Doctors told how toxoplasma captures body cells

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(ORDO NEWS) — Researchers at Indiana University School of Medicine (USA) have discovered new information about how the dangerous parasitic feline protist Toxoplasma gondii , which can also be transmitted to other animals and humans, controls cells and thereby spreads throughout the body. The study , published in the journal mBio , according to its authors, was an important discovery that will help in the development of new drugs for the treatment of toxoplasmosis.

Toxoplasma gondii affects up to a third of the world’s population. Typically, humans contract Toxoplasma through contact with cat feces or through contaminated food and water. The parasite is able to spread to the brain and provoke changes in behavior in some patients: slow down the reaction rate, cause anxiety, influence the propensity to take risks, and so on. In the brain and other tissues, the parasite remains in the form of a hidden cyst, waiting for activation when the immune system is weakened (in particular, when it comes to patients with HIV and AIDS).

“Cells infected with Toxoplasma gondii exhibit increased hypermigration activity, which contributes to the spread of infection. We have identified a novel mechanism that Toxoplasma uses to capture a host cell and increase its mobility. <…> After invasion of the host cell, Toxoplasma forms a parasitophorous vacuole (PV), which serves as a protective niche and can interact with the cytoplasm of the host cell to release nutrients,” the experts explain.

According to the authors of the study, one of the key problems in the fight against toxoplasmosis is that the spread of the parasites that cause this disease is extremely difficult to control: they turn off the signaling system in the host cell, which leads to the activation of the IRE1 protein. This, in turn, helps the cell deal with stress, which can include moving it to another location and hence spreading Toxoplasma gondii.

In vitro experiments in rodents have shown that removal of IRE1 from infected host cells reduces their migration and prevents the spread of Toxoplasma in vivo. So, when doctors infected cells that were deprived of RE1, they could no longer move that way.

“Noticeable levels of Toxoplasma spread in IRE1 depleted infected individuals into the spleen were not detected until three days after inoculation of mice. Even on the third day, loss of IRE1 caused reduced levels of parasitemia in the spleen. We also measured the spread of Toxoplasma on the third day – and found that there were 200 times fewer parasites. Mice lacking the IRE1 protein survived significantly longer. These results demonstrate a new role for the host protein IRE1 in the pathogenesis of parasites, since IRE1 is crucial for the migration of immune cells that are exploited as a Trojan horse for the spread of parasites,” the authors of the study concluded.


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