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3. Non-SARS Coronaviruses in Individuals with Psychiatric Disorders

Author

Dickerson, Faith B., Severance, Emily G., Yolken, Robert H., Geyer, Mark A., Series Editor, Marsden, Charles A., Series Editor, Ellenbroek, Bart A., Series Editor, Barnes, Thomas R. E., Series Editor, Andersen, Susan L., Series Editor, Paulus, Martin P., Series Editor, Olivier, Jocelien, Series Editor, Savitz, Jonathan, editor, and Yolken, Robert H., editor

Published
2023
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4. The Microbiome and Mental Health Across the Lifespan

Author

Dickerson, Faith, Dilmore, Amanda Hazel, Godoy-Vitorino, Filipa, Nguyen, Tanya T., Paulus, Martin, Pinto-Tomas, Adrian A., Moya-Roman, Cristofer, Zuniga-Chaves, Ibrahim, Severance, Emily G., Jeste, Dilip V., Geyer, Mark A., Series Editor, Marsden, Charles A., Series Editor, Ellenbroek, Bart A., Series Editor, Barnes, Thomas R. E., Series Editor, Andersen, Susan L., Series Editor, Paulus, Martin P., Series Editor, Olivier, Jocelien, Series Editor, Savitz, Jonathan, editor, and Yolken, Robert H., editor

Published
2023
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5. Fungal Forces in Mental Health: Microbial Meddlers or Function Fixers?

Author

Severance, Emily G., Geyer, Mark A., Series Editor, Marsden, Charles A., Series Editor, Ellenbroek, Bart A., Series Editor, Barnes, Thomas R. E., Series Editor, Andersen, Susan L., Series Editor, Paulus, Martin P., Series Editor, Olivier, Jocelien, Series Editor, Savitz, Jonathan, editor, and Yolken, Robert H., editor

Published
2023
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8. Toxoplasma-induced behavior changes - is microbial dysbiosis the missing link?

Author

Prandovszky, Emese, Severance, Emily G., Splan, Victor W., Hua Liu, Jianchun Xiao, and Yolken, Robert H.

Subjects
GUT microbiome, DYSBIOSIS, IMMUNE system, TOXOPLASMA, AT-risk people, TOXOPLASMA gondii
Abstract

Toxoplasma gondii (T. gondii) is one of the most successful intracellular protozoa in that it can infect the majority of mammalian cell types during the acute phase of infection. Furthermore, it is able to establish a chronic infection for the host's entire lifespan by developing an encysted parasite form, primarily in the muscles and brain of the host, to avoid the host immune system. The infection affects one third of the world population and poses an increased risk for people with a suppressed immune system. Despite the dormant characteristics of chronic T. gondii infection, there is much evidence suggesting that this infection leads to specific behavior changes in both humans and rodents. Although numerous hypotheses have been put forth, the exact mechanisms underlying these behavior changes have yet to be understood. In recent years, several studies revealed a strong connection between the gut microbiome and the different organ systems that are affected in T. gondii infection. While it is widely studied and accepted that acute T. gondii infection can lead to a dramatic disruption of the host's normal, well-balanced microbial ecosystem (microbial dysbiosis), changes in the gut microbiome during the chronic stage of infection has not been well characterized. This review is intended to briefly inspect the different hypotheses that attempt to explain the behavior changes during T. gondii infection. Furthermore, this review proposes to consider the potential link between gut microbial dysbiosis, and behavior changes in T. gondii infection as a novel way to describe the underlying mechanism. [ABSTRACT FROM AUTHOR]

Published
2024
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14. The Microbiome and Mental Health Across the Lifespan

Author

Dickerson, Faith, primary, Dilmore, Amanda Hazel, additional, Godoy-Vitorino, Filipa, additional, Nguyen, Tanya T., additional, Paulus, Martin, additional, Pinto-Tomas, Adrian A., additional, Moya-Roman, Cristofer, additional, Zuniga-Chaves, Ibrahim, additional, Severance, Emily G., additional, and Jeste, Dilip V., additional

Published
2022
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15. Activation of Nrf2 at Critical Windows of Development Alters Tissue-Specific Protein S -Glutathionylation in the Zebrafish (Danio rerio) Embryo.

Author

Marques, Emily S., Severance, Emily G., Arsenault, Paige, Zahn, Sarah M., and Timme-Laragy, Alicia R.

