The S100A9 protein is an important proinflammatory factor of innate
immunity that has been proposed to participate in inflammation associated with the
pathogenesis of Alzheimer’s disease. Here, we provide insights into the potential
roles of extracellular S100A9 in the interaction with the immune response in human
THP-1 monocytic cells that have been challenged with amyloid β1-42 (Aβ1-42)
monomers instead of oligomers. Extracellular S100A9 alone produced a stimulatory
effect on tumor necrosis factor-α and interleukin-1β, expression as well as released
monocyte chemoattractant protein-1 into culture supernatants, which was
accompanied by an increased level of matrix metalloproteinas-9 activity.
Importantly, co-stimulation with S100A9 and Aβ1-42 resulted in a marked
enhancement of Aβ1-42-mediated release of these proinflammatory mediators under the same
experimental conditions, whereas heat inactivated S100A9 had little effect. Our findings clearly suggest
that excess S100A9 protein may play an important role in the pathological processes of Alzheimer’s
disease by exacerbating the Aβ1-42-induced innate immune response.
Keywords: Alzheimer’s disease, innate immunity, S100A9.
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