Abstract
Pathogens comprised of viruses, bacteria, gut microbiome, and parasites are a leading cause of ever-emerging diseases in humans. Studying pathogens for their ability to cause diseases is a topic of critical discussion among scientists and pharmaceutical centers for effective drug development that diagnose, treat, and prevent infection-associated disorders. Pathogens impact health either directly by invading the host or by eliciting an acute inflammatory immune response. This paradigm of inflammatory immune responses is even more consequential in people who may be immunocompromised. In this regard, pregnancy offers an altered immunity scenario, which may allow the onset of severe diseases. Viruses, such as Influenza, HIV, and now SARS-CoV-2, associated with the COVID-19 pandemic, raise new concerns for maternal and fetal/neonatal health. Intrauterine bacterial and parasitic infections are also known to impact pregnancy outcomes and neonatal health. More importantly, viral and bacterial infections during pregnancy have been identified as a common contributor to fetal brain development defects. Infection-mediated inflammatory uterine immune milieu is thought to be the main trigger for causing poor fetal brain development, resulting in long-term cognitive impairments. The concept of in utero programming of childhood and adult disorders has revolutionized the field of neurodevelopment and its associated complications. Recent findings in mice and humans clearly support the idea that uterine immunity during pregnancy controls the health trajectory of the child and considerably influences the cognitive function and mental health. In this review, we focus on the in utero programming of autism spectrum disorders (ASD) and assess the effects of pathogens on the onset of ASD-like symptoms.
Highlights
Viral and bacterial infections during pregnancy have been associated with an array of adverse pregnancy outcomes, including spontaneous abortion, premature birth, stillbirth, intrauterine growth restriction, and fetal neurological defects [1,2,3,4]
According to the research in animal models, the pro-inflammatory phenotype of uterine, not systemic, immune activation is often associated with cognitive deficits and stereotypic behavior [18]. This raises a pertinent question of how uterine immune activation (UIA) during pregnancy can result in the onset of autism spectrum disorders (ASD) in the offspring
Other cognitive and social behavior diseases are extremely complicated neurodevelopmental disorders with no definite etiology, gestational stress and pathogenic infections are emerging as causative factors
Summary
Viral and bacterial infections during pregnancy have been associated with an array of adverse pregnancy outcomes, including spontaneous abortion, premature birth, stillbirth, intrauterine growth restriction, and fetal neurological defects [1,2,3,4]. According to the research in animal models, the pro-inflammatory phenotype of uterine, not systemic, immune activation is often associated with cognitive deficits and stereotypic behavior [18] This raises a pertinent question of how uterine immune activation (UIA) during pregnancy can result in the onset of ASD in the offspring. Recent observations further suggest that UIA directly affects GABaergic interneurons, which may result in the reduction in cell numbers, redistribution across cortical regions and layers, changes in morphology and cellular activity, and altered transcriptomes in the cortex [23] This raises a question about whether IL-17A is responsible for cortical architectural defects. Fetal interface during normal pregnancy, altered transcriptomes, and the cortical architecture impairment and its association with ASD-like social behavior
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