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RESEARCH ARTICLE
Year : 2019  |  Volume : 14  |  Issue : 9  |  Page : 1594-1602

Interleukin-4 affects microglial autophagic flux


1 Department of Neurology, the First Hospital of China Medical University, Shenyang, Liaoning Province, China
2 Department of Dermatology, Key Laboratory of Immunodermatology, the First Hospital of China Medical University, Shenyang, Liaoning Province, China

Correspondence Address:
Hua-Yan Liu
Department of Neurology, the First Hospital of China Medical University, Shenyang, Liaoning Province
China
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Source of Support: This study was supported by the Natural Science Foundation of Liaoning Province of China, No. 20170541036 (to HYL), Conflict of Interest: None


DOI: 10.4103/1673-5374.255975

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Interleukin-4 plays an important protective role in Alzheimer’s disease by regulating microglial phenotype, phagocytosis of amyloid-β, and secretion of anti-inflammatory and neurotrophic cytokines. Recently, increasing evidence has suggested that autophagy regulates innate immunity by affecting M1/M2 polarization of microglia/macrophages. However, the role of interleukin-4 in microglial autophagy is unknown. In view of this, BV2 microglia were treated with 0, 10, 20 or 50 ng/mL interleukin-4 for 24, 48, or 72 hours. Subsequently, light chain 3-II and p62 protein expression levels were detected by western blot assay. BV2 microglia were incubated with interleukin-4 (20 ng/mL, experimental group), 3-methyladenine (500 μM, autophagy inhibitor, negative control group), rapamycin (100 nM, autophagy inductor, positive control group), 3-methyladenine + interleukin-4 (rescue group), or without treatment for 24 hours, and then exposed to amyloid-β (1 μM, model group) or vehicle control (control) for 24 hours. LC3-II and p62 protein expression levels were again detected by western blot assay. In addition, expression levels of multiple markers of M1 and M2 phenotype were assessed by real-time fluorescence quantitative polymerase chain reaction, while intracellular and supernatant amyloid-β protein levels were measured by enzyme-linked immunosorbent assay. Our results showed that interleukin-4 induced microglial autophagic flux, most significantly at 20 ng/mL for 48 hours. Interleukin-4 pretreated microglia inhibited blockade of amyloid-β-induced autophagic flux, and promoted amyloid-β uptake and degradation partly through autophagic flux, but inhibited switching of amyloid-β-induced M1 phenotype independent on autophagic flux. These results indicate that interleukin-4 pretreated microglia increases uptake and degradation of amyloid-β in a process partly mediated by autophagy, which may play a protective role against Alzheimer’s disease.


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