Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
6.0
Journals
Cells
Special Issues
Advances in Neuroinfections and Neuroimmunology
share announcement

Advances in Neuroinfections and Neuroimmunology

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 9344

Special Issue Editor

Prof. Dr. Lars Ove Brandenburg

E-Mail Website
Guest Editor
1. Institute of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany
2. Department of Anatomy and Cell Biology, RWTH Aachen University, 52062 Aachen, Germany
Interests: neuroinflammation; neurodegeneration; bacterial meningitis; antimicrobial peptides; Alzheimer’s disease; multiple sclerosis; glia cells; pattern recognition receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,  

The central nervous system (CNS) is protected from the environment by the skull, the meninges, the blood–brain barrier, and the innate immune system. Pathogens have developed mechanisms to pass these barriers and enter the CNS while the human organism tries to prevent this. Once pathogens have entered the brain, they cause serious damage that often leads to death despite rapid antibiotic therapy. Despite much progress in recent decades in the prevention of infectious diseases with the help of vaccines and the development of effective antibiotic agents, neurological infections remain the main cause of permanent neurological damage worldwide. Recent studies show that the control of the inflammatory response plays an important role, and the prevention of an excessive inflammatory response seems to be an important approach in the treatment of such CNS infections. This Special Issue seeks reviews and original papers covering a wide range of hot topics related to new studies around neuroinfections and neuroimmunology, to understand the interactions between the invaders and the body’s defense mechanisms, the importance of the inflammatory response for the progression of diseases, and current developments of new forms of therapy for neuroimmunological diseases. 

Dr. Lars Ove Brandenburg
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. Cells is an international peer-reviewed open access semimonthly 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

  • central nervous system
  • brain
  • inflammation
  • infection
  • neuroimmunology
  • neuroinflammation
  • innate immunity
  • specific immunity
  • blood–brain barrier

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

15 pages, 5063 KiB  
Article
Antibody Properties Associate with Clinical Phenotype in LGI1 Encephalitis
by Susann Ludewig, Leonie Salzburger, Alexander Goihl, Jana Rohne, Frank Leypoldt, Daniel Bittner, Emrah Düzel, Burkhart Schraven, Dirk Reinhold, Martin Korte and Péter Körtvélyessy
Cells 2023, 12(2), 282; https://doi.org/10.3390/cells12020282 - 11 Jan 2023
Cited by 2 | Viewed by 1900
Abstract
Autoimmune encephalitis (AE) associated with autoantibodies against leucine-rich glioma-inactivated protein-1 (LGI1) can present with faciobrachial dystonic seizures (FBDS) and/or limbic encephalitis (LE). The reasons for this heterogeneity in phenotypes are unclear. We performed autoantibody (abs) characterization per patient, two patients suffering from LE [...] Read more.
Autoimmune encephalitis (AE) associated with autoantibodies against leucine-rich glioma-inactivated protein-1 (LGI1) can present with faciobrachial dystonic seizures (FBDS) and/or limbic encephalitis (LE). The reasons for this heterogeneity in phenotypes are unclear. We performed autoantibody (abs) characterization per patient, two patients suffering from LE and two from FBDS, using isolated antibodies specified with single amino acid epitope mapping. Electrophysiological slice recordings were conducted alongside spine density measurements, postsynaptic Alpha-amino-3-hydoxy-5-methyl-4-isoaxole-proprionate-receptors (AMPA-R) and N-methyl-D-aspartate-receptors receptor (NMDA-R) cluster counting. These results were correlated with the symptoms of each patient. While LGI1 abs from LE patients mainly interacted with the Leucine-rich repeat section of LGI1, abs from both FBDS patients also recognized the Epitempin section as well. Six-hour incubation of mouse hippocampal slices with LE patients autoantibodies but not from the FBDS patients resulted in a significant decline in long-term potentiation (p = 0.0015) or short-term plasticity at CA3-CA1 neurons and in decreased hippocampal synaptic density. Cluster differentiation showed no decrease in postsynaptic AMPA-R and NMDA-R. LGI1 autoantibodies selected by phenotype show an almost distinct epitope pattern, elicit disparate functional effects on hippocampal neurons, and cause divergent effects on spine density. This data illuminates potential pathomechanisms for disease heterogeneity in LGI1 AE. Full article
(This article belongs to the Special Issue Advances in Neuroinfections and Neuroimmunology)
►▼ Show Figures

