Absence of CD14 Delays Progression of Prion Diseases Accompanied by Increased Microglial Activation

• DOI: 10.1128/jvi.02072-13
• Publication Date: 2013-10-03T00:59:30Z
• Authors: Keiko Sakai; Rie Hasebe; Yusuke Takahashi; Chang-Hyun Song; Akio Suzuki; Takeshi Yamasaki; Motohiro Horiuchi
• Keywords: Astrocytosis

ABSTRACT Prion diseases are fatal neurodegenerative disorders characterized by accumulation of PrP Sc , vacuolation neurons and neuropil, astrocytosis, microglial activation. Upregulation gene expressions innate immunity-related factors, including complement factors CD14, is observed in the brains mice infected with prions even early stage infections. When CD14 knockout (CD14 −/− ) were intracerebrally Chandler Obihiro prion strains, survived longer than wild-type (WT) mice, suggesting that influences progression disease. Immunofluorescence staining can distinguish normal protein from disease-specific form (PrP revealed deposition was delayed compared WT middle infection. Immunohistochemical Iba1, a marker for activated microglia, showed an increased activation prion-infected to mice. Interestingly, accompanied activation, anti-inflammatory cytokines interleukin-10 (IL-10) transforming growth factor β (TGF-β) appeared be expressed earlier In contrast, IL-1β expression reduced Double immunofluorescence demonstrated CD11b- Iba1-positive microglia mainly produced cytokines, status These results imply plays role disease suppressing responses brain