Effects Of Maternal Infection Research Articles

ОТДАЛЕННЫЕ ПОСЛЕДСТВИЯ ПРЕНАТАЛЬНОГО СТРЕССА И ПОДХОДЫ К КОРРЕКЦИИ НАРУШЕНИЙ В РАННЕМ РАЗВИТИИ

This work published and original data about the effects of various stressful stimuli on neuroendocrine and immune system development in animals and humans, with particular focus on effects of maternal infection, inducing inflammation, on developing fetus. Inflammatory processes may modify physiological levels of regulatory factors and hence disrupt developmental mechanisms. The central nervous system is particularly affected by inflammatory products during critical periods of ontogenesis. It leads in prospect to an increase of risk of different psychoneurological diseases, such as autism, Alzheimer’s disease, Parkinson’s disease, schizophrenia and depression, in the offspring. Inflammation-induced disorders of reproductive axis can lead to suppressed reproductive ability and infertility. Epigenetic mechanisms of development are highly sensitive to various regulatory factors, that opens up opportunities for disorder correction. Attempts to prevent the after-effects of prenatal inflammation are made over recent years. The approaches aimed at timely detection and correction of the perinatal disorders open a prospect of health maintenance in adult offspring.

REVIEW ARTICLE: HISTOPATHOLOGICAL CHANGES IN PLACENTA AND RELATIONSHIP WITH CORONAVIRUS INFECTION DURING PREGNANCY

During Covid-19 pandemic, Severe Acute Respiratory Syndrome - Coronavirus 2 (SARS-CoV-2) was significantly more severe in pregnant women than in non-pregnant women, leading in a number of health-related consequences that impacted healthcare, including fetal and maternal ramifications. Infection by coronavirus 2 can harm placental tissue by causing a variety of alterations.
 The majority of patients with SARS-CoV-2 are asymptomatic or have moderate symptoms related to upper respiratory infections that could sometimes escalate to severely sickness, injury of multi-organ, system failure, and death.
 Evidence about the effects of maternal infection is growing. Emerging information points to an increase in the dangers associated with obstetrics, such as stillbirth, gestational diabetes, maternal problems, preterm births, hypertensive disorder, reduced intrauterine fetal growth, and a chance of neonatal impairments of development. Generally, it remains contradictory concerns regarding the possibility of vertical transmission. 
 Further analysis is needed on the placenta and its role in pregnancies with COVID-19 since impairment of placental function effects on fate of pregnancy. The reviewed studies referred to present of changes in the architecture of tissues as histopathological alterations accompanied coronavirus 2 outbreaks. The current review study can be a guide that helps doctors and researchers in the future to clarify effective plans in diagnosing and treating cases of this epidemic to prevent the risks it causes.

SARS-CoV-2 Infection in Unvaccinated High-Risk Pregnant Women in the Bronx, NY, USA Is Associated with Decreased Apgar Scores and Placental Villous Infarcts.

Babies born to severe acute respiratory syndrome corona virus-2 (SARS-CoV-2)-infected mothers are at greater risk for perinatal morbidity and more likely to receive a neurodevelopmental diagnosis in the first year of life. However, the effect of maternal infection on placental function and neonatal outcomes varies depending upon the patient population. We set out to test our hypothesis that maternal SARS-CoV-2 infection in our underserved, socioeconomically disadvantaged, mostly unvaccinated, predominantly African American and Latina population in the Bronx, NY would have effects evident at birth. Under IRB approval, 56 SARS-CoV-2-positive patients infected during the "first wave" of the pandemic with alpha and beta strains of the virus, 48 patients infected during the "second wave" of the pandemic with delta and omicron strains and 61 negative third-trimester high-risk patients were randomly selected from Montefiore Medical Center (MMC), Bronx, NY. In addition, two positive cases from Yale New Haven Hospital, CT were included as controls. All 104 placentas delivered by SARS-CoV-2-positive mothers were uninfected by the virus, based on immunohistochemistry, in situ hybridization, and qPCR analysis. However, placental villous infarcts were significantly increased in first-wave cases compared to second-wave cases or negative controls. Significantly lower Apgar scores at 1 min and 5 min were observed in neonates born to infected mothers with severe symptoms. These findings suggest that even without entering the placenta, SARS-CoV-2 can affect various systemic pathways, culminating in altered placental development and function, which may adversely affect the fetus, especially in a high-risk patient population such as ours. These results underline the importance of vaccination among pregnant women, particularly in low-resource areas.