Figure 1

13 pages, 3390 KiB  
Article
Regulatory T-Cells Suppress Cytotoxic T Lymphocyte Responses against Microglia
by Priyanka Chauhan, Shuxian Hu, Wen S. Sheng and James R. Lokensgard
Cells 2022, 11(18), 2826; https://doi.org/10.3390/cells11182826 - 09 Sep 2022
Cited by 1 | Viewed by 2081
Abstract
Regulatory T-cells (Tregs) play pivotal roles during infection, cancer, and autoimmunity. In our previous study, we demonstrated a role for the PD-1:PD-L1 pathway in controlling cytolytic responses of CD8+ T lymphocytes against microglial cells presenting viral peptides. In this study, we investigated [...] Read more.
Regulatory T-cells (Tregs) play pivotal roles during infection, cancer, and autoimmunity. In our previous study, we demonstrated a role for the PD-1:PD-L1 pathway in controlling cytolytic responses of CD8+ T lymphocytes against microglial cells presenting viral peptides. In this study, we investigated the role of Tregs in suppressing CD8+ T-cell-mediated cytotoxicity against primary microglial cells. Using in vitro cytotoxicity assays and flow cytometry, we demonstrated a role for Tregs in suppressing antigen-specific cytotoxic T-lymphocyte (CTL) responses against microglia loaded with a model peptide (SIINFEKL). We went on to show a significant decrease in the frequency of IFN-γ- and TNF-producing CD8+ T-cells when cultured with Tregs. Interestingly, a significant increase in the frequency of granzyme B- and Ki67-producing CTLs was observed. We also observed a significant decrease in the production of interleukin (IL)-6 by microglia. On further investigation, we found that Tregs significantly reduced MHC class 1 (MHC-1) expression on IFN-γ-treated microglial cells. Taken together, these studies demonstrate an immunosuppressive role for Tregs on CTL responses generated against primary microglia. Hence, modulation of Treg cell activity in combination with negative immune checkpoint blockade may stimulate anti-viral T-cell responses to more efficiently clear viral infection from microglial cell reservoirs. Full article
(This article belongs to the Special Issue Advances in Neuroinfections and Neuroimmunology)
►▼ Show Figures

Figure 1

22 pages, 2587 KiB  
Article
Serum Cytokines Predict Neurological Damage in Genetically Diverse Mouse Models
by Aracely A. Pérez Gómez, Moumita Karmakar, Raymond J. Carroll, Koedi S. Lawley, Katia Amstalden, Colin R. Young, David W. Threadgill, C. Jane Welsh and Candice Brinkmeyer-Langford
Cells 2022, 11(13), 2044; https://doi.org/10.3390/cells11132044 - 28 Jun 2022
Cited by 2 | Viewed by 1872
Abstract
Viral infections contribute to neurological and immunological dysfunction driven by complex genetic networks. Theiler’s murine encephalomyelitis virus (TMEV) causes neurological dysfunction in mice and can model human outcomes to viral infections. Here, we used genetically distinct mice from five Collaborative Cross mouse strains [...] Read more.
Viral infections contribute to neurological and immunological dysfunction driven by complex genetic networks. Theiler’s murine encephalomyelitis virus (TMEV) causes neurological dysfunction in mice and can model human outcomes to viral infections. Here, we used genetically distinct mice from five Collaborative Cross mouse strains and C57BL/6J to demonstrate how TMEV-induced immune responses in serum may predict neurological outcomes in acute infection. To test the hypothesis that serum cytokine levels can provide biomarkers for phenotypic outcomes of acute disease, we compared cytokine levels at pre-injection, 4 days post-injection (d.p.i.), and 14 d.p.i. Each strain produced unique baseline cytokine levels and had distinct immune responses to the injection procedure itself. Thus, we eliminated the baseline responses to the injection procedure itself and identified cytokines and chemokines induced specifically by TMEV infection. Then, we identified strain-specific longitudinal cytokine profiles in serum during acute disease. Using stepwise regression analysis, we identified serum immune markers predictive for TMEV-induced neurological phenotypes of the acute phase, e.g., IL-9 for limb paralysis; and TNF-α, IL-1β, and MIP-1β for limb weakness. These findings indicate how temporal differences in immune responses are influenced by host genetic background and demonstrate the potential of serum biomarkers to track the neurological effects of viral infection. Full article
(This article belongs to the Special Issue Advances in Neuroinfections and Neuroimmunology)
►▼ Show Figures

Figure 1

Review

Jump to: Research

31 pages, 2166 KiB  
Review
Drosophila as a Model for Human Viral Neuroinfections
by Ilena Benoit, Domenico Di Curzio, Alberto Civetta and Renée N. Douville
Cells 2022, 11(17), 2685; https://doi.org/10.3390/cells11172685 - 29 Aug 2022
Cited by 2 | Viewed by 2585
Abstract
The study of human neurological infection faces many technical and ethical challenges. While not as common as mammalian models, the use of Drosophila (fruit fly) in the investigation of virus–host dynamics is a powerful research tool. In this review, we focus on the [...] Read more.
The study of human neurological infection faces many technical and ethical challenges. While not as common as mammalian models, the use of Drosophila (fruit fly) in the investigation of virus–host dynamics is a powerful research tool. In this review, we focus on the benefits and caveats of using Drosophila as a model for neurological infections and neuroimmunity. Through the examination of in vitro, in vivo and transgenic systems, we highlight select examples to illustrate the use of flies for the study of exogenous and endogenous viruses associated with neurological disease. In each case, phenotypes in Drosophila are compared to those in human conditions. In addition, we discuss antiviral drug screening in flies and how investigating virus–host interactions may lead to novel antiviral drug targets. Together, we highlight standardized and reproducible readouts of fly behaviour, motor function and neurodegeneration that permit an accurate assessment of neurological outcomes for the study of viral infection in fly models. Adoption of Drosophila as a valuable model system for neurological infections has and will continue to guide the discovery of many novel virus–host interactions. Full article
(This article belongs to the Special Issue Advances in Neuroinfections and Neuroimmunology)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop