as a reference LPS. P. gingivalis A7436 LPS induced lower secreted levels of NO from the tested cells than S. typhosa LPS but induced similar levels of TNF-alpha. In contrast, LPS from P. gingivalis W50 did not induce NO or TNF-alpha secretion. Preincubation of macrophages with LPS from S. typhosa or P. gingivalis A7436 prior to stimulation with S. typhosa LPS upregulated NO secretion and downregulated TNF-alpha secretion, while preincubation with P. gingivalis W50 LPS enhanced both TNF-alpha and NO secretory responses. These results demonstrate that LPSs derived from different strains of P. gingivalis vary in their biological activities in vitro. The findings may have an impact on our understanding of the range of P. gingivalis virulence in vivo.

摘要

牙龈卟啉单胞菌是与牙周疾病相关的病原体之一,其脂多糖(LPS)被认为是一种可能的毒力因子,通过刺激宿主细胞分泌促炎介质发挥作用。然而,最近的研究表明牙龈卟啉单胞菌LPS抑制了炎症反应的某些成分。本研究旨在验证牙龈卟啉单胞菌LPS引发宿主炎症反应的能力存在菌株依赖性差异这一假说。通过使用牙龈卟啉单胞菌W50和A7346两个菌株的LPS制剂,通过测量一氧化氮(NO)和肿瘤坏死因子α(TNF-α)的分泌来评估小鼠巨噬细胞和人单核细胞的反应。研究了直接和间接(引发)效应。伤寒沙门氏菌的LPS用作参考LPS。牙龈卟啉单胞菌A7436 LPS诱导受试细胞分泌的NO水平低于伤寒沙门氏菌LPS,但诱导的TNF-α水平相似。相比之下,牙龈卟啉单胞菌W50的LPS未诱导NO或TNF-α分泌。在用伤寒沙门氏菌LPS刺激之前,用伤寒沙门氏菌或牙龈卟啉单胞菌A7436的LPS预孵育巨噬细胞会上调NO分泌并下调TNF-α分泌,而用牙龈卟啉单胞菌W50 LPS预孵育则会增强TNF-α和NO分泌反应。这些结果表明,源自不同牙龈卟啉单胞菌菌株的LPS在体外的生物活性存在差异。这些发现可能会影响我们对牙龈卟啉单胞菌体内毒力范围的理解。

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