Biological complexity:how toxoplasmosis parasitizes (Introduction)

by David Turell , Friday, January 24, 2020, 21:31 (1553 days ago) @ David Turell

They produce a protein chemical to lower the immune reaction in their hosts:

https://phys.org/news/2020-01-protein-delivery-parasite-suppress-host.html

"Toxoplasma's "success," scientists believe, owes in part to its ability to evade the immune response of its host, whichever warm-blooded vertebrate it has infected. Now a new study suggests the parasite employs a sophisticated manipulation to suppress that immune response.

"The work, ... shows that T. gondii parasites inject their host's macrophages, a type of immune cell, with a protein that changes the activity of the macrophage itself, creating what is known as an M2 macrophage. Those changes, the team showed, rein in the response of T cells that are normally responsible for killing parasites.

"'This is the first time that it's been shown that injection alone is sufficient to drive the creation of M2 macrophages," says Christopher A. Hunter, an immunologist at Penn Vet and senior author of the paper.

***

"For T. gondii, infection is a careful balancing act. It wants to spread far and wide within a host—and eventually be passed on to other hosts—but protective immunity is needed to prevent the death of the host. Scientists have long known that macrophages are critical players in maintaining this balance.

"Macrophages are the cells normally responsible for cleaning up infections by consuming foreign invaders. Around a decade ago, scientists found that they come in different "flavors."

"'Some macrophages are profoundly pro-inflammatory and kill pathogens; these are known as M1 macrophages." Hunter says. "M2 macrophages are profoundly anti-inflammatory but are less able to kill parasites. So M1 macrophages induce inflammation, and M2s help clear it up."

***

"'In an infected cell you see nearly 2,000 genes are changed," says Hunter. "But if they're only injected, you still see about 600 genes changing in expression."

"These changes alone were enough to sway macrophages over to the M2 type and to suppress the activity of T cells that normally act to kill parasites.

"Finally, to investigate the effect of ROP16 on the parasite itself and its ability to infect mice, Josh Kochanowsky of the University of Arizona engineered a ROP16-deficient strain of T. gondii.

"'If you put these parasites in immune-deficient mice, they grow normally" says Christian, "but if you put them in immune competent mice you get a reduced amount of M2s and a reduced parasite burden. So, we're seeing that taking away ROP16 leads to a more effective immune response.'"

Comment: finding just the right protein to adjust the immune system cannot be by chance. The toxoplasma organisms rely on an active life cycle and must have had this ability from the beginning. Only design fits.