scholarly journals Long-Term Effects of prophylactic MgSO4 in Maternal Immune Activation Rodent Model at Adolescence and Adulthood

2022 ◽  
Vol 226 (1) ◽  
pp. S311
Author(s):  
Ron Beloosesky ◽  
Sally Rashid ◽  
Idit Golani ◽  
Alon Rubinstein ◽  
Ravid doron ◽  
...  
2014 ◽  
Vol 4 (2) ◽  
pp. e363-e363 ◽  
Author(s):  
D Khan ◽  
P Fernando ◽  
A Cicvaric ◽  
A Berger ◽  
A Pollak ◽  
...  

Author(s):  
Mian Bao ◽  
Naomi Hofsink ◽  
Torsten Plösch

A prominent health issue nowadays is the COVID-19 pandemic, which poses acute risks to human health. However, the long-term health consequences are largely unknown and cannot be neglected. An especially vulnerable period for infection is pregnancy, when infections could have long-term health effect on the child. Evidence suggests that maternal immune activation (MIA) induced by either bacteria or viruses presents various effects on the offspring, leading to adverse phenotypes in many organ systems. This review compares the mechanisms of bacterial and viral MIA and the possible long-term outcomes for the offspring by summarizing the outcome in animal LPS and Poly I:C models. Both models are activated immune responses mediated by Toll-like receptors. The outcomes for MIA offspring include neurodevelopment, immune response, circulation, metabolism and reproduction. Some of these changes keep existing until later life. Besides different doses and batches of LPS and Poly I:C, the injection day, administration route and also different animal species influence the outcomes. Here, we specifically aim to support colleagues when choosing their animal models for future studies.


2020 ◽  
Vol 226 ◽  
pp. 113130 ◽  
Author(s):  
Samira Rahimi ◽  
Maghsoud Peeri ◽  
Mohammad Ali Azarbayjani ◽  
Leila Anoosheh ◽  
Elham Ghasemzadeh ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
José Javier Reyes-Lagos ◽  
Eric Alonso Abarca-Castro ◽  
Juan Carlos Echeverría ◽  
Hugo Mendieta-Zerón ◽  
Alejandra Vargas-Caraveo ◽  
...  

The emergent Coronavirus Disease 2019 (COVID-19) caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) could produce a maternal immune activation (MIA) via the inflammatory response during gestation that may impair fetal neurodevelopment and lead to postnatal and adulthood mental illness and behavioral dysfunctions. However, so far, limited evidence exists regarding long-term physiological, immunological, and neurodevelopmental modifications produced by the SARS-CoV-2 in the human maternal-fetal binomial and, particularly, in the offspring. Relevant findings derived from epidemiological and preclinical models show that a MIA is indeed linked to an increased risk of neurodevelopmental disorders in the offspring. We hypothesize that a gestational infection triggered by SARS-CoV-2 increases the risks leading to neurodevelopmental disorders of the newborn, which can affect childhood and the long-term quality of life. In particular, disruption of either the maternal or the fetal cholinergic anti-inflammatory pathway (CAP) could cause or exacerbate the severity of COVID-19 in the maternal-fetal binomial. From a translational perspective, in this paper, we discuss the possible manifestation of a MIA by SARS-CoV-2 and the subsequent neurodevelopmental disorders considering the role of the fetal-maternal cytokine cross-talk and the CAP. Specifically, we highlight the urgent need of preclinical studies as well as multicenter and international databanks of maternal-fetal psychophysiological data obtained pre-, during, and post-infection by SARS-CoV-2 from pregnant women and their offspring.


2014 ◽  
Vol 20 (3) ◽  
pp. 379-386 ◽  
Author(s):  
Shiliang Li ◽  
Sevil Korkmaz ◽  
Sivakkanan Loganathan ◽  
Tamás Radovits ◽  
Peter Hegedűs ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Karina S. MacDowell ◽  
Eva Munarriz-Cuezva ◽  
J. Javier Meana ◽  
Juan C. Leza ◽  
Jorge E. Ortega

Emerging evidence indicates that early-life exposure to environmental factors may increase the risk for schizophrenia via inflammatory mechanisms. Inflammation can alter the metabolism of tryptophan through the oxidative kynurenine pathway to compounds with neurotoxic and neuroprotective activity and compromise serotonin (5-HT) synthesis. Here we investigate the role of serotonergic and kynurenine pathways in the maternal immune activation (MIA) animal model of schizophrenia. The potential reversion exerted by long-term antipsychotic treatment was also evaluated. MIA was induced by prenatal administration of polyinosinic:polycytidylic acid (poly (I:C)) in mice. Expression of different proteins and the content of different metabolites involved in the function of serotonergic and kynurenine pathways was assessed by RT-PCR, immunoblot and ELISA analyses in frontal cortex of the offspring after puberty. MIA decreased tissue 5-HT content and promoted changes in the expression of serotonin transporter, 5-HT2A and 5-HT2C receptors. Expression of indoleamine 2,3-dioxygenase 2 (IDO2) and kynurenine 3-monooxygenase (KMO) was increased by poly (I:C) whereas kynurenine aminotransferase II and its metabolite kynurenic acid were not altered. Long-term paliperidone was able to counteract MIA-induced changes in 5-HT and KMO, and to increase tryptophan availability and tryptophan hydroxylase-2 expression in poly (I:C) mice but not in controls. MIA-induced increase of the cytotoxic risk ratio of kynurenine metabolites (quinolinic/kynurenic acid) was also reversed by paliperidone. MIA induces specific long-term brain effects on serotonergic activity. Such effects seem to be related with alternative activation of the kynurenine metabolic pathway towards a cytotoxic status. Atypical antipsychotic paliperodine partially remediates abnormalities observed after MIA.


2017 ◽  
Vol 63 ◽  
pp. 60-70 ◽  
Author(s):  
Destanie R. Rose ◽  
Milo Careaga ◽  
Judy Van de Water ◽  
Kim McAllister ◽  
Melissa D. Bauman ◽  
...  

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