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Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0
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Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0

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

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1387

Special Issue Editors

Prof. Dr. Zsuzsanna Helyes

E-Mail Website
Guest Editor
Department of Pharmacology and Pharmacotherapy, Medical School & Szentagothai Research Centre, University of Pecs, H-7624 Pécs, Hungary
Interests: neuropharmacology; sensory nervous system; pain; inflammation; sensory-vascular-immune interactions; neuropathy; migraine; arthritis; TRP channels; neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Szőke Éva

E-Mail Website
Guest Editor
Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, H-7624 Pécs, Hungary
Interests: neuropharmacology; capsaicin; TRP channels; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Capsaicin-sensitive peptidergic sensory nerves do not only transfer sensation and pain into the central nervous system (afferent function), but they also exert important efferent functions. They play complex regulatory roles in a broad range of inflammatory and pain conditions, such as arthritis/osteoarthritis, gastrointestinal diseases (irritable and inflammatory bowel diseases), neuropathic pain, and migraine. Several pro- and anti-inflammatory neuropeptides and other mediators (tachykinins, calcitonin gene-related peptide, pituitary adenylate cyclase-activating polypeptide, somatostatin, and purines) are released in response to their activation. Their balance and functions on immune cells and vessels determine the overall role of these nerves in different pathophysiological conditions related to unmet medical need diseases. Furthermore, inflammatory cell-derived mediators act back on these nerves to induce activation or inhibition. Exploring the molecular mechanisms of the complex sensory–immune–vascular interactions and identifying key targets can open promising novel anti-inflammatory and analgesic dug developmental perspectives.

Prof. Dr. Zsuzsanna Helyes
Dr. Szőke Éva
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • sensory neuropeptides
  • inflammation
  • neurogenic inflammation
  • pain
  • arthritis
  • colitis
  • neuropathy
  • migraine
  • novel drug targets
  • TRP channels
  • neuroinflammation

Related Special Issues

Published Papers (2 papers)

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Research

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13 pages, 816 KiB  
Article
Anti-Nociceptive Effects of Sphingomyelinase and Methyl-Beta-Cyclodextrin in the Icilin-Induced Mouse Pain Model
by Ádám Horváth, Anita Steib, Andrea Nehr-Majoros, Boglárka Kántás, Ágnes Király, Márk Racskó, Balázs István Tóth, Eszter Szánti-Pintér, Eva Kudová, Rita Skoda-Földes, Zsuzsanna Helyes and Éva Szőke
Int. J. Mol. Sci. 2024, 25(9), 4637; https://doi.org/10.3390/ijms25094637 - 24 Apr 2024
Viewed by 201
Abstract
The thermo- and pain-sensitive Transient Receptor Potential Melastatin 3 and 8 (TRPM3 and TRPM8) ion channels are functionally associated in the lipid rafts of the plasma membrane. We have already described that cholesterol and sphingomyelin depletion, or inhibition of sphingolipid biosynthesis decreased the [...] Read more.
The thermo- and pain-sensitive Transient Receptor Potential Melastatin 3 and 8 (TRPM3 and TRPM8) ion channels are functionally associated in the lipid rafts of the plasma membrane. We have already described that cholesterol and sphingomyelin depletion, or inhibition of sphingolipid biosynthesis decreased the TRPM8 but not the TRPM3 channel opening on cultured sensory neurons. We aimed to test the effects of lipid raft disruptors on channel activation on TRPM3- and TRPM8-expressing HEK293T cells in vitro, as well as their potential analgesic actions in TRPM3 and TRPM8 channel activation involving acute pain models in mice. CHO cell viability was examined after lipid raft disruptor treatments and their effects on channel activation on channel expressing HEK293T cells by measurement of cytoplasmic Ca2+ concentration were monitored. The effects of treatments were investigated in Pregnenolone-Sulphate-CIM-0216-evoked and icilin-induced acute nocifensive pain models in mice. Cholesterol depletion decreased CHO cell viability. Sphingomyelinase and methyl-beta-cyclodextrin reduced the duration of icilin-evoked nocifensive behavior, while lipid raft disruptors did not inhibit the activity of recombinant TRPM3 and TRPM8. We conclude that depletion of sphingomyelin or cholesterol from rafts can modulate the function of native TRPM8 receptors. Furthermore, sphingolipid cleavage provided superiority over cholesterol depletion, and this method can open novel possibilities in the management of different pain conditions. Full article
(This article belongs to the Special Issue Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0)

Review

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25 pages, 383 KiB  
Review
Exploring Localized Provoked Vulvodynia: Insights from Animal Model Research
by Yara Nakhleh-Francis, Yaseen Awad-Igbaria, Reem Sakas, Sarina Bang, Saher Abu-Ata, Eilam Palzur, Lior Lowenstein and Jacob Bornstein
Int. J. Mol. Sci. 2024, 25(8), 4261; https://doi.org/10.3390/ijms25084261 - 11 Apr 2024
Viewed by 842
Abstract
Provoked vulvodynia represents a challenging chronic pain condition, characterized by its multifactorial origins. The inherent complexities of human-based studies have necessitated the use of animal models to enrich our understanding of vulvodynia’s pathophysiology. This review aims to provide an exhaustive examination of the [...] Read more.
Provoked vulvodynia represents a challenging chronic pain condition, characterized by its multifactorial origins. The inherent complexities of human-based studies have necessitated the use of animal models to enrich our understanding of vulvodynia’s pathophysiology. This review aims to provide an exhaustive examination of the various animal models employed in this research domain. A comprehensive search was conducted on PubMed, utilizing keywords such as “vulvodynia”, “chronic vulvar pain”, “vulvodynia induction”, and “animal models of vulvodynia” to identify pertinent studies. The search yielded three primary animal models for vulvodynia: inflammation-induced, allergy-induced, and hormone-induced. Additionally, six agents capable of triggering the condition through diverse pathways were identified, including factors contributing to hyperinnervation, mast cell proliferation, involvement of other immune cells, inflammatory cytokines, and neurotransmitters. This review systematically outlines the various animal models developed to study the pathogenesis of provoked vulvodynia. Understanding these models is crucial for the exploration of preventative measures, the development of novel treatments, and the overall advancement of research within the field. Full article
(This article belongs to the Special Issue Molecular Links between Sensory Nerves, Inflammation, and Pain 3.0)
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