Toxoplasma gondii eIF-5A Modulates the Immune Response of Murine Macrophages In Vitro

TL;DR

This study shows that a protein from Toxoplasma gondii affects how mouse macrophages respond to infection, potentially aiding vaccine development.

Contribution

The study reveals a new role for T. gondii eIF-5A in modulating macrophage immune responses.

Findings

TgeIF-5A binds to and is partially internalized by macrophages.

TgeIF-5A reduces TLR4 levels and chemotaxis but increases phagocytosis and apoptosis in macrophages.

TgeIF-5A promotes macrophage viability and induces secretion of IL-6, TNF-α, and NO.

Abstract

Toxoplasma gondii (T. gondii) is an obligate intracellular protozoan that can elicit a robust immune response during infection. Macrophage cells have been shown to play an important role in the immune response against T. gondii. In our previous study, the eukaryotic translation initiation factor 5A (eIF-5A) gene of T. gondii was found to influence the invasion and replication of tachyzoites. In this study, the recombinant protein of T. gondii eIF-5A (rTgeIF-5A) was incubated with murine macrophages, and the regulatory effect of TgeIF-5A on macrophages was characterized. Immunofluorescence assay showed that TgeIF-5A was able to bind to macrophages and partially be internalized. The Toll-like receptor 4 (TLR4) level and chemotaxis of macrophages stimulated with TgeIF-5A were reduced. However, the phagocytosis and apoptosis of macrophages were amplified by TgeIF-5A. Meanwhile, the cell viability experiment indicated that TgeIF-5A can promote the viability of macrophages, and in the secretion assays, TgeIF-5A can induce the secretion of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and nitric oxide (NO) from macrophages. These findings demonstrate that eIF-5A of T. gondii can modulate the immune response of murine macrophages in vitro, which may provide a reference for further research on developing T. gondii vaccines.

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