Cellular Mechanisms of Neuroinflammation

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

Deadline for manuscript submissions: closed (31 July 2021) | Viewed by 8681

Special Issue Editors

Department of Experimental and Clinical Medicine (DMSC), Anatomy Section, School of Human Health Sciences, University of Florence, Florence, Italy
Interests: neuropathic pain; blood–brain barrier; cadmium toxicity; neuroprotection
Special Issues, Collections and Topics in MDPI journals
Department of Experimental and Clinical Medicine, Anatomy Section, School of Human Health Sciences, University of Florence, 50121 Florence, Italy
Interests: blood–brain barrier; vitamin D; cadmium toxicity; cannabidiol; neuroprotection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

I am glad to announce the Special Issue titled “Cellular Mechanisms of Neuroinflammation” of the journal Cells.

Neuroinflammation is an inflammatory reaction within the central nervous system (CNS) that occurs in response to various pathological signals, such as traumatic brain injury, toxic molecules, and infections. This immune reaction is mediated by secreted chemical messengers, such as cytokines and chemokines, that are produced by resident CNS glia, namely, microglia and astrocytes. Microglia activation plays a fundamental role in triggering a signaling cascade that leads to the release of inflammatory mediators. This acute response to an initial pathological signal has a positive connotation, as it is adaptive and has a protective role for the organism. However, if these phenomenon becomes prolonged over time or even chronic, it assumes a detrimental significance, resulting in harmful outcomes for the nervous system. Although the role of microglia in the inflammatory response has been extensively studied, it has recently been shown that astrocytes, endowed of a neuroprotective physiological role, also play a key role in this mechanism. Indeed, the inflammatory stimulus induces an astrocyte reaction (that can also be directly set off by neurons), known as reactive astrogliosis, consisting of the unbalanced secretion of pro-inflammatory cytokines that exacerbate neuroinflammation.  The role attributed to CNS glial cells in triggering neuroinflammation parallels that of satellite cells and Schwann cells in the peripheral nervous system (PNS). After nerve injury, inflammatory mediators released from PNS glial cells and from infiltrated leukocytes give rise to a neuroinflammatory response that induces a central sensitization. The activation of microglia and astrocytes contributes to the development of a maladaptive response, triggering a perpetuation of several neurological disorders like painful neuropathies.

Another important structure whose alteration can cause neuroinflammation is the blood–brain barrier (BBB). Indeed, the alteration of this highly specialized structure made of microvascular endothelium, astrocytic end feet, and pericytes, stimulates or aggravates many pathologies of the brain, including neurodegenerative disorders such as Alzheimer’s and Parkinson’s diseases, amyotrophic lateral sclerosis, and multiple sclerosis. Finally, the importance of the complex interaction between the CNS and the enteric nervous system, named gut–brain axis, has recently emerged. The most important role in this interaction is played by the gut microbiota (GM), consisting of the bacteria, viruses, fungi, and protozoa that live symbiotically in the human gut. A close association was found between variation in GM composition and CNS disorders such as depression, anxiety, autism, as well as neurodegenerative diseases.

With this Special Issue, we aim to present the state of the art and novel data to increase our knowledge of the cellular mechanisms of neuroinflammation. We welcome experts in the field to contribute research papers and critical reviews on neuroinflammation signaling pathways. Also, a greater understanding of glial role, including epigenetic alterations that regulate their functions, could provide targets for neuroprotective therapies.

We are looking forward to your contributions to this Special Issue.

Dr. Alessandra Pacini
Dr. Jacopo Junio Valerio Branca
Guest Editors

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Keywords

  • neuroinflammation
  • neurodegenerative disorders
  • microglia activation
  • astrogliosis
  • blood-brain barrier
  • gut-brain axis
  • neuropathic pain
  • neuroprotection

Published Papers (2 papers)