Effect of infection with severe acute respiratory syndrome coronavirus 2 on the fetus in pregnant women who recovered from infection.

The effect of maternal infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on the fetus is unclear, and there is no data from Saudi Arabia. Assess the effect of maternal SARS-CoV-2 infection on fetal growth. Retrospective case-control SETTING: Tertiary care hospital, Riyadh, Saudi Arabia PATIENTS AND METHODS: We selected pregnant women who underwent an obstetric growth scan and umbilical artery Doppler ultra-sound examination between 28 and 41 weeks of pregnancy. Women with multiple pregnancy, fetal abnormalities, maternal body mass index >30, maternal hypertension, any other chronic diseases that might affect fetal growth or pregnant women suffering from cancer were excluded. Fetal growth parameters assessed included fetal biometry (biparietal diameter, head circumference, abdominal circumference and femur length). We also did an umbilical artery Doppler assessment, which includes the umbilical artery pulsatility index, resistive index and the systolic/diastolic ratio. Fetal biometry and biophysical profile SAMPLE SIZE: 48 SARS-CoV-2; 98 non-SARS-CoV-2 RESULTS: More women who had recovered from SARS-CoV-2 infection had small for gestational age fetuses compared with the control group (P=.001). Maternal SARS-CoV-2 infection during pregnancy was associated with a higher prevalence of small for gestational age (SGA) fetuses. Retrospective, middle cerebral artery and uterine artery Doppler data were not included nor were the effect of tobacco use and socioeconomic status, the relationship between the date of infection with the date of conceiving or the relationship between the severity of infection in the mother and fetal biometry and growth. None.

Altered dendritic morphology in dorsolateral prefrontal cortex of nonhuman primates prenatally exposed to maternal immune activation

Women who contract a viral or bacterial infection during pregnancy have an increased risk of giving birth to a child with a neurodevelopmental or psychiatric disorder. The effects of maternal infection are likely mediated by the maternal immune response, as preclinical animal models have confirmed that maternal immune activation (MIA) leads to long lasting changes in offspring brain and behavior development. The present study sought to determine the impact of MIA-exposure during the first or second trimester on neuronal morphology in dorsolateral prefrontal cortex (DLPFC) and hippocampus from brain tissue obtained from MIA-exposed and control male rhesus monkey (Macaca mulatta) during late adolescence. MIA-exposed offspring display increased neuronal dendritic branching in pyramidal cells in DLPFC infra- and supragranular layers relative to controls, with no significant differences observed between offspring exposed to maternal infection in the first and second trimester. In addition, the diameter of apical dendrites in DLPFC infragranular layer is significantly decreased in MIA-exposed offspring relative to controls, irrespective of trimester exposure. In contrast, alterations in hippocampal neuronal morphology of MIA-exposed offspring were not evident. These findings demonstrate that a maternal immune challenge during pregnancy has long-term consequences for primate offspring dendritic structure, selectively in a brain region vital for socioemotional and cognitive development.

Pregnancy and malaria: the perfect storm.

