Toxoplasmosis is generally a mild infection, but it can have serious and potentially fatal effects in pregnant women, their fetuses and others with weakened immune systems.
Studies conducted over mice have shown that T gondii directly activates a specific immune protein in the host, called toll-like receptor 11 (TLR-11), which helps control the animals' immune response to the parasite. Humans, however, don't have an active form of this receptor.
In the new study, researchers suggest that instead of activating toll-like receptors directly, T gondii's first interaction in the human gut is with the helpful bacteria that live inside the body.
Those bacteria then release signaling molecules, alerting the human host to the invader.
"While this is very early data, our results suggest that looking at the bacteria present in each patient's gut could help physicians understand their susceptibility to infectious diseases," said Dr. Felix Yarovinsky, assistant professor of immunology at UT Southwestern and senior author of the paper.
"It also suggests the possibility of developing novel probiotic strategies for treating parasitic infections such as toxoplasmosis and cryptosporidiosis, a related disease caused by the parasite Cryptosporidium," Yarovinsky added.
The primary host of protozoan parasite is the house cat, which are generally infected with T gondii by ingesting contaminated meat, water or the feces of a cat that has recently been infected; however, the parasite also can be passed from mother to fetus. Once a person is infected, the parasite penetrates the intestine and spreads throughout all organs.
The researchers studied mice in which TLR-11 had been genetically eliminated. This mimics the human immune response to T gondii. They then infected the TRL-11-deficient mice with T gondii.
They found that the commensal - or good - bacteria in the gut activated their immune system, thereby inducing various inflammatory responses against the invading pathogen.
In humans it is those helpful bacteria that send activating signals to the three toll-like receptors that are functional, inducing various inflammatory responses against invading pathogens like T gondii.
The study appears in journal of Cell Host and Microbe.