Abstract
Epidemiological studies suggest that prenatal exposure to different types of viral or bacterial infections may be associated with similar outcomes; i.e., an increased risk of mental illness disorders in the offspring. Infections arising from various causes have similar debilitating effects in later life, suggesting that the exact pathogen may not be the critical factor in determining the neurological and cognitive outcome in the offspring. Instead, it is thought that response of the innate immune system, specifically the increased production of inflammatory cytokines, may be the critical mediator in altering fetal brain development pre-disposing the offspring to mental illness disorders later in life. Inflammatory cytokines are essential for normal brain development. Factors such as the site of cytokine production, a change in balance between anti- and pro- inflammatory cytokines, placental transfer of cytokines, the effects of cytokines on glial cells, and the effects of glucocorticoids are important when evaluating the impact of maternal infection on fetal brain development. Although it is clear that cytokines are altered in the fetal brain following maternal infection, further evidence is required to determine if cytokines are the critical factor that alters the trajectory of brain development, subsequently leading to postnatal behavioral and neurological abnormalities.
Highlights
Genetic background and environmental factors can predispose an individual to neuropsychiatric disorders, the prevalence of conditions such as schizophrenia and autism cannot be accounted for by these factors alone (Williams et al, 2006; Tandon et al, 2008)
We propose two mechanisms by which an induction or a change in inflammatory cytokines during fetal life can have long term consequences on development; The effects of cytokines on 1) glial cells and 2) the hypothalamic-pituitaryadrenal axis
DNA modification by methylation can alter long term gene function, for example by silencing gene expression, without altering sequence variation. It possible that a prenatal stress response, caused by exposure to an infection or inflammatory event, may result in the long lasting, epigenetic reprogramming of genes involved in HPA axis function. While mental illnesses such as schizophrenia and autism have been associated with prenatal infection, the variety of infections producing similar outcomes suggest that a response by the immune system common to all infections may be the important factor in the etiology of mental illness disorders
Summary
Reviewed by: Sophie Laye, Université de Bordeaux, France Aldo Lucion, Universidade Federal do Rio Grande do Sul, Brazil. Epidemiological studies suggest that prenatal exposure to different types of viral or bacterial infections may be associated with similar outcomes; i.e., an increased risk of mental illness disorders in the offspring. Infections arising from various causes have similar debilitating effects in later life, suggesting that the exact pathogen may not be the critical factor in determining the neurological and cognitive outcome in the offspring. It is thought that response of the innate immune system, the increased production of inflammatory cytokines, may be the critical mediator in altering fetal brain development pre-disposing the offspring to mental illness disorders later in life. Inflammatory cytokines are essential for normal brain development Factors such as the site of cytokine production, a change in balance between anti- and pro- inflammatory cytokines, placental transfer of cytokines, the effects of cytokines on glial cells, and the effects of glucocorticoids are important when evaluating the impact of maternal infection on fetal brain development. It is clear that cytokines are altered in the fetal brain following maternal infection, further evidence is required to determine if cytokines are the critical factor that alters the trajectory of brain development, subsequently leading to postnatal behavioral and neurological abnormalities
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