Abstract
BackgroundEgress is a vital step in the life cycle of Toxoplasma gondii which attracts attentions of many groups. Previous studies have shown that exogenous nitric oxide (NO) stimulates the early egress of T. gondii from infected peritoneal macrophages, a kind of immune cells. However, because Toxoplasma forms cysts in brain and muscle tissues, the development of autonomous immunity in non-immune cells is vital for limiting parasite burden and cyst formation. Therefore, we attempted to investigate whether exogenous NO could induce the early egress of T. gondii from infected non-immune cells.MethodsT. gondii tachyzoites were cultured in human foreskin fibroblast (HFF) cells and were then treated with NO released by sodium nitroferricyanide (III) dihydrate (SNP). The egressed parasites were analysed by flow cytometry.ResultsThe results showed that NO induced the early egress of parasites from HFF cells before completing their intracellular life cycles. We also found that the occurrence of egress was dependent on intracellular calcium (Ca2+) levels and the mobility of the parasite. Compared with freshly isolated tachyzoites, the developmental ability and virulence of egressed tachyzoites presented no difference.ConclusionsTaken together, our findings demonstrate a novel assay for the analysis of egress signalling mechanisms and an avenue of parasite clearance by hosts of T. gondii.
Highlights
Egress is a vital step in the life cycle of Toxoplasma gondii which attracts attentions of many groups
Our results showed that nitric oxide (NO) could trigger the early egress of T. gondii tachyzoites from infected human foreskin fibroblast (HFF) cells by elevating the concentration of the cytoplasmic Ca2+ of the parasites and that the occurrence of egress required the parasite motility
SNP-released NO triggered early egress of T. gondii tachyzoites from infected HFF cells A previous study reported that exogenous NO released by SNP could trigger the egress of T. gondii tachyzoites from infected peritoneal macrophages [16]
Summary
Egress is a vital step in the life cycle of Toxoplasma gondii which attracts attentions of many groups. Previous studies have shown that exogenous nitric oxide (NO) stimulates the early egress of T. gondii from infected peritoneal macrophages, a kind of immune cells. We attempted to investigate whether exogenous NO could induce the early egress of T. gondii from infected non-immune cells. One of the characterised mechanisms of resistance to T. gondii in human non-immune cells involves a disruption of the intracellular life cycle of the parasite. Many studies have focused on early egress from non-immune cells induced by immune molecules. Death receptor ligation in T. gondii infected cells results in the early egress of infectious parasites via an active process mediated by the release of intracellular Ca2+ [10]. Yan et al Parasites & Vectors (2015) 8:420 interferon-γ (IFN-γ)-induced cell death leads to early egress of Toxoplasma, which may promote the clearance of the parasite by immune cells [11]
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