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Immune Mediators and Disruptors of Neural Functions

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 16812

Special Issue Editor

Special Issue Information

While inflammation is considered a threat to nervous system integrity, increasing evidence indicates that a large range of immune molecules behave as mediators of neural functions. A still underestimated number of cytokines and chemokines modulate neuronal and glial functions in the normal nervous system. Similarly, increasing evidence indicates that naturally occurring autoantibodies directed against neural antigens may be involved in maintenance functions and the prevention of neurodegenerative processes. It is thus of major importance to determine if and how such immune mediators may become immune disruptors of neural functions under pathological conditions. This Special Issue is aimed at providing a global and updated view on such a duality of immune molecules, under physiological or pathological conditions. Only the crossing of knowledge and mutual feeding of distinct research fields (physiology, development, cognitive neurosciences, pathology) may allow uncovering new neuroimmune mechanisms and designing new therapeutic strategies for neurological diseases. Research works based on cellular or in vivo experimental approaches are welcome. Bioinformatics and data mining studies are acceptable, however, ad hoc systems biology methods should be applied and explored data should rely on experimental biology approaches. Pure simulation studies will not be considered.

Prof. Serge Nataf
Guest Editor

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Keywords

  • glial cells
  • neurons
  • cytokines
  • chemokines
  • autoantibodies
  • pathology
  • physiology
  • systems biology

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Published Papers (3 papers)

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Research

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16 pages, 1072 KiB  
Article
Molecular Insights into SARS-CoV2-Induced Alterations of the Gut/Brain Axis
by Serge Nataf and Laurent Pays
Int. J. Mol. Sci. 2021, 22(19), 10440; https://doi.org/10.3390/ijms221910440 - 28 Sep 2021
Cited by 21 | Viewed by 4941
Abstract
For a yet unknown reason, a substantial share of patients suffering from COVID-19 develop long-lasting neuropsychiatric symptoms ranging from cognitive deficits to mood disorders and/or an extreme fatigue. We previously reported that in non-neural cells, angiotensin-1 converting enzyme 2 (ACE2), the [...] Read more.
For a yet unknown reason, a substantial share of patients suffering from COVID-19 develop long-lasting neuropsychiatric symptoms ranging from cognitive deficits to mood disorders and/or an extreme fatigue. We previously reported that in non-neural cells, angiotensin-1 converting enzyme 2 (ACE2), the gene coding for the SARS-CoV2 host receptor, harbors tight co-expression links with dopa-decarboxylase (DDC), an enzyme involved in the metabolism of dopamine. Here, we mined and integrated data from distinct human expression atlases and found that, among a wide range of tissues and cells, enterocytes of the small intestine express the highest expression levels of ACE2, DDC and several key genes supporting the metabolism of neurotransmitters. Based on these results, we performed co-expression analyses on a recently published set of RNA-seq data obtained from SARS-CoV2-infected human intestinal organoids. We observed that in SARS-CoV2-infected enterocytes, ACE2 co-regulates not only with DDC but also with a specific group of genes involved in (i) the dopamine/trace amines metabolic pathway, (ii) the absorption of microbiota-derived L-DOPA and (iii) the absorption of neutral amino acids serving as precursors to neurotransmitters. We conclude that in patients with long COVID, a chronic infection and inflammation of small intestine enterocytes might be indirectly responsible for prolonged brain alterations. Full article
(This article belongs to the Special Issue Immune Mediators and Disruptors of Neural Functions)
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Review

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27 pages, 2120 KiB  
Review
The Importance of CXCL1 in Physiology and Noncancerous Diseases of Bone, Bone Marrow, Muscle and the Nervous System
by Jan Korbecki, Magdalena Gąssowska-Dobrowolska, Jerzy Wójcik, Iwona Szatkowska, Katarzyna Barczak, Mikołaj Chlubek and Irena Baranowska-Bosiacka
Int. J. Mol. Sci. 2022, 23(8), 4205; https://doi.org/10.3390/ijms23084205 - 11 Apr 2022
Cited by 28 | Viewed by 7528
Abstract
This review describes the role of CXCL1, a chemokine crucial in inflammation as a chemoattractant for neutrophils, in physiology and in selected major non-cancer diseases. Due to the vast amount of available information, we focus on the role CXCL1 plays in the physiology [...] Read more.
This review describes the role of CXCL1, a chemokine crucial in inflammation as a chemoattractant for neutrophils, in physiology and in selected major non-cancer diseases. Due to the vast amount of available information, we focus on the role CXCL1 plays in the physiology of bones, bone marrow, muscle and the nervous system. For this reason, we describe its effects on hematopoietic stem cells, myoblasts, oligodendrocyte progenitors and osteoclast precursors. We also present the involvement of CXCL1 in diseases of selected tissues and organs including Alzheimer’s disease, epilepsy, herpes simplex virus type 1 (HSV-1) encephalitis, ischemic stroke, major depression, multiple sclerosis, neuromyelitis optica, neuropathic pain, osteoporosis, prion diseases, rheumatoid arthritis, tick-borne encephalitis (TBE), traumatic spinal cord injury and West Nile fever. Full article
(This article belongs to the Special Issue Immune Mediators and Disruptors of Neural Functions)
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16 pages, 1745 KiB  
Review
Connections between Immune-Derived Mediators and Sensory Nerves for Itch Sensation
by Sumika Toyama, Mitsutoshi Tominaga and Kenji Takamori
Int. J. Mol. Sci. 2021, 22(22), 12365; https://doi.org/10.3390/ijms222212365 - 16 Nov 2021
Cited by 11 | Viewed by 3634
Abstract
Although histamine is a well-known itch mediator, histamine H1-receptor blockers often lack efficacy in chronic itch. Recent molecular and cellular based studies have shown that non-histaminergic mediators, such as proteases, neuropeptides and cytokines, along with their cognate receptors, are involved in [...] Read more.
Although histamine is a well-known itch mediator, histamine H1-receptor blockers often lack efficacy in chronic itch. Recent molecular and cellular based studies have shown that non-histaminergic mediators, such as proteases, neuropeptides and cytokines, along with their cognate receptors, are involved in evocation and modulation of itch sensation. Many of these molecules are produced and secreted by immune cells, which act on sensory nerve fibers distributed in the skin to cause itching and sensitization. This understanding of the connections between immune cell-derived mediators and sensory nerve fibers has led to the development of new treatments for itch. This review summarizes current knowledge of immune cell-derived itch mediators and neuronal response mechanisms, and discusses therapeutic agents that target these systems. Full article
(This article belongs to the Special Issue Immune Mediators and Disruptors of Neural Functions)
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