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Biomolecules
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Neuroimmune Interactions in Neuropsychiatric Diseases
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Neuroimmune Interactions in Neuropsychiatric Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 6680

Special Issue Editor

Dr. Luciana Frick

E-Mail Website
Guest Editor
Departments of Neurology and Medicine, Jacobs School of Medicine and Biomedical Sciences, The State University of New York, Buffalo, NY, USA
Interests: neuroimmune interactions in health and disease; neuroglia; cytokines; autoimmunity; neurological and psychiatric disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, the peripheral immune system and glial cells have emerged as key players in neurological and psychiatric diseases. Neuroimmune interactions are important contributors to the pathophysiology and sometimes etiology of neuropsychiatric disorders. Understanding these interactions is critical for the treatment of such diseases. In this Special Issue, authors are invited to submit novel findings of basic, translational, and clinical research and state-of-the-art reviews of the current literature on the topic of “Neuroimmune Interactions in Neuropsychiatric Diseases”.

Dr. Luciana Frick
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurology
  • psychiatry
  • immunity
  • glia

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Published Papers (3 papers)

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Research

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15 pages, 639 KiB  
Article
Altered Monocyte Populations and Activation Marker Expression in Children with Autism and Co-Occurring Gastrointestinal Symptoms
by Rachel J. Moreno, Yasmin W. Azzam, Serena Eng, Destanie Rose and Paul Ashwood
Biomolecules 2025, 15(2), 207; https://doi.org/10.3390/biom15020207 - 1 Feb 2025
Viewed by 913
Abstract
Autism spectrum disorder (ASD) is an early-onset neurodevelopmental condition that now impacts 1 in 36 children in the United States and is characterized by deficits in social communication, repetitive behaviors, and restricted interests. Children with ASD also frequently experience co-morbidities including anxiety and [...] Read more.
Autism spectrum disorder (ASD) is an early-onset neurodevelopmental condition that now impacts 1 in 36 children in the United States and is characterized by deficits in social communication, repetitive behaviors, and restricted interests. Children with ASD also frequently experience co-morbidities including anxiety and ADHD, and up to 80% experience gastrointestinal (GI) symptoms such as constipation, diarrhea, and/or abdominal pain. Systemic immune activation and dysregulation, including increased pro-inflammatory cytokines, are frequently observed in ASD. Evidence has shown that the innate immune system may be impacted in ASD, as altered monocyte gene expression profiles and cytokine responses to pattern recognition ligands have been observed compared to typically developing (TD) children. In humans, circulating monocytes are often categorized into three subpopulations—classical, transitional (or “intermediate”), and nonclassical monocytes, which can vary in functions, including archetypal inflammatory and/or reparative functions, as well as their effector locations. The potential for monocytes to contribute to immune dysregulation in ASD and its comorbidities has so far not been extensively studied. This study aims to determine whether these monocyte subsets differ in frequency in children with ASD and if the presence of GI symptoms alters subset distribution, as has been seen for T cell subsets. Whole blood from ASD children with (ASD+GI+) and without gastrointestinal symptoms (ASD+GI−) and their TD counterparts was collected from children enrolled in the Childhood Autism Risk from Genetics and Environment (CHARGE) study. Peripheral blood mononuclear cells were isolated and stained for commonly used subset identifiers CD14 and CD16 as well as activation state markers CCR2, HLA-DR, PD-1, and PD-L1 for flow cytometry analysis. We identified changes in monocyte subpopulations and their expression of surface markers in children with ASD compared to TD children. These differences in ASD appear to be dependent on the presence or absence of GI symptoms. We found that the ASD+GI+ group have a different monocyte composition, evident in their classical, transitional, and nonclassical populations, compared to the ASD+GI− and TD groups. Both the ASD+GI+ and ASD+GI− groups exhibited greater frequencies of classical monocytes compared to the TD group. However, the ASD+GI+ group demonstrated lower frequencies of transitional and nonclassical monocytes than their ASD+GI− and TD counterparts. CCR2+ classical monocyte frequencies were highest in the ASD+GI− group. HLA-DR+ classical, transitional, and nonclassical monocytes were statistically comparable between groups, however, HLA-DR− nonclassical monocyte frequencies were lower in both ASD groups compared to TD. The frequency of classical monocytes displaying exhaustion markers PD-1 and PD-L1 were increased in the ASD+GI+ group compared to ASD+GI− and TD, suggesting potentially impaired ability for clearance of foreign pathogens or debris, typically associated with worsened inflammation. Taken together, the findings of differential proportions of the monocyte subpopulations and altered surface markers may explain some of the characteristics of immune dysregulation, such as in the gastrointestinal tract, observed in ASD. Full article
(This article belongs to the Special Issue Neuroimmune Interactions in Neuropsychiatric Diseases)
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23 pages, 9441 KiB  
Article
Quantitative Spatial Analysis of Neuroligin-3 mRNA Expression in the Enteric Nervous System Reveals a Potential Role in Neuronal–Glial Synapses and Reduced Expression in Nlgn3R451C Mice
by Madushani Herath, Ellie Cho, Ulrika Marklund, Ashley E. Franks, Joel C. Bornstein and Elisa L. Hill-Yardin
Biomolecules 2023, 13(7), 1063; https://doi.org/10.3390/biom13071063 - 30 Jun 2023
Cited by 6 | Viewed by 2748
Abstract
Mutations in the Neuroligin-3 (Nlgn3) gene are implicated in autism spectrum disorder (ASD) and gastrointestinal (GI) dysfunction, but cellular Nlgn3 expression in the enteric nervous system remains to be characterised. We combined RNAScope in situ hybridization and immunofluorescence to measure Nlgn3 [...] Read more.
Mutations in the Neuroligin-3 (Nlgn3) gene are implicated in autism spectrum disorder (ASD) and gastrointestinal (GI) dysfunction, but cellular Nlgn3 expression in the enteric nervous system remains to be characterised. We combined RNAScope in situ hybridization and immunofluorescence to measure Nlgn3 mRNA expression in cholinergic and VIP-expressing submucosal neurons, nitrergic and calretinin-containing myenteric neurons and glial cells in both WT and Nlgn3R451C mutant mice. We measured Nlgn3 mRNA neuronal and glial expression via quantitative three-dimensional image analysis. To validate dual RNAScope/immunofluorescence data, we interrogated available single-cell RNA sequencing (scRNASeq) data to assess for Nlgn3, Nlgn1, Nlgn2 and their binding partners, Nrxn1-3, MGDA1 and MGDA2, in enteric neural subsets. Most submucosal and myenteric neurons expressed Nlgn3 mRNA. In contrast to other Nlgns and binding partners, Nlgn3 was strongly expressed in enteric glia, suggesting a role for neuroligin-3 in mediating enteric neuron–glia interactions. The autism-associated R451C mutation reduces Nlgn3 mRNA expression in cholinergic but not in VIPergic submucosal neurons. In the myenteric plexus, Nlgn3 mRNA levels are reduced in calretinin, nNOS-labelled neurons and S100 β -labelled glia. We provide a comprehensive cellular profile for neuroligin-3 expression in ileal neuronal subpopulations of mice expressing the R451C autism-associated mutation in Nlgn3, which may contribute to the understanding of the pathophysiology of GI dysfunction in ASD. Full article
(This article belongs to the Special Issue Neuroimmune Interactions in Neuropsychiatric Diseases)
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Review