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Research

18 pages, 4613 KiB  
Article
Roles of Crosstalk between Astrocytes and Microglia in Triggering Neuroinflammation and Brain Edema Formation in 1,2-Dichloroethane-Intoxicated Mice
by Jinhan Yang, Tong Wang, Xiaoxia Jin, Gaoyang Wang, Fenghong Zhao and Yaping Jin
Cells 2021, 10(10), 2647; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10102647 - 03 Oct 2021
Cited by 16 | Viewed by 4567
Abstract
We have previously reported that the activation of astrocytes and microglia may lead to the overproduction of proinflammatory mediators, which could induce neuroinflammation and cause brain edema in 1,2-dichloroethane (1,2-DCE)-intoxicated mice. In this research, we further hypothesized that astrocyte–microglia crosstalk might trigger neuroinflammation [...] Read more.
We have previously reported that the activation of astrocytes and microglia may lead to the overproduction of proinflammatory mediators, which could induce neuroinflammation and cause brain edema in 1,2-dichloroethane (1,2-DCE)-intoxicated mice. In this research, we further hypothesized that astrocyte–microglia crosstalk might trigger neuroinflammation and contribute to brain edema in 1,2-DCE-intoxicated mice. The present research revealed, for the first time, that subacute intoxication with 1,2-DCE might provoke the proinflammatory polarization of microglia, and pretreatment with minocycline, a specific inhibitor of microglial activation, may attenuate the enhanced protein levels of ionized calcium-binding adapter molecule1 (Iba-1), cluster of differentiation 11b (CD11b), glial fibrillary acidic protein (GFAP), soluble calcium-binding protein 100B (S100B), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase-9 (MMP-9), Toll-like receptor 4 (TLR4), MyD88, and p-p65, and ameliorate the suppressed protein expression levels of occludin and claudin 5; we also observed changes in water content and made pathological observations on edema in the brains of 1,2-DCE-intoxicated mice. Moreover, pretreatment with fluorocitrate, an inhibitor of reactive astrocytes, could also reverse the alteration in protein expression levels of GFAP, S100B, Iba-1, CD11b, TNF-α, IL-6, iNOS, VCAM-1, ICAM-1, MMP-9, occludin, and claudin 5 in the brain of 1,2-DCE intoxicated mice. Furthermore, pretreatment with melatonin, a well-known anti-inflammatory drug, could also attenuate the above-mentioned changes in the brains of 1,2-DCE-intoxicated mice. Altogether, the findings from this research indicated that microglial activation might play an important role in triggering neuroinflammation, and hence may contribute to brain edema formation; additionally, the findings suggested that molecular crosstalk between reactive astrocytes and activated microglia may amplify the neuroinflammatory reaction, which could induce secondary brain injury in 1,2-DCE-intoxicated mice. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Neuroinflammation)
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17 pages, 5973 KiB  
Article
Neuropathology and Inflammatory Cell Characterization in 10 Autoptic COVID-19 Brains
by Daniele Colombo, Laura Falasca, Luisa Marchioni, Antonella Tammaro, Ganiyat Adenike Ralitsa Adebanjo, Giuseppe Ippolito, Alimuddin Zumla, Mauro Piacentini, Roberta Nardacci and Franca Del Nonno
Cells 2021, 10(9), 2262; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10092262 - 31 Aug 2021
Cited by 33 | Viewed by 3140
Abstract
COVID-19 presents with a wide range of clinical neurological manifestations. It has been recognized that SARS-CoV-2 infection affects both the central and peripheral nervous system, leading to smell and taste disturbances; acute ischemic and hemorrhagic cerebrovascular disease; encephalopathies and seizures; and causes most [...] Read more.
COVID-19 presents with a wide range of clinical neurological manifestations. It has been recognized that SARS-CoV-2 infection affects both the central and peripheral nervous system, leading to smell and taste disturbances; acute ischemic and hemorrhagic cerebrovascular disease; encephalopathies and seizures; and causes most surviving patients to have long lasting neurological symptoms. Despite this, typical neuropathological features associated with the infection have still not been identified. Studies of post-mortem examinations of the cerebral cortex are obtained with difficulty due to laboratory safety concerns. In addition, they represent cases with different neurological symptoms, age or comorbidities, thus a larger number of brain autoptic data from multiple institutions would be crucial. Histopathological findings described here are aimed to increase the current knowledge on neuropathology of COVID-19 patients. We report post-mortem neuropathological findings of ten COVID-19 patients. A wide range of neuropathological lesions were seen. The cerebral cortex of all patients showed vascular changes, hyperemia of the meninges and perivascular inflammation in the cerebral parenchyma with hypoxic neuronal injury. Perivascular lymphocytic inflammation of predominantly CD8-positive T cells mixed with CD68-positive macrophages, targeting the disrupted vascular wall in the cerebral cortex, cerebellum and pons were seen. Our findings support recent reports highlighting a role of microvascular injury in COVID-19 neurological manifestations. Full article
(This article belongs to the Special Issue Cellular Mechanisms of Neuroinflammation)
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