Aβ-Induced Proinflammatory Cytokine Release from Differentiated Human THP-1 Monocytes

Brunden, Kurt R.; Kocsis-Angle, June; Embury, Paula; Yates, Stephen L.

doi:10.1385/1-59259-195-7:101

Cited by 2 publications

(3 citation statements)

References 26 publications

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“…THP‐1 cells . The THP‐1 human monocyte cell line (ATCC, Rockville, MD, U.S.A.; Tsuchiya et al, 1980) was grown in RPMI 1640 medium containing 10% fetal bovine serum as previously described (Brunden et al., 1999; Yates et al, 1999). The fetal bovine serum content was lowered to 2% before the cells were seeded at a density of 1.5 × 10 4 cells/well into 96‐well plates.…”

Section: Methodsmentioning

confidence: 99%

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Amyloid β and Amylin Fibrils Induce Increases in Proinflammatory Cytokine and Chemokine Production by THP‐1 Cells and Murine Microglia

Yates

Burgess

Kocsis-Angle

et al. 2000

Journal of Neurochemistry

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195

137

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Activated microglia surrounding amyloid ␤-containing senile plaques synthesize interleukin-1, an inflammatory cytokine that has been postulated to contribute to Alzheimer's disease pathology. Studies have demonstrated that amyloid ␤ treatment causes increased cytokine release in microglia and related cell cultures. The present work evaluates the specificity of this cellular response by comparing the effects of amyloid ␤ to that of amylin, another amyloidotic peptide. Both lipopolysaccharide-treated THP-1 monocytes and mouse microglia showed significant increases in mature interleukin-1␤ release 48 h following amyloid ␤ or human amylin treatment, whereas nonfibrillar rat amylin had no effect on interleukin-1␤ production by THP-1 cells. Lipopolysaccharide-stimulated THP-1 cells treated with amyloid ␤ or amylin also showed increased release of the proinflammatory cytokines tumor necrosis factor-␣ and interleukin-6, as well as the chemokines interleukin-8 and macrophage inflammatory protein-1␣ and -1␤. THP-1 cells incubated with fibrillar amyloid ␤ or amylin in the absence of lipopolysaccharide also showed significant increases of both interleukin-1␤ and tumor necrosis factor-␣ mRNA. Furthermore, treatment of THP-1 cells with amyloid fibrils resulted in an elevated expression of the immediate-early genes c-fos and junB. These studies provide further evidence that fibrillar amyloid peptides can induce signal transduction pathways that initiate an inflammatory response that is likely to contribute to Alzheimer's disease pathology.

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Section: Methodsmentioning

confidence: 99%

“…IL‐1β was measured as previously described (Brunden et al, 1999; Yates et al, 1999). In brief, the wells of Costar medium binding 96‐well plates were coated overnight at 4°C with 1.5 μg of a monoclonal antibody to human IL‐1β in 100 μl of phosphate‐buffered saline (PBS; R & D Systems, Minneapolis, MN, U.S.A.).…”

Section: Methodsmentioning

confidence: 99%

Amyloid β and Amylin Fibrils Induce Increases in Proinflammatory Cytokine and Chemokine Production by THP‐1 Cells and Murine Microglia

Yates

Burgess

Kocsis-Angle

et al. 2000

Journal of Neurochemistry

Self Cite

195

137

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“…However, once they assemble and aggregate to form its multimers, they become more insoluble and neuritic plaques [22]. Amyloid-beta aggregation stimulates excessive production of pro-inflammatory cytokines including interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha in monocytes and microglia [23,24,25]. Excessive levels of systemic and neuronal inflammation aggravate the progression of AD [22,26].…”

Section: Introductionmentioning

confidence: 99%

Supplementation with Nicotinamide Riboside Reduces Brain Inflammation and Improves Cognitive Function in Diabetic Mice

Lee

Yang

2019

IJMS

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The purpose of this study is to investigate whether nicotinamide riboside (NR) can improve inflammation and cognitive function in diabetic mice. ICR male mice were fed for 14 weeks with either high-fat chow diet (HF, 60% kcal fat) or standard chow diet (CON, 10% kcal fat). HF, streptozotocin, and nicotinamide were used to induce hyperglycemia. NR or vehicle was delivered via stomach gavage for six weeks. Oral glucose tolerance test, Y-maze test, and nest construction test were conducted before and after the NR treatment period. NR treatment induced down-regulation of NLRP3, ASC, and caspase-1. NR reduced IL-1 expression significantly by 50% in whole brains of hyperglycemic mice. Other inflammatory markers including TNF-α and IL-6 were also attenuated by NR. Brain expression of amyloid-β precursor protein and presenilin 1 were reduced by NR. In addition, NR induced significant reduction of amyloid-β in whole brains of diabetic mice. NR treatment restored hyperglycemia-induced increases in brain karyopyknosis to the levels of controls. Nest construction test showed that NR improved hippocampus functions. Spatial recognition memory and locomotor activity were also improved by NR supplementation. These findings suggest that NR may be useful for treating cognitive impairment by inhibiting amyloidogenesis and neuroinflammation.

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Aβ-Induced Proinflammatory Cytokine Release from Differentiated Human THP-1 Monocytes

Cited by 2 publications

References 26 publications

Amyloid β and Amylin Fibrils Induce Increases in Proinflammatory Cytokine and Chemokine Production by THP‐1 Cells and Murine Microglia

Amyloid β and Amylin Fibrils Induce Increases in Proinflammatory Cytokine and Chemokine Production by THP‐1 Cells and Murine Microglia

Supplementation with Nicotinamide Riboside Reduces Brain Inflammation and Improves Cognitive Function in Diabetic Mice

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