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Pain–Neuroinflammation Dyad: New Therapeutic Strategies or Pharmacological Targets to Counter...
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Pain–Neuroinflammation Dyad: New Therapeutic Strategies or Pharmacological Targets to Counter Them

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 7755

Special Issue Editors

Dr. Giada Amodeo

E-Mail Website
Guest Editor
Department of Pharmacological and Biomolecular Sciences, University of Milan, Via Vanvitelli 32, 20129 Milano, Italy
Interests: pain; neuroinflammation; aging; mood disorders
Dr. Silvia Franchi

E-Mail Website
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

Special Issue Information

Dear Colleagues,

Chronic pain persistence can be traced back to a plethora of factors. Very often, the chronicization of pain does not derive from the initial damage progression but rather from central sensitization, where the neuroinflammatory condition plays a key role. The pathogenesis of chronic pain is a large and active field of research that has led to a rapid increase in knowledge in this area. Many recent studies suggest that neuroinflammation is triggered and maintained by multiple and complex interactions between the nervous and immune systems. Indeed, although the first studies had only focused on investigations at the neuron level, to date, the role of microglia and astrocytes, resulting in the production of cytokines, chemokines, neuropeptides, reactive oxygen species, second messengers, etc., has been slowly uncovered. Additionally, the neuroinflammation that occurs can also reach higher brain structures, especially those involved in pain modulation and in pain-related emotional and cognitive aspects. Indeed, mounting evidence suggests a close link between the presence of chronic pain and the development of psychiatric symptoms. Despite this, effective treatments, free of side effects, capable of blocking the pain and therefore of interrupting the vicious circle that is estab-lished, are currently not yet available. For these reasons, the identification of new targets or therapeutic strategies appears to be of great interest. 
This Special Issue will mainly focus on the study of pain, neuroinflammation and related comorbidities, with a particular focus on finding solutions to prevent/slow down/suppress pain, neuroinflammation and related comorbidities. Both original articles and reviews will be considered for inclusion.

Dr. Giada Amodeo
Dr. Silvia Franchi
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • chronic pain
  • neuroinflammation
  • mood disorders

Published Papers (4 papers)

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Research

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12 pages, 2927 KiB  
Article
The Potential of Glucose Treatment to Reduce Reactive Oxygen Species Production and Apoptosis of Inflamed Neural Cells In Vitro
by Juin-Hong Cherng, Shu-Jen Chang, Hsin-Da Tsai, Chung-Fang Chun, Gang-Yi Fan, Kenneth Dean Reeves, King Hei Stanley Lam and Yung-Tsan Wu
Biomedicines 2023, 11(7), 1837; https://doi.org/10.3390/biomedicines11071837 - 26 Jun 2023
Viewed by 2640
Abstract
Neuroinflammation is a key feature in the pathogenesis of entrapment neuropathies. Clinical trial evidence suggests that perineural injection of glucose in water at entrapment sites has therapeutic benefits beyond a mere mechanical effect. We previously demonstrated that 12.5–25 mM glucose restored normal metabolism [...] Read more.
Neuroinflammation is a key feature in the pathogenesis of entrapment neuropathies. Clinical trial evidence suggests that perineural injection of glucose in water at entrapment sites has therapeutic benefits beyond a mere mechanical effect. We previously demonstrated that 12.5–25 mM glucose restored normal metabolism in human SH-SYFY neuronal cells rendered metabolically inactive from TNF-α exposure, a common initiator of neuroinflammation, and reduced secondary elevation of inflammatory cytokines. In the present study, we measured the effects of glucose treatment on cell survival, ROS activity, gene-related inflammation, and cell cycle regulation in the presence of neurogenic inflammation. We exposed SH-SY5Y cells to 10 ng/mL of TNF-α for 24 h to generate an inflammatory environment, followed by 24 h of exposure to 3.125, 6.25, 12.5, and 25 mM glucose. Glucose exposure, particularly at 12.5 mM, preserved apoptotic SH-SY5Y cell survival following a neuroinflammatory insult. ROS production was substantially reduced, suggesting a ROS scavenging effect. Glucose treatment significantly increased levels of CREB, JNK, and p70S6K (p < 0.01), pointing to antioxidative and anti-inflammatory actions through components of the MAPK family and Akt pathways but appeared underpowered (n = 6) to reach significance for NF-κB, p38, ERK1/2, Akt, and STAT5 (p < 0.05). Cell regulation analysis indicated that glucose treatment recovered/restored function in cells arrested in the S or G2/M-phases. In summary, glucose exposure in vitro restores function in apoptotic nerves after TNF-α exposure via several mechanisms, including ROS scavenging and enhancement of MAPK family and Akt pathways. These findings suggest that glucose injection about entrapped peripheral nerves may have several favorable biochemical actions that enhance neuronal cell function. Full article
(This article belongs to the Special Issue Pain–Neuroinflammation Dyad: New Therapeutic Strategies or Pharmacological Targets to Counter Them)
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Review

