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A Proinflammatory Immune Response Might Determine Toxoplasma gondii Vertical Transmission and Severity of Clinical Features in Congenitally Infected Newborns.

ABSTRACT: Toxoplasma gondii is the etiological agent of toxoplasmosis. Mother-to-child transmission of this parasite can occur during pregnancy. Newborns with congenital toxoplasmosis may develop central nervous system impairment, with severity ranging from subclinical manifestations to death. A proinflammatory/regulated specific immune profile is crucial in the defense against the parasite; nevertheless, its role in the infected pregnant women and the congenitally infected offspring has been poorly explored, and there is still no consensus about its relation to parasite vertical transmission or to severity and dissemination in the congenitally infected newborns. This work aimed to characterize these relations by means of principal component and principal factor analyses. For this purpose, we determined the specific production of the four immunoglobulin G antibody subclasses, cytokines, and lymphocyte proliferation in the T. gondii-infected pregnant women-10 who transmitted the infection to their offspring and seven who did not-as well as in 11 newborns congenitally infected and grouped according to disease severity (five mild and six moderate/severe) and dissemination (four local and seven disseminated). We found that the immune response of nontransmitter women differed from that of the transmitters, the latter having a stronger proinflammatory response, supporting a previous report. We also found that newborns who developed moderate/severe disease presented higher levels of lymphocyte proliferation, particularly of CD8+ and CD19+ cells, a high proportion of tumor necrosis factor ? producers, and reduced expression of the immune modulator transforming growth factor ?, as opposed to children who developed mild clinical complications. Our results suggest that a distinctive, not regulated, proinflammatory immune response might favor T. gondii vertical transmission and the development of severe clinical manifestations in congenitally infected newborns.

SUBMITTER: Gomez-Chavez F

PROVIDER: S-EPMC7082359 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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A Proinflammatory Immune Response Might Determine <i>Toxoplasma gondii</i> Vertical Transmission and Severity of Clinical Features in Congenitally Infected Newborns.

Gómez-Chávez Fernando F Cañedo-Solares Irma I Ortiz-Alegría Luz Belinda LB Flores-García Yevel Y Figueroa-Damián Ricardo R Luna-Pastén Héctor H Gómez-Toscano Valeria V López-Candiani Carlos C Arce-Estrada G Emmanuel GE Bonilla-Ríos Christian A CA Mora-González Juan Carlos JC García-Ruiz Ricardo R Correa Dolores D

Frontiers in immunology 20200313

<i>Toxoplasma gondii</i> is the etiological agent of toxoplasmosis. Mother-to-child transmission of this parasite can occur during pregnancy. Newborns with congenital toxoplasmosis may develop central nervous system impairment, with severity ranging from subclinical manifestations to death. A proinflammatory/regulated specific immune profile is crucial in the defense against the parasite; nevertheless, its role in the infected pregnant women and the congenitally infected offspring has been poorl ...[more]

PMID: 32231666

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Project description:In 1995, one of the largest outbreaks of human toxoplasmosis occurred in the Pacific Northwest region of North America. Genetic typing identified a novel Toxoplasma gondii strain linked to the outbreak, in which a wide spectrum of human disease was observed. For this globally-distributed, water-borne zoonosis, strain type is one variable influencing disease, but the inability of strain type to consistently explain variations in disease severity suggests that parasite genotype alone does not determine the outcome of infection. We investigated polyparasitism (infection with multiple parasite species) as a modulator of disease severity by examining the association of concomitant infection of T. gondii and the related parasite Sarcocystis neurona with protozoal disease in wild marine mammals from the Pacific Northwest. These hosts ostensibly serve as sentinels for the detection of terrestrial parasites implicated in water-borne epidemics of humans and wildlife in this endemic region. Marine mammals (151 stranded and 10 healthy individuals) sampled over 6 years were assessed for protozoal infection using multi-locus PCR-DNA sequencing directly from host tissues. Genetic analyses uncovered a high prevalence and diversity of protozoa, with 147/161 (91%) of our sampled population infected. From 2004 to 2009, the relative frequency of S. neurona infections increased dramatically, surpassing that of T. gondii. The majority of T. gondii infections were by genotypes bearing Type I lineage alleles, though strain genotype was not associated with disease severity. Significantly, polyparasitism with S. neurona and T. gondii was common (42%) and was associated with higher mortality and more severe protozoal encephalitis. Our finding of widespread polyparasitism among marine mammals indicates pervasive contamination of waterways by zoonotic agents. Furthermore, the significant association of concomitant infection with mortality and protozoal encephalitis identifies polyparasitism as an important factor contributing to disease severity in marine mammals.

Project description:Toxoplasma gondii is a cause of congenital diseases, miscarriages and stillbirths in production animals. In Brazil, non-archetypal genotypes of the parasite may be related to severe disease. Experimental infection with T. gondii was studied in sheep to analyse congenital transmission-related parameters in reinfections with different Brazilian parasite strains. Thirteen T. gondii-seronegative sheep were orally infected with 2 × 103oocysts for the primary infection: G1 (4 animals) were inoculated with TgCatBr71 strain (Type BrI genotype) and G2 andG3 (5 and 4 animals, respectively) withTgCatBr60 strain (Type BrIII genotype). After chronification of infection, the animals were impregnated. A second infection was performed after 60 days of gestation. TheG1 andG3 animals were inoculated withTgCatBr60BrIII and the G2 animals withTgCatBr71 BrI oocysts. The effects of reinfection were compared with a control group (5 animals) through physical examination, ultrasound imaging and serology. Ovine experimental infections were evaluated using mouse bioassays, molecular analysis, serological tests, histopathology, and immunohistochemistry. No abortions occurred; a seropositive lamb and a mummified fetus from G2-BrIIIxBrI were produced. The vertical transmission rate detected in lambs from chronically infected sheep was 31.6% (6/19). It is demonstrated that reinfection and subsequent congenital transmission occured in one sheep with a primary Brl infection challenged with BrIII genotype of T. gondii. In a twin pregnancy from G2-BrIIIxBrI, congenital transmission from a latent infection was detected in both lambs. Congenital transmission could not be tracked in three lambs. Overall, previous T. gondii infection may fail to protect against congenital transmission from a reinfection and primary infection induced insufficient protection against vertical transmission which must be taken into account in decision-making for the use of seropositive animals as breeders. Similar trials with larger groups and contemplating host cellular immune response studies should be conducted to evaluate the actual impact of T. gondii reinfection involving different strains in sheep.

Dataset Information

A Proinflammatory Immune Response Might Determine Toxoplasma gondii Vertical Transmission and Severity of Clinical Features in Congenitally Infected Newborns.

Publications

A Proinflammatory Immune Response Might Determine <i>Toxoplasma gondii</i> Vertical Transmission and Severity of Clinical Features in Congenitally Infected Newborns.

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