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Expression of serum amyloid A genes in mouse brain: unprecedented response to inflammatory mediators

The Johns Hopkins University School of Medicine, Departments of Medicine,
^* Biological Chemistry, and
^* Pediatrics, Baltimore, Maryland 21205, USA

²Correspondence: Department of Biological Chemistry, Physiology 615, The Johns Hopkins University School of Medicine, 725 N. Wolfe St., Baltimore, MD 21205, USA. E-mail: gsack{at}jhmi.edu

Serum amyloid A (SAA) proteins were originally identified as prominent acute-phase serum proteins synthesized predominantly by hepatocytes. These small proteins are remarkably lipophilic, and we have sought evidence for their synthesis in mouse brain. RT-PCR showed constitutive expression of the murine SAA₁ gene in the brains of normal BALB/cJ mice. After intracerebral inoculation with Sindbis virus, these mice predictably increase brain expression of tumor necrosis factor (TNF-), interleukin 1ß (IL-1ß), and IL-6. However, brain SAA₁ expression fell after injecting either virus or control saline and remained low despite increases in TNF- and IL-6, which are known to induce its expression in hepatocytes. Our data thus show that expression of the murine SAA₁ gene has different, unprecedented control in mouse brain, suggesting that the protein itself may have a different physiological role there.—Tucker, P. C., Sack, G. H., Jr. Expression of serum amyloid A (SAA) genes in mouse brain: unprecedented response to inflammatory mediators.

Key Words: inflammation • neuroimmunology • acute-phase reactants • gene regulation • SAA

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