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首页> 外文期刊>Infection and immunity >Impaired Immune Tolerance to Porphyromonas gingivalis Lipopolysaccharide Promotes Neutrophil Migration and Decreased Apoptosis
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Impaired Immune Tolerance to Porphyromonas gingivalis Lipopolysaccharide Promotes Neutrophil Migration and Decreased Apoptosis

机译：牙龈卟啉单胞菌脂多糖的免疫耐受受损促进中性粒细胞迁移并降低细胞凋亡。

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Periodontitis, a chronic inflammatory disease of the tissues supporting the teeth, is characterized by an exaggerated host immune and inflammatory response to periopathogenic bacteria. Toll-like receptor activation, cytokine network induction, and accumulation of neutrophils at the site of inflammation are important in the host defense against infection. At the same time, induction of immune tolerance and the clearance of neutrophils from the site of infection are essential in the control of the immune response, resolution of inflammation, and prevention of tissue destruction. Using a human monocytic cell line, we demonstrate that Porphyromonas gingivalis lipopolysaccharide (LPS), which is a major etiological factor in periodontal disease, induces only partial immune tolerance, with continued high production of interleukin-8 (IL-8) but diminished secretion of tumor necrosis factor alpha (TNF-α) after repeated challenge. This cytokine response has functional consequences for other immune cells involved in the response to infection. Primary human neutrophils incubated with P. gingivalis LPS-treated na?ve monocyte supernatant displayed a high migration index and increased apoptosis. In contrast, neutrophils treated with P. gingivalis LPS-tolerized monocyte supernatant showed a high migration index but significantly decreased apoptosis. Overall, these findings suggest that induction of an imbalanced immune tolerance in monocytes by P. gingivalis LPS, which favors continued secretion of IL-8 but decreased TNF-α production, may be associated with enhanced migration of neutrophils to the site of infection but also with decreased apoptosis and may play a role in the chronic inflammatory state seen in periodontal disease.
机译：牙周炎是支持牙齿的组织的一种慢性炎症性疾病，其特征是宿主对致病原菌的免疫和炎症反应过度。 Toll样受体活化，细胞因子网络诱导和中性粒细胞在炎症部位的积累在宿主抵抗感染中起着重要的作用。同时，诱导免疫耐受和从感染部位清除中性粒细胞对于控制免疫反应，消炎和预防组织破坏至关重要。使用人类单核细胞系，我们证明牙龈卟啉单胞菌脂多糖（LPS）是牙周疾病的主要病因，它仅诱导部分免疫耐受，并持续产生高白介素8（IL -8），但反复攻击后肿瘤坏死因子α（TNF-α）的分泌减少。这种细胞因子应答对参与感染应答的其他免疫细胞具有功能性后果。用 P孵育的原代人中性粒细胞。牙龈炎LPS处理的幼稚单核细胞上清液具有较高的迁移指数并增加了细胞凋亡。相反，用 P处理的中性粒细胞。牙龈炎LPS耐受的单核细胞上清液具有较高的迁移指数，但凋亡明显减少。总体而言，这些发现表明 P诱导单核细胞免疫耐受失衡。牙龈脂多糖（LPS）有利于IL-8的持续分泌，但TNF-α的产生减少，可能与嗜中性粒细胞向感染部位的迁移增加有关，但与凋亡减少有关，并可能在慢性炎症状态中起作用见于牙周疾病。

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