Malaria in pregnancy continues to exert a toll on pregnant women and their offspring. The burden of Plasmodium falciparum infection is especially large in Africa, and new data show lasting effects of maternal infection on the infant's neurocognitive development. Elsewhere, P. vivax infection causes relapsing infections that are challenging to prevent. Infection in first trimester of pregnancy is an area of increasing focus, and its adverse effects on pregnancy outcome are increasingly recognised. First-trimester infection is common and frequently acquired prior to conception. Although newer rapid diagnostic tests still have limited sensitivity, they may be useful in detection of early pregnancy malaria for treatment. Artemisinin-based combination therapies are efficacious in later pregnancy but have yet to be recommended in first trimester because of limited safety data. In Africa, intermittent preventive treatment in pregnancy (IPTp) with monthly sulfadoxine-pyrimethamine improves pregnancy outcomes, but sulfadoxine-pyrimethamine resistance is worsening. The alternative, IPTp with dihydroartemisinin-piperaquine, has greater antimalarial efficacy, but does not appear to improve pregnancy outcomes, because sulfadoxine-pyrimethamine has poorly understood nonmalarial benefits on birthweight. Novel IPTp regimens must be combined with interventions to strengthen protection from malaria infection acquired before and in early pregnancy.

Severe maternal infectious morbidity during the second half of pregnancy is an independent risk factor for a small for gestational age neonate

The effect of severe maternal infectious morbidity on fetal growth during the second half of pregnancy is under debate. Preliminary evidence suggests that such association may be plausible. The objectives of this study were to determine: 1) The association between severe maternal infectious morbidity and adverse pregnancy outcome; and 2) The effect of maternal infection during pregnancy on fetal growth. This retrospective population - based cohort study included 4771 women who gave birth at our medical center during the study period. Parturients were allocated into two groups: 1) patients with severe maternal infection during the second half of pregnancy (n=368); and 2) control group comprised of normal pregnant women who were matched to the study group by maternal age, gravidity and parity (n=4403). The severe maternal infection group included women with pneumonia (n=198), pyelonephritis (n=131), and viral pneumonitis (n=39). In comparison to the normal patients group: 1) having had pneumonia during the second half of pregnancy was associated with increased rates of fetal growth restriction, placental abruption, fetal demise (P<0.001, for all comparisons) and preeclampsia (P=0.041); 2) Pyelonephritis during the second half of gestation was associated with higher rates of fetal growth restriction (P<0.001), placental abruption (P=0.006) and labor induction (P=0.039). As a group, women with severe maternal infection had higher rates of small for gestational age neonates compared to normal parturients (P<0.001). Among women with infections, only those who had pyelonephritis (P=0.032) or pneumonia (P=0.008), had a higher rate of small for gestational age neonates than those in the control group. After adjustment to confounding factors, maternal infection (OR=1.42, 95% CI 1.085-1.85) and previous delivery of a small for gestational age neonate (OR=2.54, 95% CI 2.02-3.19), were independent risk factors for the delivery of a small for gestational age neonate. Severe maternal infectious morbidity during the second half of pregnancy is an independent risk factor for the delivery of a small for gestational age neonate and is associated with adverse pregnancy outcomes. Both, pneumonia and pyelonephritis, during the second half of gestation affect fetal growth and are related to higher rates of small for gestational age neonates.

Maternal infection during pregnancy and the risk of attention-deficit/hyperactivity disorder in the offspring: A systematic review and meta-analysis.

The effects of maternal infection during pregnancy on the risk of attention-deficit/hyperactivity disorder (ADHD) in the offspring are unclear, and no overview is available. We searched the PubMed and EMBASE databases for relevant studies and performed a systematic review and meta-analysis of the literature. We found that that maternal infection during pregnancy was associated with a small increase in the risk of ADHD (OR 1.25, 95% CI 1.09, 1.44, P<0.0001; I2 = 92.9%, p<0.0001) in the offspring. In subgroup analyses, the association remained for maternal genitourinary (GU) infection (OR, 1.19, 1.12, 1.27, P<0.001; I2 = 0%; p=0.517). However, there was no significant association when we pooled data from siblings from other pregnancies (OR = 1.06, 95% CI, 0.99-1.13, P=0.084; I2 = 0%; p=0.859), implying that the association was due to confounding. The statistically significant association between maternal infection during pregnancy and ADHD in the offspring can be partially explained by unmeasured confounding.

