Toxoplasma gondii Parasite May Protect Against Developing MS
Toxoplasmosis may have a protective effect against the development of #MultipleSclerosis (MS), according to a review study. People who had been infected with #Toxoplasma gondii were 32% less likely to develop MS than those who never had #toxoplasmosis.
Toxoplasmosis, an infection by the parasite Toxoplasma gondii, has a protective effect against the development of multiple sclerosis (MS), according to a review study. Specifically, people who had been infected with the parasite were 32% less likely to develop MS than those who never had toxoplasmosis.
While these findings support T. gondii infection as a protective factor against MS, appropriately-designed studies are needed to confirm its protective effect, to assess whether it also lessens disease progression, and to better understand the mechanisms behind these associations.
Such information may help develop new therapeutic approaches for people living with MS, the researchers noted.
The review study, “Toxoplasma gondii and Multiple Sclerosis: a systematic review and meta-analysis,” was published in the European Journal of Neurology.
MS is considered a multifactorial autoimmune disease due to a complex interaction between genetic and environmental factors. Increasing evidence supports the viewpoint that infectious agents, such as viruses and parasites, can modulate activity of the immune system.
Notably, exposure to certain infectious agents early in life may have a protective effect against autoimmune diseases such as MS, according to a theory called hygiene hypothesis.
Previous clinical trial data showed that infecting MS patients with a generally safe gut parasitic worm was associated with anti-inflammatory effects and fewer new or enlarging brain lesions, relative to those not infected with the worm.
Infection with T. gondii, a generally harmless parasite that can be transmitted to humans through ingestion of undercooked contaminated meat or exposure to infected cat feces, has been shown to promote anti-inflammatory, immunosuppressive responses in animal models.
However, research on its potential protective effect in human autoimmune diseases have provided contradictory results. While a prior study reported that the parasite was associated with an increased risk of rheumatoid arthritis, other studies suggested it may have a protective effect in MS.
Now, researchers in Italy and France evaluated the effects of T. gondii infection in MS development by systematically reviewing published studies (including those written in Portuguese, Spanish, and French) up to November 2020 reporting associations between toxoplasmosis and MS.
From the initial 562 hits, eight studies were accessed for eligibility, and seven — covering a total of 752 MS patients and 1,282 people without MS (controls) — were included in the meta-analysis. Three studies were conducted in Asia, two in Europe, one in North America, and one study used two different groups from Europe and South America.
Studies comprised 45–163 MS patients and 45–297 controls who were recruited from either the general population, unaffected family members living in the same household, or from hospital patients without MS. History of toxoplasmosis was assessed through the presence of antibodies against the parasite.
One study included also people with clinically isolated syndrome (CIS), which may precede a diagnosis of MS.
When excluding CIS patients, pooled results showed that people who had been infected with T. gondii were 32% less likely to develop MS than those with no history of infection. A similar association was found when including CIS patients, with toxoplasmosis being associated with a 34% lower likelihood of developing MS.
Notably, three of the included studies found no link between T. gondii infection and MS, which may be explained by their small samples and very low statistical power. In turn, the two studies with sufficient statistical power found a protective effect of toxoplasmosis.
Still, a causal association between T. gondii infection and MS development “cannot be inferred due to the retrospective nature of the included studies,” and as such, “it is not possible to know whether T. gondii infection has been acquired before or after the development of MS,” the researchers wrote.
These findings support “the hypothesis that T. gondii infection represents a protective factor towards the development of MS,” the team wrote.
Future, well-designed, large studies following people infected with T. gondii over time are needed to confirm these findings and to describe the immune profiles of infected and non-infected MS patients.
“In the near future, combining these scientific evidences could contribute to the development of new therapeutic strategies for patients with MS,” the researchers concluded.
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