Role of Oxidative Stress in the Pathophysiology of Pneumococcal Meningitis

Figure 2

Innate immune system in pneumococcal meningitis infection. The majority of TLRs utilize a common intracellular adapter protein known as myeloid differentiation factor 88 (MyD88): it activates IRAK, which is phosphorylated and dissociated from MyD88. Thus, it interacts with the tumor necrosis factor receptor-associated factor 6 dependent signaling pathway (TRAF6). TRAF6 stimulates to the transforming growth factor β-activated kinase (TAK1). TAK1 activates the IKK (Inhibitor of IκB kinase), resulting in the destruction of IkB and subsequently, NF-κB activation resulting in the nuclear translocation of NF-κB. This cascade provides a link to NF-κB-inducing kinase, resulting in the nuclear translocation of NF-κB, which induces the production of cytokines, chemokines, and others proinflammatory molecules in response to bacterial stimuli.