ArticleParasitology research2016
The morphological analysis of autophagy in primary skeletal muscle cells infected with Toxoplasma gondii.
Article in Parasitology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Nanoformulation-Based 1,2,3-Triazole Sulfonamides for Anti-Tropical medicine and infectious disease · 2023Article
- Article
- Autophagy in protists and their hosts: When, how and why?Autophagy reports · 2023Article
- Different Drugs, Same End: Ultrastructural Hallmarks of Autophagy in Pathogenic Protozoa.Frontiers in microbiology · 2022Review
- Host-Frontiers in immunology · 2017Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toxoplasma gondii is an obligate intracellular protozoan parasite, the causative agent of toxoplasmosis, one of the most widespread zoonoses in the world. During the host immune response, tissue cysts are formed, allowing the maintenance of the parasite within the host cell. Autophagy, a degradation process of cellular components, is critical for cellular homeostasis. Recently, it has been proposed that autophagy participates in host-pathogen interactions. Autophagic inducers (rapamycin or glucose plus serum deprivation) inhibited infection and parasite proliferation in a clinically relevant model of primary skeletal muscle cells (SkMC). The ultrastructural analysis showed in SkMC submitted to autophagic stimuli the presence of structures suggestive of autophagosomes close to the parasitophorous vacuole containing degraded parasites. Fluorescence microscopy results pointed out the increase in LC3 puncta in these cells after incubation with autophagic inducers. In the present study, SkMC autophagy controlled the proliferation of tachyzoites inside the cell, data reinforced by ultrastructural evidences and increased LC3 expression.
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