Establishment of BV2 microglia polarization model and its effect on Toxoplasma gondii proliferation.

Res Vet Sci

National Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin 150069, China. Electronic address:

Published: August 2019

AI Article Synopsis

  • Toxoplasma gondii is a parasitic protozoan that can influence microglial cells (a type of immune cell in the brain) by inducing their activation.
  • In this study, BV2 microglial cells were exposed to T. gondii and various inducing agents to assess changes in M1 and M2 marker expressions, showing significant upregulation of M1 markers shortly after infection.
  • The research highlights the activation of specific signaling pathways (JAK/STAT1 and NF-κB) in response to T. gondii infection, indicating that it promotes M1 microglial polarization and affects their function in the context of the innate immune response.

Article Abstract

Toxoplasma gondii is an intracellular opportunistic, parasitic protozoan. Microglia have been classified into two main types: M1 (classically activated macrophages) and M2 (alternatively activated macrophages). BV2 cells were used in this study, together with lipopolysaccharide (LPS) and interferon (IFN)-γ or interleukin (IL)-4, which were used to induce resting microglia. Expression levels of M1/M2 markers were determined at both mRNA and protein levels, using PCR, western blot, and flow cytometry. Furthermore, cells were infected with T. gondii PLK strain, and the dynamic changes in M1/M2 marker expression levels were determined. An in vitro polarization model was successfully established. Expression of Nos2 and M1-associated markers was significantly upregulated at 12 h post-infection in BV2 cells. Further, the JAK/STAT1 and NF-κB signaling pathways were also activated following T. gondii infection. This demonstrated that T. gondii infection induces M1-type microglial polarization in vitro. The present study demonstrated that T. gondii infection affects microglial activation in vitro and elucidated the effects of activated microglia on T. gondii proliferation. This data may serve as a useful reference for more detailed elucidation of interactions between T. gondii and the innate immune system.

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Source
http://dx.doi.org/10.1016/j.rvsc.2019.08.002DOI Listing

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