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Cells
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Pain, Itch and Sensory Nerve Endings
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Pain, Itch and Sensory Nerve Endings

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 (30 September 2021) | Viewed by 14550

Special Issue Editor

Prof. Dr. Laurent Misery

E-Mail Website
Guest Editor
1. Department of Dermatology, University Hospital of Brest, 29200 Brest, France
2. Laboratory of Neurosciences, University of Western Brittany, 29238 Brest, France
Interests: itch; pain; neurodermatology; psychodermatology; autoimmune diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pain and itch are very unpleasant sensations for patients. Fortunately, ongoing research provides new data to enhance our knowledge and address these issues as new results are followed by emerging treatments. Sensory neurons are the main cells involved in pain and itch. They can be studied using a large variety of approaches. This Special Issue will summarize the current knowledge on itch, pain, and sensory neurons through the publication of new original data in addition to presenting possible therapeutic perspectives.

Prof. Laurent Misery
Guest Editor

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Keywords

  • itch
  • pain
  • neuron
  • sensory
  • TRP

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Published Papers (4 papers)

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Research

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23 pages, 2466 KiB  
Article
Calcium Increase and Substance P Release Induced by the Neurotoxin Brevetoxin-1 in Sensory Neurons: Involvement of PAR2 Activation through Both Cathepsin S and Canonical Signaling
by Ophélie Pierre, Maxime Fouchard, Paul Buscaglia, Nelig Le Goux, Raphaël Leschiera, Olivier Mignen, Joachim W. Fluhr, Laurent Misery and Raphaële Le Garrec
Cells 2020, 9(12), 2704; https://doi.org/10.3390/cells9122704 - 17 Dec 2020
Cited by 4 | Viewed by 3179
Abstract
Red tides involving Karenia brevis expose humans to brevetoxins (PbTxs). Oral exposition triggers neurotoxic shellfish poisoning, whereas inhalation induces a respiratory syndrome and sensory disturbances. No curative treatment is available and the pathophysiology is not fully elucidated. Protease-activated receptor 2 (PAR2), cathepsin S [...] Read more.
Red tides involving Karenia brevis expose humans to brevetoxins (PbTxs). Oral exposition triggers neurotoxic shellfish poisoning, whereas inhalation induces a respiratory syndrome and sensory disturbances. No curative treatment is available and the pathophysiology is not fully elucidated. Protease-activated receptor 2 (PAR2), cathepsin S (Cat-S) and substance P (SP) release are crucial mediators of the sensory effects of ciguatoxins (CTXs) which are PbTx analogs. This work explored the role of PAR2 and Cat-S in PbTx-1-induced sensory effects and deciphered the signaling pathway involved. We performed calcium imaging, PAR2 immunolocalization and SP release experiments in monocultured sensory neurons or co-cultured with keratinocytes treated with PbTx-1 or P-CTX-2. We demonstrated that PbTx-1-induced calcium increase and SP release involved Cat-S, PAR2 and transient receptor potential vanilloid 4 (TRPV4). The PbTx-1-induced signaling pathway included protein kinase A (PKA) and TRPV4, which are compatible with the PAR2 biased signaling induced by Cat-S. Internalization of PAR2 and protein kinase C (PKC), inositol triphosphate receptor and TRPV4 activation evoked by PbTx-1 are compatible with the PAR2 canonical signaling. Our results suggest that PbTx-1-induced sensory disturbances involve the PAR2-TRPV4 pathway. We identified PAR2, Cat-S, PKA, and PKC that are involved in TRPV4 sensitization induced by PbTx-1 in sensory neurons. Full article
(This article belongs to the Special Issue Pain, Itch and Sensory Nerve Endings)
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16 pages, 4066 KiB  
Article
Granulocyte Colony Stimulating Factor (GCSF) Can Attenuate Neuropathic Pain by Suppressing Monocyte Chemoattractant Protein-1 (MCP-1) Expression, through Upregulating the Early MicroRNA-122 Expression in the Dorsal Root Ganglia
by Ming-Feng Liao, Jung-Lung Hsu, Kwok-Tung Lu, Po-Kuan Chao, Mei-Yun Cheng, Hui-Ching Hsu, Ai-Lun Lo, Yun-Lin Lee, Yu-Hui Hung, Rong-Kuo Lyu, Hung-Chou Kuo, Chun-Che Chu and Long-Sun Ro
Cells 2020, 9(7), 1669; https://doi.org/10.3390/cells9071669 - 11 Jul 2020
Cited by 12 | Viewed by 3465
Abstract
Our previous animal studies and several human clinical trials have shown that granulocyte-colony stimulating factor (GCSF) can attenuate neuropathic pain through various mechanisms. GCSF itself is also a multipotent cytokine that can modulate microribonucleic acid (microRNA) expression profiles in vitro. In this study, [...] Read more.
Our previous animal studies and several human clinical trials have shown that granulocyte-colony stimulating factor (GCSF) can attenuate neuropathic pain through various mechanisms. GCSF itself is also a multipotent cytokine that can modulate microribonucleic acid (microRNA) expression profiles in vitro. In this study, we used the NanoString nCounter analysis system to screen the expression of different rodent microRNAs at early stage after nerve injury and studied the expression of related cytokines/chemokines in the dorsal root ganglia (DRGs) of rats that underwent chronic constriction injury (CCI) to explore the underlying mechanisms of the analgesic effects of GCSF. We found that microRNA-122 expression was downregulated by CCI; in contrast, GCSF treatment significantly upregulated microRNA-122 expression in the DRGs of CCI rats on the 1st day after nerve injury. We further studied the expression of different cytokines/chemokines (IL-1β, IL-6, and monocyte chemoattractant protein-1 (MCP-1)) that were modulated by microRNA-122. MCP-1 has been reported to participate in neuropathic pain development, and its expression on the DRGs of vehicle-treated CCI rats was significantly higher than that on the DRGs of sham-operated rats; in contrast, GCSF-treated rats exhibited significantly lower MCP-1 expression in the DRG than vehicle-treated rats on the 7th day after nerve injury. An early GCSF treatment can suppress MCP-1 expressions, through upregulating microRNA-122 expressions in the DRGs of CCI rats at an earlier stage, thus indirectly attenuating neuropathic pain development. Full article
(This article belongs to the Special Issue Pain, Itch and Sensory Nerve Endings)
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Review

