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Figure 1 | Journal of Neuroinflammation

Figure 1

From: Amyloid-β peptide-induced extracellular S100A9 depletion is associated with decrease of antimicrobial peptide activity in human THP-1 monocytes

Figure 1

S100A9 release in response to Aβ1-42 monomers in human monocytic THP-1 cells. To measure the extracellular release of S100A9 in response to mostly monomeric Aβ1-42 stimulation, THP-1 cells were incubated with either vehicle only (−) or increasing amounts of Aβ1-42 for 24 hours in serum-free RPMI-1640 medium supplemented with glucose (0.5%). (A) The cell-free conditioned media were examined for S100A9 via protein immunoblot. Positive control for S100A9 was shown in human PBMC whole cell lysate. Aβ1-42 decreased S100A9 release in conditioned media in a dose-dependent manner. Results are representative of three independent experiments. (B) Densitometric quantification of analyses of (A), showing the levels of S100A9 release. All data are presented as the means ± SEM (n = 3). **P <0.01, versus vehicle treated samples. PBMC, peripheral blood mononuclear cells.

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