PSIII-12 The effect of maternal dietary isoflavone supplementation and infection with porcine reproductive and respiratory syndrome virus on the growth performance of offspring

Abstract The objective of this experiment was to evaluate the effects of maternal infection with porcine reproductive and respiratory syndrome virus (PRRSV) on piglet prenatal development and pre-weaning growth, and the potential for isoflavone supplementation to alleviate these effects. First parity gilts (n = 24) at gestational day (GD) 65 were allotted to one of three treatments: uninfected and fed a diet devoid of isoflavones (CON), infected with PRRSV and fed the control diet (POS), or infected with PRRSV and fed a diet supplemented with 1,500 ppm soy isoflavones (ISF). Gilts were inoculated intranasally with saline or 2.5×104 TCID50/mL of suspended live PRRSV (NADC20 strain) on GD 70. To determine the effects of PRRSV infection in sows, feed intake (GD 70–114) and rectal temperatures (GD 70–91) were recorded daily, while serum TNF-α concentrations were measured weekly. After farrowing (GD 114 ± 2), two piglets closest to the average litter weight were culled either at birth or weaning (21 d of age) to determine body, muscle, and organ weights of offspring pigs. Hematoxylin and eosin staining was performed on left semitendinosus muscles for determination of muscle cell number and size at each time-point. At birth, whole body, muscle, and organ weights were not different (P &amp;gt; 0.22) between groups except that relative liver weight was increased (P &amp;lt; 0.05) in POS compared with CON piglets. At weaning, ISF reduced (P ≤ 0.05) whole body and muscle weights, but greater (P &amp;lt; 0.05) kidney weight compared with CON, and greater (P &amp;lt; 0.05) relative liver weight compared with CON or POS. However, muscle fiber number and size were not different (P &amp;gt; 0.39) between groups at either time-point. These results suggest maternal PRRSV infection altered offspring organ growth, but dietary ISF did not alleviate the detrimental effects of PRRSV infection in sows or offspring.

The legacy of maternal SARS-CoV-2 infection on the immunology of the neonate.

Despite extensive studies into severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the effect of maternal infection on the neonate is unclear. To investigate this, we characterized the immunology of neonates born to mothers with confirmed SARS-CoV-2 infection during pregnancy. Here we show that maternal SARS-CoV-2 infection affects the neonatal immune system. Despite similar proportions of B cells, CD4+ T cells and CD8+ T cells, increased percentages of natural killer cells, Vδ2+ γδ T cells and regulatory T cells were detected in neonates born to mothers with recent or ongoing infection compared with those born to recovered or uninfected mothers. Increased plasma cytokine levels were also evident in neonates and mothers within the recent or ongoing infection group. Cytokine functionality was enhanced in neonates born to SARS-CoV-2-exposed mothers, compared to those born to uninfected mothers. In most neonates, this immune imprinting was nonspecific, suggesting vertical transmission of SARS-CoV-2 is limited, a finding supported by a lack of SARS-CoV-2-specific IgM in neonates despite maternal IgG transfer.

Maternal Immune Activation during Pregnancy Alters Postnatal Brain Growth and Cognitive Development in Nonhuman Primate Offspring.