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50 pages, 2825 KiB  
Review
Neuroinflammation—A Crucial Factor in the Pathophysiology of Depression—A Comprehensive Review
by Andreea Sălcudean, Cristina-Raluca Bodo, Ramona-Amina Popovici, Maria-Melania Cozma, Mariana Păcurar, Ramona-Elena Crăciun, Andrada-Ioana Crisan, Virgil-Radu Enatescu, Ileana Marinescu, Dora-Mihaela Cimpian, Andreea-Georgiana Nan, Andreea-Bianca Sasu, Ramona-Camelia Anculia and Elena-Gabriela Strete
Biomolecules 2025, 15(4), 502; https://doi.org/10.3390/biom15040502 - 30 Mar 2025
Viewed by 1776
Abstract
Depression is a multifactorial psychiatric condition with complex pathophysiology, increasingly linked to neuroinflammatory processes. The present review explores the role of neuroinflammation in depression, focusing on glial cell activation, cytokine signaling, blood–brain barrier dysfunction, and disruptions in neurotransmitter systems. The article highlights how [...] Read more.
Depression is a multifactorial psychiatric condition with complex pathophysiology, increasingly linked to neuroinflammatory processes. The present review explores the role of neuroinflammation in depression, focusing on glial cell activation, cytokine signaling, blood–brain barrier dysfunction, and disruptions in neurotransmitter systems. The article highlights how inflammatory mediators influence brain regions implicated in mood regulation, such as the hippocampus, amygdala, and prefrontal cortex. The review further discusses the involvement of the hypothalamic–pituitary–adrenal (HPA) axis, oxidative stress, and the kynurenine pathway, providing mechanistic insights into how chronic inflammation may underlie emotional and cognitive symptoms of depression. The bidirectional relationship between inflammation and depressive symptoms is emphasized, along with the role of peripheral immune responses and systemic stress. By integrating molecular, cellular, and neuroendocrine perspectives, this review supports the growing field of immunopsychiatry and lays the foundation for novel diagnostic biomarkers and anti-inflammatory treatment approaches in depression. Further research in this field holds promise for developing more effective and personalized interventions for individuals suffering from depression. Full article
(This article belongs to the Special Issue Neuroimmune Interactions in Neuropsychiatric Diseases)
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