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Protective Activity of Aβ on Cell Cultures (PC12 and THP-1 after Differentiation) Preincubated with
Benita Wiatrak1,2, Katarzyna Balon3
1Department of Pharmacology, Wroclaw Medical University, Mikulicza-Radeckiego 2, 50-345, Wrocław, Poland. benita.wiatrak@umed.wroc.pl.
Abstract:
Amyloid-β (Aβ), the influence of which is considered the pathomechanism of Alzheimer's disease, is also present in healthy people. The microbiome's impact is also taken into account, where bacterial lipopolysaccharide (LPS) activates inflammatory processes and stimulates microglia via TLRs. Molecules of bacterial origin can co-create senile plaques with Aβ. This study evaluated the activity of physiological Aβ concentrations on neuronal and microglial cells after preincubation with LPS. Two cell lines were used in the study: PC12 cells differentiated with NGF and THP-1 cells differentiated with phorbol 12-myristate 13-acetate (PMA). Cells were incubated with LPS at concentrations of 1-100 μM for 24 h and then with Aβ25-35 at a concentration of 0.001 μM or 1.0 μM for another 24 h. The viability of the culture and free oxygen radicals and the number of DNA strand breaks in both cell lines were evaluated. Additionally, for PC12 cells, neural features were assessed. Stimulation of repair processes in the presence of Aβ was observed for both studied cell lines. There was a decrease in free radical level and DNA damage number compared to control cultures (cells treated with LPS and without Aβ). The neurotrophic activity of Aβ was observed-the effect on neurites' growth even after the preincubation of PC12 cells with LPS. At the lowest concentration of LPS used, the increase in neurite length was about 50% greater than in the negative control. At low concentrations, Aβ has a protective effect on neuron-like PC12 cells pretreated with LPS.
Insights
Bacterial lipopolysaccharide (LPS) and amyloid-beta (Aβ) can interact. Low concentrations of Aβ showed protective effects on neuronal cells pretreated with LPS, reducing free radicals and DNA damage.
Area of Science:
- Neuroscience
- Immunology
- Microbiology
Background:
- Alzheimer's disease pathogenesis involves amyloid-beta (Aβ), also found in healthy individuals.
- Bacterial lipopolysaccharide (LPS) triggers inflammatory responses and microglial activation via Toll-like receptors (TLRs).
- Bacterial molecules may aggregate with Aβ in senile plaques.
Purpose of the Study:
- To investigate the effects of physiological amyloid-beta (Aβ) concentrations on neuronal and microglial cells previously exposed to lipopolysaccharide (LPS).
- To assess the impact of LPS and Aβ co-exposure on cell viability, oxidative stress, and DNA damage.
Main Methods:
- Utilized PC12 (neuronal) and THP-1 (microglial) cell lines, differentiated appropriately.
- Cells were incubated with varying concentrations of LPS (1-100 μM) for 24 hours, followed by incubation with Aβ25-35 (0.001 μM or 1.0 μM) for another 24 hours.
- Evaluated cell viability, free oxygen radical levels, DNA strand breaks, and neurite outgrowth in PC12 cells.
Main Results:
- Amyloid-beta (Aβ) demonstrated a stimulatory effect on repair processes in both cell lines.
- A reduction in free radicals and DNA damage was observed compared to control groups.
- Amyloid-beta (Aβ) exhibited neurotrophic activity, promoting neurite growth in PC12 cells even after LPS pre-incubation.
- Low concentrations of Aβ conferred a protective effect on LPS-treated PC12 cells.
Conclusions:
- Physiological concentrations of amyloid-beta (Aβ) can exert protective and neurotrophic effects on neuronal cells, particularly when co-exposed with bacterial lipopolysaccharide (LPS).
- These findings suggest a complex interplay between microbial components and Aβ in neuronal health and disease, potentially influencing Alzheimer's disease progression.
