JCI - Sustained hippocampal IL-1β overexpression mediates chronic neuroinflammation and ameliorates Alzheimer plaque pathology

Sustained hippocampal IL-1β overexpression mediates chronic neuroinflammation and ameliorates Alzheimer plaque pathology

Solomon S. Shaftel, Stephanos Kyrkanides, John A. Olschowka, Jen-nie H. Miller, Renee E. Johnson, M. Kerry O’Banion

Published in Volume 117, Issue 6

J Clin Invest. 2007; 117(6):1595–1604 doi:10.1172/JCI31450

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Figure 3

The neuroinflammatory response requires IL-1R1.

IL-1β^XAT B/b animals that were lacking (Il1r1^–/–), heterozygous for (Il1r1^+/–), or with 2 copies (Il1r1^+/+) of the gene encoding IL-1R1 were examined 2 weeks following FIV-Cre hippocampal injections. qRT-PCR analysis of ipsilateral hippocampi was performed relative to WT controls. (A) MHC class II induction was absent in Il1r1^–/– B/b animals, whereas Il1r1^+/– B/b mice exhibited a significant, intermediate phenotype compared with WT mice. (B) Histochemical analysis of MHC class II expression within the dentate gyrus of B/b mice revealed a pattern of expression mirroring the results in A. Scale bar: 25 μm. (C) GFAP induction was absent in Il1r1^–/– B/b mice, whereas Il1r1^+/– and Il1r1^+/+ B/b mice displayed significant GFAP upregulation. n = 3–5 animals per group. Data are mean ± SEM. *P < 0.05 versus WT.