About

Dr. Adrienne M. Antonson is an Assistant Professor of Animal Sciences at the University of Illinois Urbana-Champaign, where she leads the Antonson Developmental Neuroimmunology Laboratory. She completed her PhD in Animal Science, specializing in Immunophysiology and Behavior, at the University of Illinois Urbana-Champaign from 2013 to 2018. Following her doctoral studies, she pursued postdoctoral research at the Institute for Behavioral Medicine Research at The Ohio State University from 2018 to 2021. Dr. Antonson's academic background combines biology and animal sciences with a focus on neuroimmunology, reflecting her interdisciplinary expertise in these areas. Originally from Chatham, New York, Dr. Antonson balances her professional work with personal interests such as running, hiking, cycling, mountain biking, and enjoying local brews. She also enjoys listening to true crime podcasts, reading, cooking, and caring for her two cats. A fun personal note is that she has a twin sister named Hannah who lives in Austin, Texas.

Research topics

• Biology
• Neuroscience
• Internal medicine
• Genetics
• Medicine
• Endocrinology
• Immunology
• Psychology
• Bioinformatics

Selected publications

• Influenza A virus infection during pregnancy increases transfer of maternal bloodborne molecules to fetal tissues

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-31

  preprintOpen accessSenior authorCorresponding

  Abstract Influenza A virus (IAV) infection during pregnancy is linked to heightened risk for neurodevelopmental disorders (NDDs) in the offspring. The precise pathophysiological mechanism(s) underling this association remains an active topic of research. We propose that maternal immune activation (MIA) triggered by IAV infection can disrupt selective permeability at the maternal-fetal interface, leading to increased transfer of blood-derived molecules into the fetal compartment. Some of these molecules might be responsible for the initiation of inflammatory cascades implicated in NDD etiology. Using a murine model of seasonal IAV infection during pregnancy, we examined placental and fetal brain barrier properties following maternal IAV challenge. Our findings demonstrate an enhanced transplacental transfer of fluorescently labeled tracers from maternal circulation to key neurodevelopmental regions, including the subventricular zone (SVZ) and choroid plexus (ChP) of fetal brains. This effect was most pronounced in fetuses from dams exposed to the highest dose of IAV. Notably, a similar pattern was observed for accumulation of the bloodborne neuroinflammatory molecule fibrinogen in these same brain regions, which was further amplified in response to the highest IAV dose. Moreover, fibrinogen accumulation was positively correlated with Iba1 + cell immunofluorescence, suggesting a potential interaction between fibrinogen and Iba1 + cells. Collectively, these findings suggest that IAV-induced MIA enhances transplacental transfer of blood-derived molecules into fetal tissues, potentially activating proinflammatory pathways in Iba1 + cells. Highlights Maternal influenza infection increases fetal exposure to maternally derived tracers. Fetal blood brain barrier dysfunction is evident in the SVZ and ChP. Fibrinogen accumulation in the SVZ and ChP correlates with Iba1 intensity. Increased vascular permeability may contribute to altered fetal brain development.

  PublisherOA PDFDOI

• Ontogeny and colonization of embryonic border-associated macrophages and their role in neurodevelopment

  Frontiers in Cellular Neuroscience · 2025-10-30 · 1 citations

  reviewOpen accessSenior authorCorresponding

  Border-associated macrophages (BAMs) are tissue-resident macrophages in the central nervous system (CNS) that originate from yolk sac progenitors during primitive hematopoiesis. While much is known about their parenchymal counterparts, microglia, recent evidence indicates that BAMs also play roles in neurodevelopment. Located at CNS interfaces such as the meninges, choroid plexus, and perivascular space, BAMs facilitate immune surveillance, vascular modeling, debris clearance, and cerebrospinal fluid dynamics. Despite their strategic location, BAMs have historically been understudied in developmental contexts. This mini review covers their embryonic origins, regional diversification, and functional roles as development progresses. Offering new insights, we consider BAMs in the context of neurodevelopmental disorders (NDDs). Recent findings from maternal immune activation (MIA) studies suggest that fetal BAMs may contribute to aberrant cortical development through altered inflammatory signaling. We propose that, like microglia, BAMs may play previously unappreciated roles in shaping the developmental trajectory of the brain. To aid future research, we also review current tools for studying BAMs in vivo and in vitro , including new transgenic lines and organoid-based approaches. These tools will be critical for dissecting the molecular functions of BAMs during healthy and disordered development. Understanding BAM biology in early life may reveal novel mechanisms underlying NDDs and inform therapeutic strategies targeting brain–immune interfaces.

