License. The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. Permissions beyond the scope of the License are administered by Dove Medical Press Limited. Information on how to request permission may be found at: http://www.dovepress.com/permissions.php Research and Reports in Biology 2015:6 171–189 Research and Reports in Biology Dovepress

/pdf/the-maternal-immune-system-during-pregnancy-and-its-rl42mltxt7.pdf

The maternal immune system during pregnancy and its influence on fetal development

Epidemiological studies have associated infection during pregnancy with increased risk of neurodevelopmental disorders in children, which is modeled in rodents by stimulating the immune system of pregnant dams with microorganisms or their mimics, such as poly(I:C) or LPS. In two prenatal mouse models, we show that in utero exposure of the fetus to cytokines/inflammatory mediators elicited by maternal immune stimulation with poly(I:C) yields offspring that exhibit a proinflammatory phenotype due to alterations in developmental programming of their immune system. Changes in the innate and adaptive immune elements of these pro-inflammatory offspring result in more robust responses following exposure to immune stimuli than those observed in control offspring from PBS-injected pregnant dams. In the first model, offspring from poly(I:C)-injected immunologically naive dams showed heightened cellular and cytokine responses 4 h after injection of zymosan, a TLR2 agonist. In the second model, using dams with immunological memory, poly(I:C) injection during pregnancy produced offspring that showed preferential differentiation toward Th17 cell development, earlier onset of clinical symptoms of EAE, and more severe neurological deficits following immunization with MOG35-55. Such "fetal programming" in offspring from poly(I:C)-injected dams not only persists into neonatal and adult life, but also can have profound consequences on health and disease.

Maternal immune stimulation during pregnancy shapes the immunological phenotype of offspring.

Association Between Prenatal Exposure to Maternal Infection and Offspring Mood Disorders: A Review of the Literature

Introduction Epidemiological studies revealed that maternal exposure to influenza A (H1N1) and Toxoplasma gondii (T. gondii) infection during pregnancy may increase the risk for mood disorders of the offspring. However, the impact of maternal infections in different stages of neural development and the nature of antigens remain to be elucidated. Objective This study investigated behavioral impairments induced by maternal immune activation (MIA) due to H1N1 or T. gondii infection during preborn neurodevelopment. Methods Maternal infection with influenza or toxoplasma was mimicked by administration of influenza vaccine antigens or suspension of soluble T. gondii antigen (STAg) in pregnant Balb/c mice at E6 or E16. Adult male offspring were evaluated for anxiety-like and depressive-like behavior in elevated plus maze (EPM) and forced swimming test (FST). Results In FST, immobility time at E6 and E16 increased when the mothers were treated with both antigen solutions. There was increased immobility in the pups whose mothers were treated with STAg at E16. MIA with influenza antigens reduced the exploration of the open arms of EPM for the pups whose progenitors received treatment at E6 and E16. The animals at E6 exhibited a greater number of stretch-attend postures compared with the saline group. STAg at E6 reduced the time of exploration in the open arms and increased the number of stretch-attend postures compared with the saline group. Conclusion These results suggest that immunological responses to H1N1 or T. gondii during pregnancy may impact differently the susceptibility of adult offspring to mood disorder.

Maternal Immune Activation with H1N1 or Toxoplasma gondii Antigens Induces Behavioral Impairments Associated with Mood Disorders in Rodents.

Contributions of Maternal Prenatal Infection and Antibiotic Exposure to Offspring Infection and Risk for Allergic Respiratory Conditions through Age 5

There is consensus among investigators studying Autism Spectrum Disorders (ASD) that the etiological basis involves environmental factors acting on the genetic susceptibility of the individual [1-5]. Over 100 candidate genes that may contribute to ASD susceptibility have been identified, and numerous environmental “triggers” have been suggested. Yet, the cause of ASD eludes clear definition and most likely is, as in most diseases, multi-factorial. However, several common immunological themes emerge from clinical and experimental studies of ASD, including persistent neuroinflammation, immune dysregulation, or autoim‐ mune manifestations in many autistic children. Thus, in addition to genetic and environ‐ mental factors, there is compelling evidence that immune factors also play a role in ASD. Abnormalities consistent with immune dysregulation, including abnormal or skewed T helper (Th) cell subsets and cytokine profiles, decreased lymphocyte numbers, decreased T cell mitogen responses, and an imbalance of serum immunoglobulin levels have been re‐ ported in children with ASD [6-11].

/pdf/pro-inflammatory-phenotype-induced-by-maternal-immune-2rezw07hee.pdf

Pro-Inflammatory Phenotype Induced by Maternal Immune Stimulation During Pregnancy

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Pro-Inflammatory Phenotype Induced by Maternal Immune Stimulation During Pregnancy