scholarly journals Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6

2007 ◽  
Vol 27 (40) ◽  
pp. 10695-10702 ◽  
Author(s):  
S. E. P. Smith ◽  
J. Li ◽  
K. Garbett ◽  
K. Mirnics ◽  
P. H. Patterson
Keyword(s):  
Brain Development ◽  
Immune Activation ◽  
Interleukin 6 ◽  
Fetal Brain ◽  
Maternal Immune Activation ◽  
Fetal Brain Development

scholarly journals Maternal Immune Activation Alters Fetal Brain Development and Enhances Proliferation of Neural Precursor Cells in Rats

2020 ◽  
Vol 11 ◽  
Author(s):  
Kelly J. Baines ◽  
Dendra M. Hillier ◽  
Faraj L. Haddad ◽  
Nagalingam Rajakumar ◽  
Susanne Schmid ◽  
...  
Keyword(s):  
Brain Development ◽  
Immune Activation ◽  
Fetal Brain ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Maternal Immune Activation ◽  
Fetal Brain Development

scholarly journals Mycobacterium tuberculosis-Induced Maternal Immune Activation Promotes Autism-Like Phenotype in Infected Mice Offspring

2021 ◽  
Vol 18 (9) ◽  
pp. 4513
Author(s):  
Wadzanai Manjeese ◽  
Nontobeko E. Mvubu ◽  
Adrie J. C. Steyn ◽  
Thabisile Mpofana
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Immune Activation ◽  
Fetal Brain ◽  
Autism Spectrum ◽  
Necrosis Factor Alpha ◽  
Altered Expression ◽  
Maternal Immune Activation ◽  
Persistent Inflammation ◽  
Cytokine Levels ◽  
Fetal Brain Development

The maternal system’s exposure to pathogens during pregnancy influences fetal brain development causing a persistent inflammation characterized by elevated pro-inflammatory cytokine levels in offspring. Mycobacterium tuberculosis (Mtb) is a global pathogen that causes tuberculosis, a pandemic responsible for health and economic burdens. Although it is known that maternal infections increase the risk of autism spectrum disorder (ASD), it is not known whether Mtb infection is sufficient to induce ASD associated behaviors, immune dysregulation and altered expression of synaptic regulatory genes. The current study infected pregnant Balb/c mice with Mtb H37Rv and valproic acid (VPA) individually and in combination. Plasma cytokine profiles were measured in offspring using the Bio-plex Th17 pro mouse cytokine panel. Mtb infection increased plasma interleukin (IL)-6 and IL-17A, while tumor necrosis factor alpha (TNF-α), interferon (IFN)-γ and IL-1β were reduced when compared with saline. Mtb-induced maternal immune activation (MIA) offspring displayed increased grooming behavior. The study also revealed dysregulation in gene expression of synaptic molecules in the cerebellum. MIA rescued the VPA-induced effects on self-grooming and social interaction behaviors. Our finding therefore highlights a potential role of Mtb as a MIA agent that can potentially contribute to ASD.

scholarly journals Fetal innate immunity contributes to the induction of atypical behaviors in a mouse model of maternal immune activation

2020 ◽  
Author(s):  
Eva K. Nichols ◽  
Hsiu-Chun Chuang ◽  
Matthew T. Davis ◽  
Kristina M. Geiger ◽  
Rick Z. Li ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Immune Activation ◽  
Repetitive Behavior ◽  
Fetal Brain ◽  
Toll Like Receptor ◽  
Neurodevelopmental Outcomes ◽  
Behavioral Phenotypes ◽  
Maternal Immune Activation ◽  
Fetal Brain Development ◽  
Adapter Molecule

