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Effect of interferon regulatory factor 5 in LPS‐induced neuro‐inflammation
Author(s) -
Fan Ziqi
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.040170
Subject(s) - irf5 , microglia , inflammation , interferon regulatory factors , immunology , lipopolysaccharide , tumor necrosis factor alpha , macrophage , cytokine , interferon , medicine , biology , immune system , innate immune system , in vitro , biochemistry
Background Activated microglia plays a central role in neuro‐inflammation in central nervous system (CNS), which is involved in the progress of disease. Interferon regulatory factor 5 (IRF5) has been well established relating to inflammatory responses and is highly expressed in M1 macrophage in periphery, the role of which in the CNS remains elusive. Method Down‐regulation of IRF5 by siRNA in C57/BL6 mice and BV2 microglial cells was employed. Lipopolysaccharide (LPS) challenge activates the response of neuro‐inflammation, Pro‐inflammatory cytokines were evaluated by ELISA, western blot, and real‐time PCR. Result LPS induced the activation of microglia, which co‐localized with the significantly increase expression of IRF5. Down‐regulation of IRF5 significantly quenched the pro‐inflammatory responses. The levels of pro‐inflammatory cytokine TNF‐α, IL‐1βand IL‐6 were significantly up‐regulated at 4h after LPS treatment, which were reduced with the down‐regulation of IRF5. However, LPS did not up‐regulate the expression of IRF5 in BV2 microglial cells, indicating that LPS induced inflammation does not involve IRF5 signaling. Conclusion IRF5 plays an important role in the inflammatory responses in the CNS, which might serve as a therapeutic target for CNS inflammatory diseases. BV2 microglia is not an ideal cell line for the studies involves IRF5.