Macrolide-affected Toll-like receptor 4 expression from Helicobacter pylori-infected monocytes does not modify interleukin-8 production

Joon Yong Park , Hak Yang Kim , Ja Young Lee , Kyung Ho Kim , Myung Kook Jang , Jin Heon Lee , Jae Young Yoo , Dong Soo Han , Joon Soo Hahm
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引用次数: 15

Abstract

Macrolide antibiotics have an anti-inflammatory effect by suppressing lipopolysaccharide-induced IL-8 production. IL-8 secretion from monocytes is observed in Helicobacter pylori infection. Although cag gene products are known to induce IL-8 secretion, whether other bacterial substances can initiate the reaction is not determined. In this study, we show that clarithromycin induced down-regulation of Toll-like receptor 4 expression and did not lead to a decrease in IL-8 production and H. pylori lipopolysaccharide. However, Toll-like receptor 4 activation was possibly not the main cause in the induction of inflammation during H. pylori infection.

大环内酯影响的toll样受体4在幽门螺杆菌感染单核细胞中的表达不改变白细胞介素8的产生
大环内酯类抗生素通过抑制脂多糖诱导的IL-8产生而具有抗炎作用。幽门螺杆菌感染时单核细胞分泌IL-8。虽然已知cag基因产物可诱导IL-8分泌,但尚不确定其他细菌物质是否可以引发该反应。在这项研究中,我们发现克拉霉素诱导toll样受体4表达下调,但不导致IL-8的产生和幽门螺杆菌脂多糖的减少。然而,toll样受体4的激活可能不是幽门螺杆菌感染诱导炎症的主要原因。
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