MyD88-dependent signals are essential for the host immune response in experimental brain abscess.

摘要: Brain abscesses form in response to a parenchymal infection by pyogenic bacteria, with Staphylococcus aureus representing common etiologic agent of human disease. Numerous receptors that participate immune responses including the majority TLRs, IL-1R, and IL-18R, use adaptor molecule, MyD88, for transducing activation signals leading proinflammatory mediator expression effector functions. To delineate importance MyD88-dependent brain abscesses, we compared disease pathogenesis using MyD88 knockout (KO) wild-type (WT) mice. Mortality rates were significantly higher KO mice, which correlated significant reduction several mediators, but not limited IL-1β, TNF-α, MIP-2/CXCL2. These changes associated neutrophil macrophage recruitment into animals. In addition, microglia, macrophages, neutrophils isolated from mice produced less IL-6, MIP-1α/CCL3, IFN-γ-induced protein 10/CXCL10 WT cells. The lack had dramatic effect on extent tissue injury, larger typified exaggerated edema necrosis Interestingly, despite these striking bacterial burdens did differ between two strains at early time points examined. Collectively, findings indicate plays an essential role establishing protective CNS host during stages abscess development, whereas MyD88-independent pathway(s) are responsible pathogen containment.