  PublisherOA PDFDOI

• Maternal vaccination partially protects piglets against influenza A virus associated alteration of the microbiome and hippocampal gene expression

  Veterinary Microbiology · 2025-05-08 · 1 citations

  articleOpen access

  Influenza A virus (IAV) causes respiratory disease with systemic complications in a variety of avian and mammalian hosts, including humans and pigs. Infection with IAV in newborns can be particularly damaging as viral infection is known to disrupt the rapid developmental processes that occur during this period. Maternal IAV vaccination can reduce the risk of IAV infection in infants, but it is unknown whether passive transfer of anti-IAV antibodies protect against the downstream complications of infection. In this study, we evaluated the impact of maternal vaccination on the gut and nasal microbiota development and hippocampal transcriptome in neonatal piglets infected with influenza A virus. Sows were either vaccinated with an experimental influenza A vaccine at 70- and 90-days gestation, or mock-vaccinated with PBS. Neonatal piglets born from vaccinated and unvaccinated sows were challenged with a pathogenic IAV isolate or mock-challenged with PBS at 6 days post-farrowing and euthanized five days post challenge. Vaccination significantly reduced lung lesions and infectious viral load in piglets. Nasal and gut microbial community development was also partially protected from viral disruption as indicated by increased deviation from pre-challenge timepoints compared to animals challenged with the virus from unvaccinated mothers. Bulk RNA sequencing of hippocampal tissue identified 1146 differentially expressed genes (FDR < 0.05) between groups. IAV-infected piglets from vaccinated sows showed increases in genes related to viral immune responses, while IAV-infected piglets from unvaccinated sows showed increases in genes related to neurogenesis and decreases in genes related to vascular development. Many of these differentially regulated genes were strongly correlated with microbial community abundances, indicating that the microbiota may contribute to IAV outcomes. Notably, nasal microbial abundances intricately connected with hippocampal gene expression patterns, suggesting a strong nasal microbiome-brain communication axis in early development. Together, our results indicate that maternal vaccination partially protects neonatal piglets against influenza virus infection and mitigates the potential long-term impacts of IAV infection on the microbiome and cognition.

  PublisherDOI

• Influenza A virus infection during pregnancy increases transfer of maternal bloodborne molecules to fetal tissues

  Brain Behavior and Immunity · 2025-08-06 · 3 citations

  articleOpen accessSenior authorCorresponding

  • Maternal influenza infection increases fetal exposure to maternally derived tracers. • Fetal blood brain barrier dysfunction is evident in the SVZ and ChP. • Fibrinogen accumulation in the SVZ and ChP correlates with Iba1 intensity. • Increased vascular permeability may contribute to altered fetal brain development. Influenza A virus (IAV) infection during pregnancy is linked to heightened risk for neurodevelopmental disorders (NDDs) in the offspring. The precise pathophysiological mechanism(s) underling this association remains an active topic of research. We propose that maternal immune activation (MIA) triggered by IAV infection can disrupt selective permeability at the maternal-fetal interface, leading to increased transfer of blood-derived molecules into the fetal compartment. Some of these molecules might be responsible for the initiation of inflammatory cascades implicated in NDD etiology. Using a murine model of seasonal IAV infection during pregnancy, we examined placental and fetal brain barrier properties following maternal IAV challenge. Our findings demonstrate an enhanced transplacental transfer of fluorescently labeled tracers from maternal circulation to key neurodevelopmental regions, including the subventricular zone (SVZ) and choroid plexus (ChP) of fetal brains. This effect was most pronounced in fetuses from dams exposed to the highest dose of IAV. Notably, a similar pattern was observed for accumulation of the bloodborne neuroinflammatory molecule fibrinogen in these same brain regions, which was further amplified in response to the highest IAV dose. Moreover, fibrinogen accumulation was positively correlated with Iba1 + cell immunofluorescence, suggesting a potential interaction between fibrinogen and Iba1 + cells. Collectively, these findings suggest that IAV-induced MIA enhances transplacental transfer of blood-derived molecules into fetal tissues, potentially activating proinflammatory pathways in Iba1 + cells.

  PublisherDOI

• Influenza A virus during pregnancy disrupts maternal immunity and fetal neocortical development in a dose- and time-dependent manner

  Brain Behavior and Immunity · 2024-11-01

  articleSenior author
  PublisherDOI

• Immune and metabolic challenges induce changes in pain sensation and related pathways in the hypothalamus

  Physiological Genomics · 2024-01-08 · 8 citations

  articleOpen access

  The interaction of infection during gestation and insults later in life influences the molecular mechanisms in the hypothalamus that participate in pain sensation. The response of the hypothalamic transcriptome varies between sexes and can also affect synapses and immune signals. The findings from this study assist in the identification of agonists or antagonists that can guide pretranslational studies to ameliorate the effects of gestational insults interacting with postnatal challenges on physiological or behavioral disorders.