Human epidemiological studies implicate exposure to infection during gestation in the etiology of neurodevelopmental disorders. Animal models of maternal immune activation (MIA) have identified the maternal immune response as the critical link between maternal infection and aberrant offspring brain and behavior development. Here we evaluate neurodevelopment of male rhesus monkeys (Macaca mulatta) born to MIA-treated dams (n = 14) injected with a modified form of the viral mimic polyinosinic:polycytidylic acid at the end of the first trimester. Control dams received saline injections at the same gestational time points (n = 10) or were untreated (n = 4). MIA-treated dams exhibited a strong immune response as indexed by transient increases in sickness behavior, temperature, and inflammatory cytokines. Although offspring born to control or MIA-treated dams did not differ on measures of physical growth and early developmental milestones, the MIA-treated animals exhibited subtle changes in cognitive development and deviated from species-typical brain growth trajectories. Longitudinal MRI revealed significant gray matter volume reductions in the prefrontal and frontal cortices of MIA-treated offspring at 6 months that persisted through the final time point at 45 months along with smaller frontal white matter volumes in MIA-treated animals at 36 and 45 months. These findings provide the first evidence of early postnatal changes in brain development in MIA-exposed nonhuman primates and establish a translationally relevant model system to explore the neurodevelopmental trajectory of risk associated with prenatal immune challenge from birth through late adolescence.SIGNIFICANCE STATEMENT Women exposed to infection during pregnancy have an increased risk of giving birth to a child who will later be diagnosed with a neurodevelopmental disorder. Preclinical maternal immune activation (MIA) models have demonstrated that the effects of maternal infection on fetal brain development are mediated by maternal immune response. Since the majority of MIA models are conducted in rodents, the nonhuman primate provides a unique system to evaluate the MIA hypothesis in a species closely related to humans. Here we report the first longitudinal study conducted in a nonhuman primate MIA model. MIA-exposed offspring demonstrate subtle changes in cognitive development paired with marked reductions in frontal gray and white matter, further supporting the association between prenatal immune challenge and alterations in offspring neurodevelopment.

Maternal infection programmes offspring immunity.

A preprint by Lim et al. looks at the effects of maternal infection on long-term immunity in offspring, showing that maternal IL-6-induced signalling in mice induces epigenetic changes in fetal intestinal epithelial cells.

Acute congenital Toxoplasma gondii infection alters fetal hematopoiesis via interferon-gamma

Abstract In adulthood, infection drives cytokine-mediated inflammation that can directly influence hematopoietic stem and progenitor cell (HSPC) function and differentiation, but the effects of maternal infection on the trajectory of fetal hematopoietic and immune cells have not been elucidated. Toxoplasma gondii is a TORCH pathogen that can be vertically transmitted upon acute infection during pregnancy, with dire consequences for the developing fetus. Maternal IFNγ production during congenital infection is required to prevent vertical transmission and promote parasite clearance, but at the cost of lowered birth weights and premature abortion. Here, we investigated the effects of acute congenital toxoplasmosis on fetal hematopoiesis. Our examination of fetal hematopoiesis in response to maternal T. gondii infection of varying virulence revealed that discrete HSPC populations, including subsets of fetal hematopoietic stem cells, B1 precursors, and myeloid progenitors are fundamentally altered in response to congenital toxoplasmosis. To assess the ability of IFNγ to mediate these observed changes and directly cross the placental barrier, we performed epistatic crosses of mice deficient for IFNγ receptor. Our results indicate that maternal IFNy produced in response to T. gondii infection may drive observed changes to the fetal HSPC compartment and that fetal HSPCs respond directly to maternal sources of IFNγ in a manner distinct from adult HSPCs. Ongoing experiments attempt to resolve the mechanisms by which vertical transmission and maternal inflammation perturb the establishment of the fetal immune system, and the direct role of IFNγ in mediating these phenomena.

Effect of maternal infection on fetal and infant growth: a review

Effect of maternal infection on fetal and infant growth: a review

Maternal viral infection during pregnancy elicits anti-social behavior in neonatal piglet offspring independent of postnatal microglial cell activation

