Jacinta Bowler
Our feline friends have a habit of infecting us with more than just love and affection. There’s also parasites. Specifically, Toxoplasma gondii – a parasite capable of infecting almost all warm-blooded animals, but which uses only cats as a ‘host’ for reproduction. Depending on who you ask, studies suggest it could have infected up to 50% of all humans!
In the last few years there’s been a push to be able to understand how the parasite works. We know it changes the behaviour of mice to make it easier for cats to nab them, it’s been implicated in a wide range of human diseases (although the jury is still out on how many), and can hitch rides on microplastics.
A new study, published in Cell Host & Microbe, has zoomed down to the cellular level to investigate why the parasite can so successfully spread through the body, looking at cells from both mice and humans.
“We have now discovered a protein that the parasite uses to reprogram the immune system,” says Stockholm University molecular biologist Arne ten Hoeve.
It all comes down to a decision a cell makes once the parasite has been detected and engulphed by a type of immune cell, or ‘phagocyte’ called a macrophage.
Usually once a pathogen has been engulfed, macrophages will stay put, happily digesting the problem, and then recruiting other immune cells to scout for more.
But another type of immune cell called dendritic cells take sections of the pathogen and travel to the lymphatic system to sound the alarm.
But when a macrophage cell is infected with T. gondii, the parasite releases a protein called ‘GRA28’ which creates chemicals and instructions normally used by dendritic cells. This allows the parasite to hijack the cell and travel towards the lymphatic system instead, spreading the infection further throughout the body.
“It is astonishing that the parasite succeeds in hijacking the identity of the immune cells in such a clever way,” says senior author and Stockhom University molecular biologist Professor Antonio Barragan.
“We believe that the findings can explain why Toxoplasma spreads so efficiently in the body when it infects humans and animals.”
The team confirmed this by creating genetically engineered T. gondii which were unable to produce GRA28. These deficient strains were much less effective in migrating to new locations.
“It is becoming increasingly clear that bacterial, viral, and fungal microorganisms use elaborate strategies to thrive inside macrophages and other phagocytes,” the team write in their new paper.
“The findings unveil putative alternative pathways by which mononuclear phagocytes can be made migratory or activated, which could – by extension – be exploited, for example, in cell therapies.”