ArticleJournal of inflammation research2021
Exposure to Maternal Immune Activation Causes Congenital Unfolded Protein Response Defects and Increases the Susceptibility to Postnatal Inflammatory Stimulation in Offspring.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Aberrant IL-17 Levels in Rodent Models of Autism Spectrum Disorder: A Systematic Review.Frontiers in immunology · 2022Pooled it
- The Role of Prenatal Microglial Activation and Its Sex Differences in the Development of Neuropsychiatric Disorders and Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- IgG4 elevation dilemma at the crossroads of helminth infection and IgG4-related disease: insights from a case report of pediatric paragonimiasis with persistent pericardial effusion.Translational pediatrics · 2025Article
- Interleukin-6 produces behavioral deficits in pre-pubescent mice independent of neuroinflammation.Brain, behavior, and immunity · 2025Article
- The fetal programming effect of maternal immune activation (MIA) on the offspring's immune system.Seminars in immunopathology · 2024Review
- Abnormal neutrophil-to-lymphocyte ratio in children with autism spectrum disorder and history of maternal immune activation.Scientific reports · 2023Article
- Maternal Th17 Profile after Zika Virus Infection Is Involved in Congenital Zika Syndrome Development in Children.Viruses · 2023Article
- Influence of Immune System Abnormalities Caused by Maternal Immune Activation in the Postnatal Period.Cells · 2023Review
- Distinct effects of interleukin-6 and interferon-γ on differentiating human cortical neurons.Brain, behavior, and immunity · 2022Article
- Maternal immune activation and neuroinflammation in human neurodevelopmental disorders.Nature reviews. Neurology · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA number of childhood diseases have been identified, such as severe infection or autoinflammatory disease, in which immune overreaction against inflammation is a possible underlying mechanism. Previous reports have demonstrated that fetal cells exposed to maternal immune activation (MIA) induced by polyriboinosinic-polyribocytidylic acid [poly(I:C)] exhibited hypersensitivity to inflammation in vitro. However, the details of this mechanism remain unclear. Therefore, this study aimed to reveal the reaction to inflammation in offspring exposed to MIA in the prenatal period, as well as its molecular mechanism, using a viral infection mouse model. MATERIALS AND
methodsPregnant mice at 12.5, 14.5, and 16.5 days post coitum were injected intraperitoneally with poly(I:C) 20 mg/kg body weight (BW) or saline. Offspring aged 3-4 weeks received the second injection of 20 mg/kg BW or 4 mg/kg BW poly(I:C) or saline. Serum and tissues were collected at 2, 24, 48, and 72 h after the postnatal injection. The cytokine profile, histopathology of organs, and unfolded protein response (UPR) in offspring were examined.
resultsThe serum levels of interleukin (IL)-6, IL-17, and interferon-γ were significantly higher in the MIA group, and acute liver necrosis was detected. Moreover, failure in UPR was observed in the MIA group compared with that in the control group.
conclusionOverall, MIA exposure in utero caused failure in UPR as well as immune overreaction to the second attack of inflammation in offspring. Our results suggested that prenatal exposure to MIA might contribute to the congenital inflammatory constitution after birth.
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