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Temporal Gene Expression in the Hippocampus and Peripheral Organs to Endotoxin-Induced Systemic Inflammatory Response in Caspase-1-Deficient Mice
Author(s) -
Claudio A. Mastronardi,
Gilberto Paz-Filho,
Martina Zai,
Nicolás Molano-González,
Mauricio ArcosBurgos,
Júlio Licinio,
Ma Li Wong
Publication year - 2015
Publication title -
neuroimmunomodulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.635
H-Index - 65
eISSN - 1423-0216
pISSN - 1021-7401
DOI - 10.1159/000368310
Subject(s) - proinflammatory cytokine , lipopolysaccharide , endocrinology , cxcl1 , caspase 1 , medicine , microbiology and biotechnology , knockout mouse , chemistry , gene expression , biology , chemokine , receptor , inflammation , inflammasome , biochemistry , gene
Caspase-1 (casp1), a key protease involved in the systemic inflammatory response syndrome (SIRS), controls the brain expression of a set of eight genes: Nos2 and Ptgs2 (nitric oxide synthase 2 and prostaglandin-endoperoxide synthase 2, two inducible enzymes), Cxcl1 and Cxcl10 (C-X-C motif chemokine ligand 1 and ligand 10), Tgtp and Gbp2 (T cell-specific GTPase 1 and guanylate-binding protein 2, two GTPases), Adamts1 (a disintegrin-like and metallopeptidase with thrombospondin type 1 motif, 1, a metalloprotease) and Il1rn (interleukin-1 receptor antagonist). Our objective was to ascertain whether casp1 also controlled the peripheral expression of these genes and, if so, to compare their central versus peripheral patterns of gene expression in immune and endocrine tissues during SIRS.

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