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https://hdl.handle.net/2142/132824
Description
Title
Evaluating fetal neocortical development in germ-free mice in response to maternal IL-17A administration
Author(s)
Chalen, Izan
Wang, Selena
Otero, Ashley
Gonzalez-Ricon, Rafael
Best-Popescu, Catherine
Issue Date
2024-10-06
Keyword(s)
neurodevelopmental disorders
Date of Ingest
2026-02-22T17:01:26-06:00
Abstract
Maternal inflammation during pregnancy has been identified as an environmental factor that can trigger the pathogenesis of neurodevelopmental disorders (NDDs) in offspring. The mechanisms behind this trigger are still not fully understood. However, previous research in mice has shown that interleukin-17 (IL-17) is potentially a key mediator in this phenomenon. A commonly used physiological marker of proper neurological development is the patterning of the cerebral cortex. Abnormalities in the somatosensory cortex are correlated with behavioral phenotypes in mice that resemble those of NDDs. Notably, the gut microbiota is key for the differentiation and expansion of T helper 17 cell that produce IL-17, and some studies have shown that maternal microbial composition dictates the ability of IL-17 to influence offspring neurodevelopment and behavior. Our study aims to determine if IL-17A is sufficient to cause NDD-like malformations in the fetal brain in the total absence of maternal microbes. We used pregnant germ-free (GF) mice and administered either 1 µg recombinant IL-17A or 0.1 mL sterile saline (vehicle) intraperitoneally once daily from gestational day (GD) 10.5 through GD15.5. Fetal brains were collected on GD 16.5 and postfixed in 10% formalin before being sectioned coronally and immunohistochemically (IHC) stained for TBR1, a marker for excitatory neurons, and DAPI. Counts of TBR1+ cells and TBR1 fluorescence intensity were measured to determine layer patterns across the cortical plate. DAPI staining was used to measure layer thickness and total cortical plate thickness. Additionally, Spatial Light Interference Microscopy (SLIM), a label-free imaging technology, was used to quantify layer thickness. This technique, which for the first time is used in prenatal samples, allows researchers to overcome limitations of traditional IHC. Our preliminary findings indicate that IL-17A does not trigger the emergence of malformations as measured by TBR1 patterning and overall cortical thickness, suggesting that IL-17A alone may not be sufficient for triggering fetal neurodevelopmental abnormalities in the absence of maternal microbes.
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