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Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
Published on: February 16, 2018
Microglial proliferation attenuates sickness responses in adult mice during endotoxin-induced inflammation
Katsuhiro Torii1, Shohei Takagi1, Ryoichi Yoshimura1
1Department of Applied Biology, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto 606-8585, Japan.
Abstract:
We previously reported that the single peripheral administration of lipopolysaccharide (LPS) induced robust and transient microglial proliferation or increased the microglial population in the circumventricular organs (CVOs) and other regions, including the hypothalamus, medulla oblongata, and limbic system. However, the functional significance of an increased microglial population during endotoxin-induced inflammation remains unclear. The present study showed microglial proliferation in the mouse brain during inflammation induced by 50 mg/kg zymosan, 160 nmol/kg prostaglandin E2, and 5 mg/kg LPS. The inhibition of LPS-induced microglial proliferation with a continuous i.c.v. infusion of mitotic inhibitor cytosine arabinoside (AraC) caused persistent decreases in body weight and food and water intakes. The continuous infusion of AraC also prolonged LPS-induced sickness responses, such as lower locomotor activity and core body temperature. Collectively, the present results indicate that a transient increase in the microglial population is beneficial during endotoxin-induced inflammation in the mouse brain because it attenuates sickness responses.
Insights
A transient increase in brain microglia benefits mice during endotoxin-induced inflammation. Inhibiting this microglial proliferation prolonged sickness responses, indicating a protective role.
Area of Science:
- Neuroscience
- Immunology
- Neuroinflammation
Background:
- Peripheral administration of lipopolysaccharide (LPS) induces microglial proliferation in specific brain regions.
- The functional significance of this increased microglial population during inflammation is not fully understood.
Purpose of the Study:
- To investigate the functional significance of microglial proliferation during inflammation induced by various agents.
- To determine the role of LPS-induced microglial proliferation in sickness responses.
Main Methods:
- Induced inflammation using zymosan, prostaglandin E2, and LPS in mice.
- Inhibited LPS-induced microglial proliferation using continuous intracerebroventricular (i.c.v.) infusion of cytosine arabinoside (AraC).
- Monitored body weight, food and water intake, locomotor activity, and core body temperature.
Main Results:
- Microglial proliferation was observed in response to zymosan, prostaglandin E2, and LPS.
- Inhibition of LPS-induced microglial proliferation with AraC led to sustained decreases in body weight and intake.
- AraC infusion prolonged LPS-induced sickness behaviors, including reduced activity and body temperature.
Conclusions:
- A transient increase in the brain's microglial population is beneficial during endotoxin-induced inflammation.
- Microglial proliferation plays a protective role by attenuating sickness responses in the mouse brain.
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