Abstract
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.
CNS & Neurological Disorders - Drug Targets
Title:S100A9 Exacerbates the Aβ1-42-mediated Innate Immunity in Human THP-1 Monocytes
Volume: 15 Issue: 8
Author(s): Kyoung A. Jhang, Eun Ok Lee, Hee-Sun Kim, Keun-A Chang, Yoo-Hun Suh and Young Hae Chong
Affiliation:
Keywords: Alzheimer’s disease, innate immunity, S100A9.
Abstract: 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.
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Cite this article as:
Jhang A. Kyoung, Lee Ok Eun, Kim Hee-Sun, Chang Keun-A, Suh Yoo-Hun and Chong Hae Young, S100A9 Exacerbates the Aβ1-42-mediated Innate Immunity in Human THP-1 Monocytes, CNS & Neurological Disorders - Drug Targets 2016; 15 (8) . https://dx.doi.org/10.2174/1871527315666160815161922
DOI https://dx.doi.org/10.2174/1871527315666160815161922 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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