ArticleParasite (Paris, France)2017
Exogenous tumor necrosis factor-alpha could induce egress of Toxoplasma gondii from human foreskin fibroblast cells.
Article in Parasite (Paris, France), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Effective factors in the pathogenesis ofHeliyon · 2024Review
- A Combination of Four Nuclear Targeted Effectors ProtectsbioRxiv : the preprint server for biology · 2023Article
- Egress Regulatory Factors: HowPathogens (Basel, Switzerland) · 2023Review
- Overview of Apoptosis, Autophagy, and Inflammatory Processes inPathogens (Basel, Switzerland) · 2023Review
- Regulated necrosis, a proinflammatory cell death, potentially counteracts pathogenic infections.Cell death & disease · 2022Review
- Overexpression screen of interferon-stimulated genes identifies RARRES3 as a restrictor ofeLife · 2021Article
- The potential role of necroptosis in clinical diseases (Review).International journal of molecular medicine · 2021Review
- Exogenous nitric oxide stimulates early egress of Eimeria tenella sporozoites from primary chicken kidney cells in vitro.Parasite (Paris, France) · 2021Article
- A Window toPathogens (Basel, Switzerland) · 2018Review
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Authors and funding
5 authors.
Funding
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Abstract
Toxoplasma gondii is an intra-cellular protozoan parasite that can infect almost all nucleated cells, eliciting host immune responses against infection. Host tissue damage is mainly caused by cellular lysis when T. gondii egresses from infected cells. However, the effects of cytokines released by host immune cells on egression of T. gondii remain elusive. This study aimed to investigate the role of tumor necrosis factor-alpha (TNF-α) on the egress of T. gondii from infected human foreskin fibroblast (HFF) cells and to elucidate the underlying mechanisms that regulate TNF-α-induced egress. Using flow cytometry to count tachyzoites of T. gondii released into cell culture medium, we found that egress of T. gondii from infected HFF cells could be induced by 10 ng/mL TNF-α in a time-dependent manner. Pre-treatment of infected HFF cells with BAPTA-AM to chelate intra-parasitic calcium could greatly inhibit TNF-α-induced egress. Similar results were obtained when using cytochalasin D to block parasite motility before the TNF-α-induced egress assay. In addition, blocking host apoptosis by Z-VAD-FMK could decrease TNF-α induced egress, while blocking necroptosis by necrostatin-1 has little impact on TNF-α-induced egress. The egressed tachyzoites displayed a normal growth rate and lost no virulence. Our results suggest that host cytokines could influence the cellular lytic processes of T. gondii, providing new insights into the relationship between host TNF-α and T. gondii pathogenesis.
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