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

中耳细菌感染引起炎症细胞因子和趋化因子的合成。认为细胞因子的过量产生在慢性中耳炎的发病机制中起关键作用。细菌成分，如LPS，积聚在中耳可能会继续诱导炎症反应。该项目使用人上皮细胞系。上皮细胞暴露于来自非分型流感嗜血杆菌（NTHi）和LPS的病原体成分，表现出NF-κB的激活。使用蛋白酶体抑制剂和p38 MAPK抑制剂的研究表明，细菌感染引起的NF-κB激活需要IKK-IkBα和p38 MAPK途径。总之，我们的研究表明NTHi感染引起的炎症反应需要ikk - i - κ b α和p38 MAPK通路。两种途径也涉及调节炎症细胞因子和趋化因子，如TNF-α， il - 1 β和IL-8。我们未来的研究将集中在研究炎性细胞浸润所需的细胞粘附分子的合成。我们未来的研究将集中在研究炎性细胞浸润所需的细胞粘附分子的合成。

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.