The imbalance in the relationship between inflammatory and regulatory cytokines during gestational toxoplasmosis can be harmful to fetuses: A systematic review

Abstract

ObjectiveTo evaluate the available information on inflammatory and regulatory plasma mediators in pregnant women (PW) diagnosed with toxoplasmosis. Source: The PubMed, Embase, Scopus, and Lilacs databases were evaluated until October 2022. Study eligibility criteria: This review was carried out following the PRISMA and registered on the PROSPERO platform (CRD42020203951). Studies that reported inflammatory mediators in PW with toxoplasmosis were considered.Evaluation methodsAfter excluding duplicate articles, two authors independently carried out the process of title and abstract exclusion, and a third resolved disagreements when necessary. The full text was evaluated to detect related articles. The extraction table was built from the following data: Author, year of publication, journal name and impact factors, country, study design, number of gestations and maternal age (years), gestational period, diagnosis of toxoplasmosis, levels of inflammatory markers, laboratory tests, and clinical significance. Methodological quality was assessed using Joanna Briggs Institute tools.ResultsOf the 1,024 studies reported, only eight were included. Of the 868 PW included in this review, 20.2% were IgM+/IgG- and 50.8% were IgM-/IgG+ to T. gondii, and 29.0% uninfected. Infected PW presented higher plasma levels ofIL-5, IL-6, IL-8, IL-17, CCL5, and IL-10. Regarding the methodological quality, four studies obtained high quality. Data from this review pointed out the maintenance of the inflammatory pattern during pregnancy with a closely related to the parasite.ConclusionImmune status in PW defined the course of the T. gondii infection, where the equilibrium between inflammatory and regulatory cytokines mitigated the harmful placenta and fetus effects.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD420203951.

Neuroserpin, IL-33 and IL-17A as potential markers of mild symptoms of depressive syndrome in Toxoplasma gondii-infected pregnant women

“…We observed elevated levels of three mediators-neuroserpin, IL-33, and IL-17A-in women with mild DS. Previously, our group demonstrated the involvement of IL-33, CCL2, and IL-17A in pregnant women with T. gondii infection (36)(37)(38). However, neuroserpin was a novel target of this investigation in the context of T. gondii infection and was the only marker elevated in plasma of pregnant women with T. gondii infection having both mild and moderate/severe DS.…”

“…The alarmin IL-33, IL-17A, and the chemokine CCL2 have been highlighted in studies of depressive disorders ( 45 – 47 ), and their high production/expression was demonstrated in chronic T. gondii research in both experimental models and humans ( 38 , 48 – 50 ). IL-33, which shows high expression in glial cells and astrocytes, has been associated with neurological diseases such as Alzheimer’s, post-traumatic stress disorder, major depressive disorder, and schizophrenia ( 51 , 52 ).…”

New advances in immune mechanism and treatment during ocular toxoplasmosis

“…that topical application of IL-6 antibodies significantly improved retinal structure and reduced parasite load, suggesting that IL-6 can induce retinopathy in mice (49). Similarly, T. gondii infection upregulates IL-17 expression, and IL-17 neutralization is partially protective against fatal T. gondii-associated inflammation (43,50). IL-17 is secreted by astrocytes during acute inflammation and is protective against neural cell apoptosis and tissue damage in active uveitis by maintaining homeostasis and inhibiting intracellular calcium increase (51).…”

“…IL-10 is a potent immunomodulatory cytokine and its deficiency increases the susceptibility to T. gondii infection in mice. IL-10 has been shown to inhibit T. gondii-induced inflammation (43) by suppressing Th1 cell differentiation (44), whereas IL-10 deficiency leads to 4-to 6fold increase in IL-12 and IFN-g (43,45). Thus, IL-10 plays a key role in dampening inflammation and restricting excessive proinflammatory response.…”

“…IL-17 is secreted by astrocytes during acute inflammation and is protective against neural cell apoptosis and tissue damage in active uveitis by maintaining homeostasis and inhibiting intracellular calcium increase (51). However, excess IL-17 can also lead to unwanted tissue damage (43). Therefore, inflammatory cytokines must be used with caution in the treatment of toxoplasmosis as they may hinder parasite eradication and exacerbate patient discomfort.…”