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10 pages, 963 KiB  
Review
What Do We Know about Pruritus in Very Young Infants? A Literature Review
by Camille Le Pors, Matthieu Talagas, Claire Abasq-Thomas, Séverine Henry, Laurent Misery and Jean-Michel Roué
Cells 2021, 10(10), 2788; https://doi.org/10.3390/cells10102788 - 18 Oct 2021
Cited by 2 | Viewed by 2416
Abstract
In infants, pruritus is frequently considered as absent because they do not scratch themselves. Because pruritus could induce severe adverse effects in this vulnerable population, we aimed to review existing evidence on the ability of young infants to experience itch and on how [...] Read more.
In infants, pruritus is frequently considered as absent because they do not scratch themselves. Because pruritus could induce severe adverse effects in this vulnerable population, we aimed to review existing evidence on the ability of young infants to experience itch and on how to assess itch-related discomfort in this population. A literature review was performed (Pubmed, Google Scholar). Neurological itch pathways are well described. Skin development starts early during gestation. At 34 weeks of gestation, skin is almost complete while skin adaptations occur after birth. Newborn skin is neurologically functional, including the ability for young infants to feel pain. Similarities and interactions between pain and pruritus support the hypothesis that infants could feel pruritus. However, the existence of pruritus in infants has never been evidenced. Many itchy conditions can affect them, suggesting non-negligible prevalence of infant pruritus among which atopic dermatitis (AD) is the most studied disease. Studies reported a negative impact of AD on children and their families. There is no existing validated method to assess pruritus in infants, although they may feel pruritus and chronic pruritus can lead to serious adverse effects. To appropriately diagnose pruritus appears of great interest among young infants. Development of a method is required to this aim. Full article
(This article belongs to the Special Issue Pain, Itch and Sensory Nerve Endings)
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27 pages, 1565 KiB  
Review
Neurological Disturbances of Ciguatera Poisoning: Clinical Features and Pathophysiological Basis
by Killian L’Herondelle, Matthieu Talagas, Olivier Mignen, Laurent Misery and Raphaele Le Garrec
Cells 2020, 9(10), 2291; https://doi.org/10.3390/cells9102291 - 14 Oct 2020
Cited by 21 | Viewed by 4562
Abstract
Ciguatera fish poisoning (CFP), the most prevalent seafood poisoning worldwide, is caused by the consumption of tropical and subtropical fish contaminated with potent neurotoxins called ciguatoxins (CTXs). Ciguatera is a complex clinical syndrome in which peripheral neurological signs predominate in the acute phase [...] Read more.
Ciguatera fish poisoning (CFP), the most prevalent seafood poisoning worldwide, is caused by the consumption of tropical and subtropical fish contaminated with potent neurotoxins called ciguatoxins (CTXs). Ciguatera is a complex clinical syndrome in which peripheral neurological signs predominate in the acute phase of the intoxication but also persist or reoccur long afterward. Their recognition is of particular importance in establishing the diagnosis, which is clinically-based and can be a challenge for physicians unfamiliar with CFP. To date, no specific treatment exists. Physiopathologically, the primary targets of CTXs are well identified, as are the secondary events that may contribute to CFP symptomatology. This review describes the clinical features, focusing on the sensory disturbances, and then reports on the neuronal targets and effects of CTXs, as well as the neurophysiological and histological studies that have contributed to existing knowledge of CFP neuropathophysiology at the molecular, neurocellular and nerve levels. Full article
(This article belongs to the Special Issue Pain, Itch and Sensory Nerve Endings)
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