Host autophagy is exploited by the intracellular parasite Toxoplasma gondii to enhance amino acids levels.
Matthew D WhiteRajendra K AngaraLeticia Torres DiasDhananjay D ShindeVinai C ThomasLeonardo AugustoPublished in: bioRxiv : the preprint server for biology (2023)
induces the host's autophagic pathway to boost amino acid levels in infected cells. The depletion of amino acids, in turn, influences the persistence of the parasite's chronic forms, resulting in a reduction of neurological alterations caused by chronic infection in mice. Significantly, our investigation establishes the crucial role of host ER-phagy in the parasite's persistence within the host during latent infection.
Keyphrases
- toxoplasma gondii
- amino acid
- cell death
- plasmodium falciparum
- induced apoptosis
- cell cycle arrest
- trypanosoma cruzi
- oxidative stress
- signaling pathway
- type diabetes
- life cycle
- fluorescent probe
- metabolic syndrome
- cell proliferation
- breast cancer cells
- living cells
- single molecule
- estrogen receptor
- blood brain barrier
- endoplasmic reticulum