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The Role of Neuroimmune Inflammation in Chemotherapy-Induced Side Effects
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The Role of Neuroimmune Inflammation in Chemotherapy-Induced Side Effects

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

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 5057

Special Issue Editors

Dr. Silvia Franchi

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Guest Editor
Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milano, Italy
Interests: pain; cytokines; neuroinflammation; mood
Special Issues, Collections and Topics in MDPI journals
Dr. Lorenzo Di Cesare Mannelli

E-Mail Website
Guest Editor
Department of Neuroscience, Psychology, Drug Research and Child Health (NEUROFARBA), Pharmacology and Toxicology Section, University of Florence, 50139 Florence, Italy
Interests: pharmacology; medicinal plants; chronic pain; nervous system pathologies and treatment; glia; cholinergic receptors; opioid receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Chemotherapy has increased the survival rate in cancer patients; however, despite the undisputed benefits, antitumoral drugs cause a wide range of known and little-known side effects, such as chemotherapy-induced neuropathy (CIN), chemotherapy-induced cognitive impairment (CICI), and the development of mood alterations such as anxiety and depression. All of these complications seem to be independent of the antitumoral effect, are also common to newer antitumoral molecules, and are often connected to and dependent on each other. Emerging evidence indicates that neuroimmune inflammation at the peripheral and central nervous system level plays a pivotal role in the development of such complications. Infiltrated and resident immune cells or glial cells interact with the neuronal component, promoting a sensitization process and maladaptive plasticity that contribute to the progression of damage and finally result in clinical complications. In this scenario, both classic and newer biomolecules could represent novel pharmacological targets to counteract the development of chemotherapy-induced side effects but could also represent potential biomarkers to predict them.This Special Issue aims to collect recent findings regarding the role of neuroimmune inflammation in chemotherapy-induced side effects, identifying mechanisms and novel controlling networks or suggesting new potential pharmacological approaches to counteract or predict them.

Prof. Dr. Silvia Franchi
Prof. Dr. Lorenzo Di Cesare Mannelli
Guest Editors

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Keywords

  • neuroimmune inflammation
  • chemotherapy-induced side effects
  • neuropathy
  • chemobrain
  • mood
  • cytokines
  • chemokines
  • glia

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Published Papers (2 papers)

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Research

11 pages, 869 KiB  
Article
Interplay between Prokineticins and Histone Demethylase KDM6A in a Murine Model of Bortezomib-Induced Neuropathy
by Laura Rullo, Silvia Franchi, Giada Amodeo, Francesca Felicia Caputi, Benedetta Verduci, Loredana Maria Losapio, Paola Sacerdote, Patrizia Romualdi and Sanzio Candeletti
Int. J. Mol. Sci. 2021, 22(21), 11913; https://doi.org/10.3390/ijms222111913 - 3 Nov 2021
Cited by 9 | Viewed by 2195
Abstract
Chemotherapy-induced neuropathy (CIN) is a major adverse effect associated with many chemotherapeutics, including bortezomib (BTZ). Several mechanisms are involved in CIN, and recently a role has been proposed for prokineticins (PKs), a chemokine family that induces proinflammatory/pro-algogen mediator release and drives the epigenetic [...] Read more.
Chemotherapy-induced neuropathy (CIN) is a major adverse effect associated with many chemotherapeutics, including bortezomib (BTZ). Several mechanisms are involved in CIN, and recently a role has been proposed for prokineticins (PKs), a chemokine family that induces proinflammatory/pro-algogen mediator release and drives the epigenetic control of genes involved in cellular differentiation. The present study evaluated the relationships between epigenetic mechanisms and PKs in a mice model of BTZ-induced painful neuropathy. To this end, spinal cord alterations of histone demethylase KDM6A, nuclear receptors PPARα/PPARγ, PK2, and pro-inflammatory cytokines IL-6 and IL-1β were assessed in neuropathic mice treated with the PK receptors (PKRs) antagonist PC1. BTZ treatment promoted a precocious upregulation of KDM6A, PPARs, and IL-6, and a delayed increase of PK2 and IL-1β. PC1 counteracted allodynia and prevented the increase of PK2 and of IL-1β in BTZ neuropathic mice. The blockade of PKRs signaling also opposed to KDM6A increase and induced an upregulation of PPAR gene transcription. These data showed the involvement of epigenetic modulatory enzymes in spinal tissue phenomena associated with BTZ painful neuropathy and underline a role of PKs in sustaining the increase of proinflammatory cytokines and in exerting an inhibitory control on the expression of PPARs through the regulation of KDM6A gene expression in the spinal cord. Full article
(This article belongs to the Special Issue The Role of Neuroimmune Inflammation in Chemotherapy-Induced Side Effects)
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17 pages, 3850 KiB  
Article
The Antagonism of the Prokineticin System Counteracts Bortezomib Induced Side Effects: Focus on Mood Alterations
by Giada Amodeo, Benedetta Verduci, Patrizia Sartori, Patrizia Procacci, Vincenzo Conte, Gianfranco Balboni, Paola Sacerdote and Silvia Franchi
Int. J. Mol. Sci. 2021, 22(19), 10256; https://doi.org/10.3390/ijms221910256 - 23 Sep 2021
Cited by 8 | Viewed by 2194
Abstract
The development of neuropathy and of mood alterations is frequent after chemotherapy. These complications, independent from the antitumoral mechanism, are interconnected due to an overlapping in their processing pathways and a common neuroinflammatory condition. This study aims to verify whether in mice the [...] Read more.
The development of neuropathy and of mood alterations is frequent after chemotherapy. These complications, independent from the antitumoral mechanism, are interconnected due to an overlapping in their processing pathways and a common neuroinflammatory condition. This study aims to verify whether in mice the treatment with the proteasome inhibitor bortezomib (BTZ), at a protocol capable of inducing painful neuropathy, is associated with anxiety, depression and supraspinal neuroinflammation. We also verify if the therapeutic treatment with the antagonist of the prokineticin (PK) system PC1, which is known to contrast pain and neuroinflammation, can prevent mood alterations. Mice were treated with BTZ (0.4 mg/kg three times/week for 4 weeks); mechanical allodynia and locomotor activity were evaluated over time while anxiety (dark light and marble burying test), depression (sucrose preference and swimming test) and supraspinal neuroinflammation were checked at the end of the protocol. BTZ treated neuropathic mice develop anxiety and depression. The presence of mood alterations is related to the presence of neuroinflammation and PK system activation in prefrontal cortex, hippocampus and hypothalamus with high levels of PK2 and PKR2 receptor, IL-6 and TNF-α, TLR4 and an upregulation of glial markers. PC1 treatment, counteracting pain, prevented the development of supraspinal inflammation and depression-like behavior in BTZ mice. Full article
(This article belongs to the Special Issue The Role of Neuroimmune Inflammation in Chemotherapy-Induced Side Effects)
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