  PublisherDOI

• Epigenetic disruptions in the offspring hypothalamus in response to maternal infection

  Gene · 2024-02-29 · 5 citations

  articleOpen access
  PublisherOA PDFDOI

• Influenza A virus during pregnancy disrupts maternal intestinal immunity and fetal cortical development in a dose- and time-dependent manner

  Molecular Psychiatry · 2024-07-03 · 19 citations

  articleOpen accessSenior author

  Abstract Epidemiological studies link exposure to viral infection during pregnancy, including influenza A virus (IAV) infection, with increased incidence of neurodevelopmental disorders (NDDs) in offspring. Models of maternal immune activation (MIA) using viral mimetics demonstrate that activation of maternal intestinal T helper 17 (T H 17) cells, which produce effector cytokine interleukin (IL)-17, leads to aberrant fetal brain development, such as neocortical malformations. Fetal microglia and border-associated macrophages (BAMs) also serve as potential cellular mediators of MIA-induced cortical abnormalities. However, neither the inflammation-induced T H 17 cell pathway nor fetal brain-resident macrophages have been thoroughly examined in models of live viral infection during pregnancy. Here, we inoculated pregnant mice with two infectious doses of IAV and evaluated peak innate and adaptive immune responses in the dam and fetus. While respiratory IAV infection led to dose-dependent maternal colonic shortening and microbial dysregulation, there was no elevation in intestinal T H 17 cells nor IL-17. Systemically, IAV resulted in consistent dose- and time-dependent increases in IL-6 and IFN-γ. Fetal cortical abnormalities and global changes in fetal brain transcripts were observable in the high-but not the moderate-dose IAV group. Profiling of fetal microglia and BAMs revealed dose- and time-dependent differences in the numbers of meningeal but not choroid plexus BAMs, while microglial numbers and proliferative capacity of Iba1 + cells remained constant. Fetal brain-resident macrophages increased phagocytic CD68 expression, also in a dose- and time-dependent fashion. Taken together, our findings indicate that certain features of MIA are conserved between mimetic and live virus models, while others are not. Overall, we provide consistent evidence of an infection severity threshold for downstream maternal inflammation and fetal cortical abnormalities, which recapitulates a key feature of the epidemiological data and further underscores the importance of using live pathogens in NDD modeling to better evaluate the complete immune response and to improve translation to the clinic.

  PublisherOA PDFDOI

• Fetal blood-brain barrier breakdown during gestational influenza virus infection allows large glycoprotein fibrinogen to reach the fetal brain

  Brain Behavior and Immunity · 2023-11-01

  articleSenior author
  PublisherDOI

• Influenza A virus during pregnancy disrupts maternal intestinal immunity and fetal cortical development in a dose- and time-dependent manner

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-12-19 · 7 citations

  preprintOpen accessSenior authorCorresponding

  Abstract Epidemiological studies link neurodevelopmental disorders (NDDs) with exposure to maternal viral infection in utero. It is hypothesized that the mechanism governing this link involves the activation of maternal intestinal T helper 17 (T H 17) cells, which produce effector cytokine interleukin (IL)-17. While IL-17 is implicated as a major driver of fetal brain abnormalities, this inflammation-induced T H 17 pathway has not been thoroughly examined in models of live viral infection during pregnancy. Influenza A virus (IAV) infection is consistently linked to offspring NDDs and can result in host intestinal dysregulation. Therefore, it is possible that intestinal T H 17 cells and subsequent production of IL-17 could drive fetal brain abnormalities during gestational IAV infection. To test this, we inoculated pregnant mice with two infectious doses of IAV and evaluated peak innate and adaptive immune responses in the dam and fetus. While respiratory IAV infection led to dose-dependent maternal colonic shortening and microbial dysregulation, there was no elevation in intestinal T H 17 cells nor IL-17. Fetal cortical abnormalities and global changes in fetal brain transcripts were observable in the high-dose IAV group, despite a lack of IL-17 signaling. Profiling fetal microglia and border-associated macrophages (BAMs) –potential cellular mediators of IAV-induced cortical abnormalities –revealed dose-dependent differences in the numbers of BAMs but not microglia. Overall, our data support the idea of an infection severity threshold for downstream maternal inflammation and fetal cortical abnormalities, confirming the use of live pathogens in NDD modeling to better evaluate the complete immune response and to improve translation to the clinic.

  PublisherOA PDFDOI

Frequent coauthors

• Tamar Gur

  The Ohio State University Wexner Medical Center

  38 shared

• Helen J. Chen

  The Ohio State University Wexner Medical Center

  29 shared

• Michael T. Bailey

  The Ohio State University Wexner Medical Center

  18 shared

• Rodney W. Johnson

  University of Illinois Urbana-Champaign

  14 shared

• Therese Rajasekera

  Institute for Behavioral Medicine

  14 shared

• Jeffrey D. Galley

  The Ohio State University Wexner Medical Center

  14 shared

• Sydney Lammers

  13 shared

• Ashley Otero

  University of Illinois Urbana-Champaign

  9 shared

Education

• PhD, Animal Sciences

  University of Illinois at Urbana-Champaign

  2018