Abstract
High mobility group box 1 (HMGB1) is abundantly expressed in intracellular engaged DNA binding ability. However, more importantly, it is a weapon against infection through proinflammatory response and immune regulation while released to extracellular. Toxoplasma gondii causes inflammatory pathological changes including ileitis and encephalitis in chronic infection. To investigate whether HMGB1 contributes to the toxoplasmosis lesions, we examined HMGB1 changes during T. gondii infection. The results showed that HMGB1 transcription was down-regulated in the murine macrophage ANA1 cell line and mouse peritoneal macrophages (PMΦs) after T. gondii inoculation, but up-regulated in the IFN-γ treated macrophages and the intraperitoneal exudate cells from the T. gondii infected mice. The content of intracellular HMGB1 are basically consistent with the transcription levels in ANA1 assay, while there were no obvious changes in the mouse PMΦs. Both ANA1 and mouse PMΦs released HMGB1 after parasites infection, and no obvious HMGB1 aggregation in cytoplasm compare to the IFN-γ treatment group. Furthermore, we demonstrated that T. gondii invasion led to HMGB1 release, which was dependent on the Caspase 1 activity. These finding should promote to further investigate the functions of extracellular HMGB1 in the toxoplasmosis.
Highlights
Toxoplasma gondii is an obligate intracellular protozoan, which invades almost all nucleated cells and resists phagosome-lysosome fusion killing through forming parasitophorous vacuoles (PV)
High mobility group box 1 (HMGB1) transcription continuously declined in ANA1 cells over the first 24 h after T. gondii infection, which may suggest inhibition of cell growth by T. gondii invasion
HMGB1 transcription increased at 12 h after T. gondii infection, and declined before a sharp increase at 48 h in the IFN-γ pretreated ANA1 cells (Figure 1A)
Summary
Toxoplasma gondii is an obligate intracellular protozoan, which invades almost all nucleated cells and resists phagosome-lysosome fusion killing through forming parasitophorous vacuoles (PV). European and North American strains of T. gondii belong to three distinct clonal lineages: types I, II, and III, which differ genetically by 1% or less (Sibley and Ajioka, 2008). Type I (high virulence) strains are categorically lethal with an LD100 = 1, whereas the LD50 of type II (intermediate virulence) and III strains (low virulence) are ∼103 and 105, respectively (Sibley and Boothroyd, 1992; Sibley and Ajioka, 2008). Many genes have been identified to be responsible for the difference between biological phenotypes, virulence and dissemination (Dubremetz and Lebrun, 2012). T. gondii can carefully regulate immune responses and host cell effector mechanisms, mostly by its ROPs (ROP18, ROP5, ROP17, ROP16, and ROP38), GRAs
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