Maternal infection during pregnancy increases risk for neurodevelopmental disorders and reduced stress resilience in offspring, but the mechanisms are not fully understood. We hypothesized that piglets born from gilts infected with a respiratory virus during late gestation would exhibit aberrant microglia activity, cognitive deficits and reduced sociability. Pregnant gilts were inoculated with porcine reproductive and respiratory syndrome virus (PRRSV; 5×105 TCID50 of live PRRSV) or saline at gestational day 76. Gilts infected with PRRSV exhibited fever (p<0.01) and reduced appetite (p<0.001) for 2weekspost-inoculation and were PRRSV-positive at parturition. Piglets born from infected and control gilts were weaned at postnatal day (PD) 1 and assigned to two groups. Group 1 was challenged with lipopolysaccharide (LPS, 5μg/kg body weight i.p.) or saline on PD 14 and tissues were collected. Group 2 was tested in a T-maze task to assess spatial learning and in a 3-chamber arena with unfamiliar conspecifics to assess social behavior from PD 14-27. Microglia (CD11b+ CD45low) isolated from Group 2 piglets at PD 28 were challenged ex vivo with LPS; a subset of cells was analyzed for MHCII expression. Maternal infection did not affect offspring circulating TNFα, IL-10, or cortisol levels basally or 4h post-LPS challenge. While performance in the T-maze task was not affected by maternal infection, both sociability and preference for social novelty were decreased in piglets from infected gilts. There was no effect of maternal infection on microglial MHCII expression or LPS-induced cytokine production. Taken together, these results suggest the reduced social behavior elicited by maternal infection is not due to aberrant microglia activity postnatally.

Abstract # 1745 Maternal viral infection during pregnancy elicits anti-social behavior in neonatal piglets independent of postnatal microglia cell activity

Maternal infection during pregnancy increases risk for neurodevelopmental disorders and reduced stress resilience in offspring, but the mechanisms are not fully understood. We hypothesized that piglets born from gilts infected with a respiratory virus during late gestation would exhibit aberrant microglia activity, cognitive deficits and reduced sociability. Piglets born from infected and control gilts were weaned at postnatal day (PD) 1 and assigned to two groups. Group 1 was challenged with LPS (5 μ g/kg body weight i.p.) or saline on PD 14 and tissues were collected. Group 2 was tested in a T-maze task to assess spatial learning and in a 3-chamber arena with unfamiliar conspecifics to assess social behavior from PD 14-27. Microglia (CD11b+ CD45low) isolated from group 2 piglets at PD 28 were challenged ex vivo with LPS; a subset of cells was analyzed for MHCII expression. Maternal infection did not affect offspring circulating TNF α , IL-10, or cortisol levels basally or 4 h post-LPS challenge. While performance in the T-maze task was not affected by maternal infection, both sociability and preference for social novelty were decreased in piglets from infected gilts. There was no effect of maternal infection on microglial MHCII expression or LPS-induced cytokine production. Taken together, these results suggest the reduced social behavior elicited by maternal infection is not due to aberrant microglia activity postnatally. Supported by NIH HD069899 to RWJ.

Effects of maternal and post‐natal infection with porcine reproductive and respiratory syndrome virus on muscle growth and development in piglets (731.10)

Prenatal muscle development is altered by maternal nutrition, the effect of maternal infection during pregnancy on offspring muscle growth and development is less clear. We assessed muscle development in piglets born of dams infected with porcine reproductive and respiratory syndrome virus (PRRSV) during pregnancy and in postnatally infected PRRSV pigs. In study 1, pregnant gilts were inoculated with PRRSV or sterile culture medium (control) at d76 of gestation. Data collected from offspring at d0 and d28 of age included body and muscle weights and gene expression of longissumus dorsi muscle. In study 2, similar measurements were collected from pigs inoculated with PRRSV at d35 and sacrificed at d49 of age. Longissumus dorsi weight was reduced (P&lt;0.01) at d28 in piglets from PRRSV inoculated gilts compared with control, but body or other muscle weights were unaffected at d0 and d28 of age. Furthermore, IGF1, IL‐6, and Pax7 expression tended to be reduced (P&lt;0.10) at d28 in piglets from PRRSV inoculated gilts compared with controls, while myostatin and UCP3 expression did not differ. In addition, TNF‐α expression was increased (P&lt;0.05) at d28 in piglets from PPRSV inoculated gilts compared with controls. Postnatal infection reduced (P&lt;0.01) body and muscle weights in PRRSV inoculated‐piglets compared with controls. However, postnatal infection did not alter expression of myostatin, IGF1, Pax7, IL‐6, or TNF‐α.

