Department of Otolaryngology, University of Minnesota Medical School, Minneapolis, Minnesota 55455, USA.
Pediatr Res. 2011 Feb;69(2):101-5. doi: 10.1203/PDR.0b013e3182055237.
Toll-like receptor 2 (TLR2) plays a key role in the host defense against Gram staining positive (Gram) bacteria and their cell wall envelope components. However, little is known about the expression of TLR2 in the middle ear under otitis media (OM) conditions, and its role in the persistent otitis media with effusion (OME). In this study, we demonstrated that the pneumococcal cell wall component, peptidoglycan-polysaccharides (PGPS), activated the expression of TLR2 in the middle ear epithelial cells through the nuclear factor kappa B (NF-κB)-cytokine signaling pathway while I kappa B alpha mutant (IκBαM), a dominant negative inhibitor of NF-κB, abrogated the expression of TLR2 induced by PGPS. This study suggests that the existence of residual PGPS may maintain a low profile of cytokine production in the middle ear mucosa and thus contribute to the pathogenesis of OME.
Toll-like receptor 2 (TLR2) 在宿主防御革兰氏染色阳性（革兰氏）细菌及其细胞壁包膜成分中发挥关键作用。然而，关于 TLR2 在中耳炎（OM）条件下中耳中的表达及其在持续性分泌性中耳炎（OME）中的作用知之甚少。在这项研究中，我们表明肺炎球菌细胞壁成分肽聚糖-多糖（PGPS）通过核因子 kappa B（NF-κB）-细胞因子信号通路激活中耳上皮细胞中 TLR2 的表达，而 I kappa B alpha 突变体（IκBαM），NF-κB 的显性负抑制剂，可阻断 PGPS 诱导的 TLR2 表达。本研究表明，残留的 PGPS 的存在可能使中耳黏膜中的细胞因子产生保持低水平，从而有助于 OME 的发病机制。