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25 pages, 7839 KiB  
Review
The Prokineticin System in Inflammatory Bowel Diseases: A Clinical and Preclinical Overview
by Giada Amodeo, Silvia Franchi, Giulia Galimberti, Benedetta Riboldi and Paola Sacerdote
Biomedicines 2023, 11(11), 2985; https://doi.org/10.3390/biomedicines11112985 - 6 Nov 2023
Viewed by 1261
Abstract
Inflammatory bowel disease (IBD) includes Crohn’s disease (CD) and ulcerative colitis (UC), which are characterized by chronic inflammation of the gastrointestinal (GI) tract. IBDs clinical manifestations are heterogeneous and characterized by a chronic relapsing-remitting course. Typical gastrointestinal signs and symptoms include diarrhea, GI [...] Read more.
Inflammatory bowel disease (IBD) includes Crohn’s disease (CD) and ulcerative colitis (UC), which are characterized by chronic inflammation of the gastrointestinal (GI) tract. IBDs clinical manifestations are heterogeneous and characterized by a chronic relapsing-remitting course. Typical gastrointestinal signs and symptoms include diarrhea, GI bleeding, weight loss, and abdominal pain. Moreover, the presence of pain often manifests in the remitting disease phase. As a result, patients report a further reduction in life quality. Despite the scientific advances implemented in the last two decades and the therapies aimed at inducing or maintaining IBDs in a remissive condition, to date, their pathophysiology still remains unknown. In this scenario, the importance of identifying a common and effective therapeutic target for both digestive symptoms and pain remains a priority. Recent clinical and preclinical studies have reported the prokineticin system (PKS) as an emerging therapeutic target for IBDs. PKS alterations are likely to play a role in IBDs at multiple levels, such as in intestinal motility, local inflammation, ulceration processes, localized abdominal and visceral pain, as well as central nervous system sensitization, leading to the development of chronic and widespread pain. This narrative review summarized the evidence about the involvement of the PKS in IBD and discussed its potential as a druggable target. Full article
(This article belongs to the Special Issue Pain–Neuroinflammation Dyad: New Therapeutic Strategies or Pharmacological Targets to Counter Them)
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15 pages, 932 KiB  
Review
Endometriosis-Related Chronic Pelvic Pain
by Soo Youn Song, Ye Won Jung, WonKyo Shin, Mia Park, Geon Woo Lee, Soohwa Jeong, Sukjeong An, Kyoungmin Kim, Young Bok Ko, Ki Hwan Lee, Byung Hun Kang, Mina Lee and Heon Jong Yoo
Biomedicines 2023, 11(10), 2868; https://doi.org/10.3390/biomedicines11102868 - 23 Oct 2023
Cited by 2 | Viewed by 1959
Abstract
Endometriosis, which is the presence of endometrial stroma and glands outside the uterus, is one of the most frequently diagnosed gynecologic diseases in reproductive women. Patients with endometriosis suffer from various pain symptoms such as dysmenorrhea, dyspareunia, and chronic pelvic pain. The pathophysiology [...] Read more.
Endometriosis, which is the presence of endometrial stroma and glands outside the uterus, is one of the most frequently diagnosed gynecologic diseases in reproductive women. Patients with endometriosis suffer from various pain symptoms such as dysmenorrhea, dyspareunia, and chronic pelvic pain. The pathophysiology for chronic pain in patients with endometriosis has not been fully understood. Altered inflammatory responses have been shown to contribute to pain symptoms. Increased secretion of cytokines, angiogenic factors, and nerve growth factors has been suggested to increase pain. Also, altered distribution of nerve fibers may also contribute to chronic pain. Aside from local contributing factors, sensitization of the nervous system is also important in understanding persistent pain in endometriosis. Peripheral sensitization as well as central sensitization have been identified in patients with endometriosis. These sensitizations of the nervous system can also explain increased incidence of comorbidities related to pain such as irritable bowel disease, bladder pain syndrome, and vulvodynia in patients with endometriosis. In conclusion, there are various possible mechanisms behind pain in patients with endometriosis, and understanding these mechanisms can help clinicians understand the nature of the pain symptoms and decide on treatments for endometriosis-related pain symptoms. Full article
(This article belongs to the Special Issue Pain–Neuroinflammation Dyad: New Therapeutic Strategies or Pharmacological Targets to Counter Them)
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14 pages, 507 KiB  
Review
Pain Modulation in Chronic Musculoskeletal Disorders: Botulinum Toxin, a Descriptive Analysis
by Daniela Poenaru, Miruna Ioana Sandulescu and Delia Cinteza
Biomedicines 2023, 11(7), 1888; https://doi.org/10.3390/biomedicines11071888 - 3 Jul 2023
Cited by 2 | Viewed by 1317
Abstract
Botulinum neurotoxin (BoNT), a product of Clostridium botulinum, reversibly inhibits the presynaptic release of the neurotransmitter acetylcholine at the neuromuscular junction. In addition, BoNT blocks the transmission of other substances involved in pain perception and, together with a soft-tissue anti-inflammatory effect, may play [...] Read more.
Botulinum neurotoxin (BoNT), a product of Clostridium botulinum, reversibly inhibits the presynaptic release of the neurotransmitter acetylcholine at the neuromuscular junction. In addition, BoNT blocks the transmission of other substances involved in pain perception and, together with a soft-tissue anti-inflammatory effect, may play a role in analgesia. When first-line treatment fails, second-line therapies might include BoNT. Studies on chronic and recurrent pain using different mechanisms offer heterogenous results that must be validated and standardized. Plantar fasciitis, severe knee osteoarthritis, painful knee and hip arthroplasty, antalgic muscular contractures, and neuropathic and myofascial pain syndromes may benefit from the administration of BoNT. Research on this topic has revealed the main musculoskeletal conditions that can benefit from BoNT, stressing the effects, modalities of administration, doses, and schedule. Full article
(This article belongs to the Special Issue Pain–Neuroinflammation Dyad: New Therapeutic Strategies or Pharmacological Targets to Counter Them)
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