SummaryMaternal immune activation (MIA) increases likelihood of altered neurodevelopmental outcomes. Maternal cytokines are proposed to affect fetal brain development in mice; however, the contribution of fetal immunity to neurodevelopmental disorders is largely unexplored. Here, we show that MIA mediated by Toll-like receptor 3 (TLR3), but not other TLRs, induces a specific set of behavioral phenotypes including decreased sociability and increased restricted repetitive behavior in offspring. Accordingly, these behavioral phenotypes were absent when offspring were deficient for Trif, the downstream adapter molecule of TLR3. Using single-cell RNA sequencing, we identified clusters of border-associated macrophages that were significantly enriched in the fetal brain following TLR3-MIA, and these clusters were diminished in Trif−/− fetal brains.Moreover, we found that triggering TLR3-TRIF in offspring can occur through transplacental viral infection, resulting in altered behavioral phenotypes. Collectively, our data indicate that fetal innate immunity contributes to MIA-induced atypical behaviors in mice.

scholarly journals The placental interleukin-6 signaling controls fetal brain development and behavior

2017 ◽  
Vol 62 ◽  
pp. 11-23 ◽  
Author(s):  
Wei-Li Wu ◽  
Elaine Y. Hsiao ◽  
Zihao Yan ◽  
Sarkis K. Mazmanian ◽  
Paul H. Patterson
Keyword(s):  
Brain Development ◽  
Interleukin 6 ◽  
Fetal Brain ◽  
Fetal Brain Development ◽  
And Behavior

scholarly journals Lessons From Zika and Other Virus Induced Skull Deformity

FACE ◽  
2020 ◽  
Vol 1 (1) ◽  
pp. 44-50
Author(s):  
Mohamad Masoumy ◽  
Emily P. Masoumy ◽  
Babak Baban ◽  
Jack C. Yu
Keyword(s):  
Brain Development ◽  
Immune Activation ◽  
Viral Infections ◽  
Fetal Brain ◽  
Growth Dynamics ◽  
Cell Loss ◽  
Maternal Immune Activation ◽  
Skull Deformity ◽  
Critical Phases ◽  
The Impact

Objective: Viral infections during pregnancy can cause disturbance in normal craniofacial morphogenesis. While some pathogens such as cytomegalovirus and herpes simplex are familiar to us, others remain obscure. This review examines the arbovirus-induced cranial deformities and combines biomechanics with growth dynamics to gain a deeper appreciation of this complex morphogenetic process. Materials and Methods: Using Wolfram Alpha, we analyzed the impact of cell population changes. The growth dynamics of the brain, and thus the size of the calvarium, followed 2 potential logistic curves: compensated and uncompensated. To understand the potential mechanism of cell loss, we performed literature review on maternal immune activation and viral tropism for neurons and glial cells. Results: With arboviral infections such as Zika, uncompensated loss of cells during the critical phases of fetal brain development reduces the intracranial mass and therefore decreases the tensile stress across the cranial sutures. The deflationary effect produces microcephaly by subduction and reduced osteogenesis seen clinically in these infants. Conclusion: Many viral infections cause intense maternal immune activation, some have neurotropism and can result in cell loss within the developing cranium. Unable to overcome this loss, the cranium assumes a new, abnormal shape and volume. Secondary calvarial deformities is due to, and should not cause, changes in brain development.

New normal range of fetal cavum septum pellucidum in the second trimester of gestation

2020 ◽  
Author(s):  
M.V. Medvedev, O.I. Kozlova, À.Yu. Romanova
Keyword(s):  
Brain Development ◽  
Reference Range ◽  
Fetal Brain ◽  
Septum Pellucidum ◽  
Second Trimester ◽  
Normal Range ◽  
Cavum Septum Pellucidum ◽  
New Normal ◽  
Biparietal Diameter ◽  
Fetal Brain Development

Fetal brain was retrospectively evaluated in 418 normal fetuses at 16–28 weeks of gestation. The multiplanar mode to obtain the axial cerebral plane and measured the width of the cavum septum pellucidum (CSP) and biparietal diameter (BD). All measurements of CSP were done from as the widest diameter across both borders in an inter-to inter fashion. The CSP width is increasing at second trimester of gestation. Normal range plotted on the reference range (mean, 5th and 95th percentiles) of fetal width CSP by measuring of its size may be useful for assessment of fetal brain development in the second trimester of gestation.

scholarly journals CB1 antagonism increases excitatory synaptogenesis in a cortical spheroid model of fetal brain development