Subjects
ZEBRA danio, DEVELOPMENTAL biology, PROTEIN S, EMBRYOLOGY, ISLANDS of Langerhans
Abstract

Activation of Nrf2—the master regulator of antioxidative response—at different stages of embryonic development has been shown to result in changes in gene expression, but the tissue-specific and downstream effects of Nrf2 activation during development remain unclear. This work seeks to elucidate the tissue-specific Nrf2 cellular localization and the downstream changes in protein S-glutathionylation during critical windows of zebrafish (Danio rerio) development. Wild-type and mutant zebrafish embryos with a loss-of-function mutation in Nrf2a were treated with two canonical activators, sulforaphane (SFN; 40 µM) or tert-butylhydroquinone (tBHQ; 1 µM), for 6 h at either pharyngula, hatching, or the protruding-mouth stage. Nrf2a protein and S-glutathionylation were visualized in situ using immunohistochemistry. At the hatching stage, Nrf2a protein levels were decreased with SFN, but not tBHQ, exposure. Exposure to both activators, however, decreased downstream S-glutathionylation. Stage- and tissue-specific differences in Nrf2a protein and S-glutathionylation were identified in the pancreatic islet and liver. Protein S-glutathionylation in Nrf2a mutant fish was increased in the liver by both activators, but not the islets, indicating a tissue-specific and Nrf2a-dependent dysregulation. This work demonstrates that critical windows of exposure and Nrf2a activity may influence redox homeostasis and highlights the importance of considering tissue-specific outcomes and sensitivity in developmental redox biology. [ABSTRACT FROM AUTHOR]

Published
2024
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42. Role of Immune and Autoimmune Dysfunction in Schizophrenia

Author

Severance, Emily G. and Yolken, Robert H.

Subjects
Gastrointestinal, animal diseases, mental disorders, bacteria, Prenatal, chemical and pharmacologic phenomena, biochemical phenomena, metabolism, and nutrition, Pathogens, Autoantigens, Article, Endothelial
Abstract

In this chapter, we review data in support of the concept that immune system dysregulation is the most plausible explanation that reconciles gene by environmental interactions in schizophrenia. Early investigations of this topic demonstrated aspects of aberrant activation of humoral immunity, including autoimmunity, associated with schizophrenia, whereas current research efforts have expanded this theme to include elements of innate immunity. Advances in our understanding of inflammation and molecules of both the adaptive and innate immune system and their functional roles in standard brain physiology provide an important context by which schizophrenia might arise as the result of the coupling of immune and neurodevelopmental dysregulation.

Published
2021

43. Activation of Nrf2 at Critical Windows of Development Alters Protein S-Glutathionylation in the Zebrafish Embryo (Danio rerio)

Author

Severance, Emily G

Subjects
respiratory system, digestive system, environment and public health
Abstract

Perturbation of cellular redox homeostasis to a more oxidized state has been linked to adverse human health effects such as diabetes and cancer. However, the impact of altering the regulation of redox homeostasis during development is not fully understood. Specifically, this project investigates the role of the Nrf2 antioxidant response pathway and its effect on glutathione (GSH; cellular redox buffer) at critical windows of development. To explore this, we used zebrafish embryos (Danio rerio) as a model due to the function of GSH and the Nrf2 being conserved among vertebrates. We exposed zebrafish embryos to three Nrf2 activators: two antioxidant enhancing molecules: sulforaphane (SFN; 40 µM) and Dimethyl fumarate (DFM; 7µM) as well as the pro-oxidant tert-Butylhydroquinone (tBHQ; 1µM) for 6 hours at critical windows development: 24, 48, 72 hours post fertilization (hpf). Following exposure, we visualized Nrf2 protein levels and glutathionylation rates using immunohistochemistry and confocal imaging. We found that changes in Nrf2 expression were dependent on the tissue type with there being significant changes in Nrf2 when looking at the pancreatic beta cells. Also in the beta cells, exposure to SFN, tBHQ, and DMF were found to increase Nrf2 translocation into the nucleus. Most notably, all three Nrf2 activators significantly altered glutathionylation levels depending on the time-point the zebrafish were exposed. SFN and tBHQ were also found to significantly increase glutathionylation at 48 and 72hpf, but led to a significant decrease at 96hpf while DMF increased glutathionylation at all three time-points. Interestingly, there was little correlation between Nrf2 protein levels and glutathionylation, but zebrafish with a mutated Nrf2 did have significantly different glutathionylation rates than the wild type fish. This suggests that oxidative stress is not the sole regulator of glutathionylation and instead Nrf2 may also be regulating glutathionylation through GSH storage. My data indicate that the effects of Nrf2 activation on Nrf2 levels and glutathionylation depend on the timing of exposure to the perturbing chemicals and the tissue type. Finding these windows of development where redox homeostasis is most sensitive in humans can allow for possible preventative and/or protective measures to oxidative stress during development.

Published
2021
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