Metabolic Modulation of Inflammasome and Reactive Gliosis in Central Nervous System

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

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 6667

Special Issue Editor


E-Mail Website
Guest Editor
Division of Human Anatomy-Neuronal Networks Morphology and Systems Biology Lab, Department of Mental, Physical Health and Preventive Medicine University of Campania “Luigi Vanvitelli”, 80138 Naples, Italy
Interests: maladaptive synaptic plasticity; reactive gliosis; neuroinflammation; spinal cord; non-invasive stimulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation of the central nervous system (CNS) is a primer of normal brain aging and many neurological disorders, including neurodegenerative disease and chronic pain states. It is well known that activation of glial cells, paralleled by energetic failure and ROS production, is a key part of the inflammatory process, boosting maladaptive synaptic changes and also cell death; however, metabolic control of inflammasome through glucose and lipid metabolism in CNS is essential for maintaining homeostasis and neural function in health and disease. To sustain neuronal function, activated glial cells undergo metabolic reprogramming (from glucose to the lipidic metabolism) that activates Toll-like receptor-4 (TLR4), caspases, NLPR1-3, sustaining neuroinflammation and leading to cell death. Therefore, it is conceivable that the overall metabolic state influences brain function and represents a new putative target for preserving long-term brain wellness and preventing neurodegenerative disorders.

Dr. Giovanni Cirillo
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

  • lipid rafts
  • glucidic metabolism
  • neuroinflammation
  • reactive gliosis
  • maladaptive plasticity

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

22 pages, 4547 KiB  
Article
Cognitive Performance during the Development of Diabetes in the Zucker Diabetic Fatty Rat
by Marcia Spoelder, Yami Bright, Martine C. Morrison, Veerle van Kempen, Lilian de Groodt, Malvina Begalli, Nikita Schuijt, Eva Kruiger, Ronald Bulthuis, Gabriele Gross, Robert Kleemann, Janna A. van Diepen and Judith R. Homberg
Cells 2023, 12(20), 2463; https://doi.org/10.3390/cells12202463 - 16 Oct 2023
Viewed by 1160
Abstract
Increased insulin levels may support the development of neural circuits involved in cognition, while chronic mild inflammation may also result in cognitive impairment. This study aimed to gain more insight into whether cognition is already impacted during adolescence in a genetic rat model [...] Read more.
Increased insulin levels may support the development of neural circuits involved in cognition, while chronic mild inflammation may also result in cognitive impairment. This study aimed to gain more insight into whether cognition is already impacted during adolescence in a genetic rat model for obesity and type 2 diabetes. Visual discrimination learning throughout adolescence and the level of motivation during early adulthood were investigated in Zucker Diabetic Fatty (ZDF) obese and ZDF lean rats using operant touchscreens. Blood glucose, insulin, and lipids were longitudinally analyzed. Histological analyses were performed in the liver, white adipose tissues, and the prefrontal cortex. Prior to the experiments with the genetic ZDF research model, all experimental assays were performed in two groups of outbred Long Evans rats to investigate the effect of different feeding circumstances. Adolescent ZDF obese rats outperformed ZDF lean rats on visual discrimination performance. During the longitudinal cognitive testing period, insulin levels sharply increased over weeks in ZDF obese rats and were significantly enhanced from 6 weeks of age onwards. Early signs of liver steatosis and enlarged adipocytes in white adipose tissue were observed in early adult ZDF obese rats. Histological analyses in early adulthood showed no group differences in the number of prefrontal cortex neurons and microglia, nor PSD95 and SIRT1 mRNA expression levels. Together, our data show that adolescent ZDF obese rats even display enhanced cognition despite their early diabetic profile. Full article
Show Figures

Figure 1

Review

Jump to: Research

24 pages, 3670 KiB  
Review
Vagus Nerve Stimulation: A Personalized Therapeutic Approach for Crohn’s and Other Inflammatory Bowel Diseases
by Giovanni Cirillo, Flor Negrete-Diaz, Daniela Yucuma, Assunta Virtuoso, Sohaib Ali Korai, Ciro De Luca, Eugenijus Kaniusas, Michele Papa and Fivos Panetsos
Cells 2022, 11(24), 4103; https://doi.org/10.3390/cells11244103 - 17 Dec 2022
Cited by 11 | Viewed by 5024
Abstract
Inflammatory bowel diseases, including Crohn’s disease and ulcerative colitis, are incurable autoimmune diseases characterized by chronic inflammation of the gastrointestinal tract. There is increasing evidence that inappropriate interaction between the enteric nervous system and central nervous system and/or low activity of the vagus [...] Read more.
Inflammatory bowel diseases, including Crohn’s disease and ulcerative colitis, are incurable autoimmune diseases characterized by chronic inflammation of the gastrointestinal tract. There is increasing evidence that inappropriate interaction between the enteric nervous system and central nervous system and/or low activity of the vagus nerve, which connects the enteric and central nervous systems, could play a crucial role in their pathogenesis. Therefore, it has been suggested that appropriate neuroprosthetic stimulation of the vagus nerve could lead to the modulation of the inflammation of the gastrointestinal tract and consequent long-term control of these autoimmune diseases. In the present paper, we provide a comprehensive overview of (1) the cellular and molecular bases of the immune system, (2) the way central and enteric nervous systems interact and contribute to the immune responses, (3) the pathogenesis of the inflammatory bowel disease, and (4) the therapeutic use of vagus nerve stimulation, and in particular, the transcutaneous stimulation of the auricular branch of the vagus nerve. Then, we expose the working hypotheses for the modulation of the molecular processes that are responsible for intestinal inflammation in autoimmune diseases and the way we could develop personalized neuroprosthetic therapeutic devices and procedures in favor of the patients. Full article
Show Figures

Figure 1

Back to TopTop