Abstract
Toxoplasma gondii has a highly clonal genetic structure classified into three major genetic types, I, II, and III, plus additional recombinant and atypical strains. In humans, type I and atypical strains usually associate with severe toxoplasmosis. Type II strains, predominantly identified in European countries and the United States, correlate with a differential course of toxoplasmosis. During pregnancy, the important protective role of the placenta against maternal–fetal T. gondii transmission has been reported. T. gondii preferentially colonizes extravillous trophoblasts as compared to syncytiotrophoblasts. The latter compartment was suggested to act as the real barrier to the fetal dissemination of T. gondii. Alterations in immune response to particular T. gondii strains were observed. Higher transcription levels of IP-10, IL-1β, IL-6, IL-10, IL-12 cytokines, and NF-κB translocation to the nucleus were more often documented for type II strains than type I strains. Since the induction of IL-12 during type II infection was Myd88-dependent, the involvement of Toll-like receptors (TLRs) in the immunity against these strains was suggested. Differential expression of TLRs depends on placental cell types and gestational age. The expression of TLR2 and TLR4 in the first trimester of pregnancy was reported only for villous cytotrophoblasts and extravillous trophoblasts, but not for syncytiotrophoblasts. The involvement of single-nucleotide polymorphisms (SNPs) in the TLR genes in infectious pathogenicity, including toxoplasmic retinochoroiditis, points at a possible involvement of TLR alterations in immunity against T. gondii. We conclude that studies on TLR contributions in the maternal–fetal transmission of particular parasite strains and congenital toxoplasmosis are warranted.
Highlights
Toxoplasma gondii has a highly clonal genetic structure classified into three major genetic types, I, II, and III, plus additional recombinant and atypical strains
Despite the fact that differential immune responses resulted from infection with various T. gondii strains, only a few studies reported that the parasite maternal–fetal transmission through the placenta might depend on strain variations
We suggest that description of the mechanisms of Toll-like receptors (TLRs) action after primary T. gondii infection of placental cells is needed
Summary
Despite the fact that differential immune responses resulted from infection with various T. gondii strains, only a few studies reported that the parasite maternal–fetal transmission through the placenta might depend on strain variations. The placenta played an important protective role against the maternal–fetal transmission of T. gondii [16]. Studies with first-trimester human placental explants described the role of two anatomical placental interfaces [the villous trophoblast (fetal cells) and the extravillous trophoblast (EVT, maternal cells)] in the maternal–fetal transmission of T. gondii [20]. Another study reported that BeWo choriocarcinoma cells went into apoptosis after infection with type II rather than type I strains In this case, host cell death versus parasite death might reflect differential strain abilities to infect the placenta with varying degrees of virulence [21]. Fetal infection was observed only in GKO B6 and not among GKO BALB/c, WT B6, and WT BALB/c mice [19]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: European Journal of Clinical Microbiology & Infectious Diseases
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.