Vaccination in Pregnancy

The recent H1N1 influenza pandemic has highlighted the potential for viral infections to cause severe disease in mothers disproportionate to the general population and have deleterious effects on the fetus. Vaccines have been used in pregnant women for over 200 years. Current guidelines recommend vaccination with only inactivated virus due to potential risk to mother and fetus with live vaccine. The exception is during times of pandemic or biological weapons attack, when the risk of life-threatening disease outweighs the risk of vaccination. A paucity of data is available regarding actual risk and mechanisms of live viral vaccine transfer from mother to fetus. Pregnancy-induced changes to the maternal immune system, effects of maternal infection on neonatal immunity, and the role of the placenta in transmission of infection and passive immunity to the fetus are incompletely understood. The aim of this paper is to review available data pertaining to newer vaccines such as the pandemic H1N1 and HPV vaccines in pregnancy, the role of Fc receptors in active transport of immunoglobulin across the placenta, and cytokine activity during maternal infection and after vaccination. We will also discuss potential areas for future research.

Altered gene expression in murine placentas in an infection-induced intrauterine growth restriction model: a microarray analysis

The biological mechanisms leading to incomplete intrauterine growth are not completely elucidated and few studies have investigated infection-mediated growth restriction. In this investigation we report the alterations induced by maternal infectious challenge in placental gene expression patterns using a murine model. Pregnant dams were challenged at day E7.5 with the oral human pathogen Campylobacter rectus to elicit fetal growth restriction. At embryonic day E16.5 placentas were collected to compare placental gene expression patterns from normal fetuses of unchallenged dams and growth restricted fetuses from infected dams. Differential gene expression patterns were determined using Agilent Oligo array (G4121A) with a false discovery rate of P<0.05 and pathway analyses were performed. Seventy-four genes were differentially expressed during infection-mediated growth restriction with 9 genes significantly up-regulated, indicating that the effects of maternal infection on gene expression were predominantly suppressive. Pathway analyses indicated that 46 of the 65 genes that were significantly down-regulated were associated with placental/fetal development, and 26 of those were imprinted genes. Among the 9 genes that were up-regulated, 4 are involved in oxygen supply to the fetus and the development of the vascular system. Microarray analysis demonstrated that in the pregnant mouse model, maternal infection that induced growth restriction was associated with down-regulated placental expression of critical growth and developmental related genes, including many imprinted genes. These findings may have significant implications for our understanding of the mechanisms underlying infection-associated human fetal growth restriction and the role of differential placental expression of imprinted genes in fetal growth.

Toxoplasma gondii: Effect of maternal infection in the development of lymphoid organs of BALB/c neonates

Toxoplasmosis is one of the worldwide parasitic zoonoses. Alterations in the lymphopoietic system are still poorly studied. We analyzed lymphoid organs of BALB/c mice neonates from Toxoplasma gondii-intraperitoneally-infected mothers on 19th day of gestation, with 30 tachyzoites of strain RH. Normal non-infected pregnant females were used as controls. At 7 days after birth, animals were classified as neonates from infected (NIM) and neonates from non-infected mothers (NNIM). Weight of the thymus and number of thymic cells in NIM were decreased, percentage of apoptosis was significantly increased. Decrease in lymphocytes and monocytes and an increase of plasma cells were observed in bone marrow of NIM. Peripheral blood of NIM showed an increase of monocytes and neutrophils and a decrease in lymphocytes. Infection of the mother during the last day of gestation provokes in the neonates changes in the lymphoid organs that could explain survival of 75% of them.