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Alexis Papariello ◽  
David Taylor ◽  
Ken Soderstrom ◽  
Karen Litwa
Keyword(s):  
Brain Development ◽  
Spontaneous Activity ◽  
Microelectrode Array ◽  
Cannabinoid Receptor ◽  
Fetal Brain ◽  
Endocannabinoid System ◽  
Autism Spectrum ◽  
Nervous System Development ◽  
Inhibitory Synapses ◽  
Fetal Brain Development

AbstractThe endocannabinoid system (ECS) plays a complex role in the development of neural circuitry during fetal brain development. The cannabinoid receptor type 1 (CB1) controls synaptic strength at both excitatory and inhibitory synapses and thus contributes to the balance of excitatory and inhibitory signaling. Imbalances in the ratio of excitatory to inhibitory synapses have been implicated in various neuropsychiatric disorders associated with dysregulated central nervous system development including autism spectrum disorder, epilepsy, and schizophrenia. The role of CB1 in human brain development has been difficult to study but advances in induced pluripotent stem cell technology have allowed us to model the fetal brain environment. Cortical spheroids resemble the cortex of the dorsal telencephalon during mid-fetal gestation and possess functional synapses, spontaneous activity, an astrocyte population, and pseudo-laminar organization. We first characterized the ECS using STORM microscopy and observed synaptic localization of components similar to that which is observed in the fetal brain. Next, using the CB1-selective antagonist SR141716A, we observed an increase in excitatory, and to a lesser extent, inhibitory synaptogenesis as measured by confocal image analysis. Further, CB1 antagonism increased the variability of spontaneous activity within developing neural networks, as measured by microelectrode array. Overall, we have established that cortical spheroids express ECS components and are thus a useful model for exploring endocannabinoid mediation of childhood neuropsychiatric disease.

scholarly journals Neuroplacentology in congenital heart disease: placental connections to neurodevelopmental outcomes

2021 ◽  
Author(s):  
Rachel L. Leon ◽  
Imran N. Mir ◽  
Christina L. Herrera ◽  
Kavita Sharma ◽  
Catherine Y. Spong ◽  
...  
Keyword(s):  
Brain Development ◽  
Congenital Heart ◽  
Fetal Brain ◽  
In Utero ◽  
Structure And Function ◽  
Brain Growth ◽  
Neurodevelopmental Outcomes ◽  
Fetal Brain Development ◽  
And Function

Abstract Children with congenital heart disease (CHD) are living longer due to effective medical and surgical management. However, the majority have neurodevelopmental delays or disorders. The role of the placenta in fetal brain development is unclear and is the focus of an emerging field known as neuroplacentology. In this review, we summarize neurodevelopmental outcomes in CHD and their brain imaging correlates both in utero and postnatally. We review differences in the structure and function of the placenta in pregnancies complicated by fetal CHD and introduce the concept of a placental inefficiency phenotype that occurs in severe forms of fetal CHD, characterized by a myriad of pathologies. We propose that in CHD placental dysfunction contributes to decreased fetal cerebral oxygen delivery resulting in poor brain growth, brain abnormalities, and impaired neurodevelopment. We conclude the review with key areas for future research in neuroplacentology in the fetal CHD population, including (1) differences in structure and function of the CHD placenta, (2) modifiable and nonmodifiable factors that impact the hemodynamic balance between placental and cerebral circulations, (3) interventions to improve placental function and protect brain development in utero, and (4) the role of genetic and epigenetic influences on the placenta–heart–brain connection. Impact Neuroplacentology seeks to understand placental connections to fetal brain development. In fetuses with CHD, brain growth abnormalities begin in utero. Placental microstructure as well as perfusion and function are abnormal in fetal CHD.

Fetal brain development of twins assessed in utero by ultrasound: implications for schizophrenia

1996 ◽  
Vol 19 (2-3) ◽  
pp. 141-149 ◽  
Author(s):  
John H. Gilmore ◽  
Diana O. Perkins ◽  
Mark A. Kliewer ◽  
Marvin L. Hage ◽  
Susan G. Silva ◽  
...  
Keyword(s):  
Brain Development ◽  
Fetal Brain ◽  
In Utero ◽  
Fetal Brain Development
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