Exploring molecular pathogenesis related to inflammatory cytokines in protracted otitis media.

中耳的细菌感染会导致炎症细胞因子和趋化因子的合成。细胞因子的过度产生在迁延性中耳炎的发病机制中起重要作用。在中耳积累的细菌成分，如脂多糖，可能会继续引发炎症反应。该项目使用了人类上皮细胞系。内皮细胞暴露于非分型流感嗜血杆菌和脂多糖的致病成分后，表现出对NF-κB的激活。使用蛋白酶体抑制剂和p38MAPK抑制剂的研究表明，细菌感染引起的NF-αB的激活需要IKK-I KB和p38MAPK两条途径。在炎性细胞因子和趋化因子的调控中也有两条途径，如肿瘤坏死因子-α、IL-Lβ和IL-8。我们未来的研究将集中在研究炎症细胞渗透所需的细胞黏附分子的合成上。

Bacterial infection in the middle ear causes synthesis of inflammatory cytokines and chemokine. It is believed overproduction of cytokines play a critical role in pathogenesis of protracted otitis media. Bacterial components, such as LPS, accumulated in the middle ear may continue to induce inflammatory response.Human epithelial cell lines were used in the project. Epithelial cells, which are exposed to pathogen components derived from Nontypeable Haemophilus influenzae (NTHi) and LPS, demonstrate activation of NF-κB.The studies using proteasome inhibitor and p38 MAPK inhibitor showed both IKK-IkBα and p38 MAPK pathways are required in NF-κB activation caused by bacterial infection.In conclusion, our studies demonstrate inflammatory response caused by NTHi infection requires both IKK-IκBα and p38 MAPK pathways. Two pathways are also implicated in regulating inflammatory cytokines and chemokine, such as TNF-α, IL-lβ, and IL-8.Our future studies will focus on investigating synthesis of cell adhesion molecules required for the infiltration of inflammatory cells.Our future studies will focus on investigating synthesis of cell adhesion molecules required for the infiltration of inflammatory cells.