We report that mRNA levels for α1-antichymotrypsin (ACT), a component of β-amyloid plaques in Alzheimer's disease, are significantly increased in the brains of two different mouse models that develop inflammation: (1) acute inflammation caused by intraperitoneal injection with lipopolysaccharide (LPS) and (2) chronic inflammation in knockout mice lacking the anti-inflammatory cytokine transforming growth factor β1 (TGF-β1). While brain mRNA levels for the inflammatory cytokines TNFα, IL-1β, and IL-6 were all elevated in the LPS-injected mice, only the mRNA for IL-1β increased significantly in TGF-β1-deficient mice. The transcription factor C/EBPβ was strongly activated in the brains of both models. These results support the hypothesis that, through induction of the ACT gene in the brain, inflammation plays an important role during the development of Alzheimer's disease and that IL-1β and C/EBPβ may be involved in this process.
|Original language||English (US)|
|Number of pages||6|
|Journal||Biochemical and Biophysical Research Communications|
|State||Published - Sep 24 1999|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology