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Biomedicines
Special Issues
Inflammation and Peripheral Nervous System
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Inflammation and Peripheral Nervous System

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

Deadline for manuscript submissions: closed (28 February 2025) | Viewed by 3759

Special Issue Editor

Dr. Nikolett Bódi

E-Mail Website
Guest Editor
Department of Physiology, Anatomy and Neuroscience, Faculty of Science and Informatics, University of Szeged, H-6726 Szeged, Hungary
Interests: enteric nervous system; gastroenterology; diabetes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Numerous factors and molecules are involved in different inflammatory processes that fundamentally determine the molecular background of several diseases with chronic inflammation in humans and animal models. Imbalance between pro-inflammatory and anti-inflammatory molecules including cytokines, metabolites, and other chemicals and regulators contributes to alterations in environmental milieu and results in neuroinflammation damaging peripheral nerves and ganglia, both in somatic and autonomic nervous systems. The aim of this Special Issue is to highlight the molecular mechanisms that trigger inflammation contributing to peripheral neuropathy or new therapeutic approaches addressing neuroinflammation in different diseases. This Special Issue is open for original research articles as well as review articles.

Dr. Nikolett Bódi
Guest Editor

Manuscript Submission Information

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Keywords

  • pro- and anti-inflammatory molecules
  • peripheral nervous system
  • peripheral neuropathy
  • neuroinflammation
  • neuronal environment
  • neuro-immune interactions
  • anti-inflammatory therapies

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Published Papers (3 papers)

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Research

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15 pages, 440 KiB  
Article
A Retrospective Assessment of Neuropathic Pain in Response to Intraneural Facilitation® Therapy and Neurovascular Index-Guided Food Elimination
by Mark Bussell, Kyan Sahba, Hailey Jahromi, Mitra Rashidian and Jamie Hankins
Biomedicines 2025, 13(3), 688; https://doi.org/10.3390/biomedicines13030688 - 11 Mar 2025
Viewed by 423
Abstract
Background/Objectives: To evaluate the effectiveness of our dual approach in treating neural ischemia. Methods: Researchers were able to retrospectively audit patient data collected from January 2022–September 2024. Patients were included if they received intraneural facilitation® (INF®), participated in [...] Read more.
Background/Objectives: To evaluate the effectiveness of our dual approach in treating neural ischemia. Methods: Researchers were able to retrospectively audit patient data collected from January 2022–September 2024. Patients were included if they received intraneural facilitation® (INF®), participated in neurovascular index (NVI)-guided food elimination, and completed pre and post pain-quality assessment scale (PQAS) forms in its entirety. Results: Eighteen of the twenty PQAS descriptive pain variables were significantly different pre- vs. post treatment: intense (p = 0.000), sharp (p = 0.002), hot (p = 0.020), dull (p = 0.022), cold (p = 0.005), sensitive (p = 0.000), shooting (p = 0.000), numb (p = 0.000), electrical (p = 0.000), tingling (p = 0.000), cramping (p = 0.000), radiating (p = 0.000), throbbing (p = 0.000), aching (p = 0.000), heavy (p = 0.000), unpleasant (p = 0.000), deep pain (p = 0.000), and intense surface pain (p = 0.000). Itchy (p = 0.058) and tender (p = 0.062) were not found to be significant. There was also significance in pain decrease in the three mean domains: paroxysmal (p = 0.000), superficial (p = 0.000), and deep (p = 0.000). Conclusions: This study suggests that blending a mechanical intervention (INF®) with a lifestyle modification (NVI-guided food elimination) is effective in improving PQAS scores in patients with peripheral neuropathy, indicating a possible reversal of neural ischemia and maintenance of capillary patency. Full article
(This article belongs to the Special Issue Inflammation and Peripheral Nervous System)
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18 pages, 30188 KiB  
Article
Intestinal Region-Dependent Impact of NFκB-Nrf Crosstalk in Myenteric Neurons and Adjacent Muscle Cells in Type 1 Diabetic Rats
by Bence Pál Barta, Benita Onhausz, Abigél Egyed-Kolumbán, Afnan AL Doghmi, János Balázs, Zita Szalai, Ágnes Ferencz, Edit Hermesz, Mária Bagyánszki and Nikolett Bódi
Biomedicines 2024, 12(10), 2347; https://doi.org/10.3390/biomedicines12102347 - 15 Oct 2024
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Abstract
Background/Objectives: Type 1 diabetes affects cytokines as potential inducers of NFκB signalling involved in inflammation and neuronal survival. Our goal was to assess the expression of NFκB p65 and its negative regulator, Nrf2, in myenteric neurons and adjacent smooth muscle of different gut [...] Read more.
Background/Objectives: Type 1 diabetes affects cytokines as potential inducers of NFκB signalling involved in inflammation and neuronal survival. Our goal was to assess the expression of NFκB p65 and its negative regulator, Nrf2, in myenteric neurons and adjacent smooth muscle of different gut segments after chronic hyperglycaemia and immediate insulin treatment. Methods: After ten weeks of hyperglycaemia, intestinal samples of control, streptozotocin-induced diabetic and insulin-treated diabetic rats were prepared for fluorescent immunohistochemistry, immunogold electron microscopy, ELISA and qPCR. Results: In the diabetic rats, the proportion of NFκB p65-immunoreactive myenteric neurons decreased significantly in the duodenum and increased in the ileum. The density of NFκB p65-labelling gold particles increased in the ileal but remained unchanged in the duodenal ganglia. Meanwhile, both total and nuclear Nrf2 density increased in the myenteric neurons of the diabetic duodenum. In smooth muscle, NFκB p65 and Nrf2 density increased in the small intestine of diabetic rats. While on the mRNA level, NFκB p65 and Nrf2 were induced, on the protein level, NFκB p65 increased and Nrf2 decreased in muscle/myenteric plexus homogenates. Insulin treatment had protective effects. Conclusions: Our findings reveal a segment-specific NFκB and Nrf expression in myenteric neurons and ganglionic muscular environments, which may contribute to regional neuronal survival and motility disturbances in diabetes. Full article
(This article belongs to the Special Issue Inflammation and Peripheral Nervous System)
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Review

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37 pages, 2119 KiB  
Review
Crumbling Pathogenesis and Biomarkers for Diabetic Peripheral Neuropathy
by Zhao Zhong Chong and Nizar Souayah
Biomedicines 2025, 13(2), 413; https://doi.org/10.3390/biomedicines13020413 - 8 Feb 2025
Viewed by 942
Abstract
Background: Diabetic sensorimotor polyneuropathy (DSP) is a common chronic diabetic complication. Traditionally, DSP was once considered irreversible with a typical loss of axon. However, the superimpose of acquired demyelination on axonal loss in DSP patients has been observed, implying that DSP may [...] Read more.
Background: Diabetic sensorimotor polyneuropathy (DSP) is a common chronic diabetic complication. Traditionally, DSP was once considered irreversible with a typical loss of axon. However, the superimpose of acquired demyelination on axonal loss in DSP patients has been observed, implying that DSP may be preventable or reversible, particularly within a subgroup of patients exhibiting early-stage acquired demyelination, underscoring the critical importance of identifying early prognostic markers. Methods: We systemically review the literature on the roles of biomarkers in predicting DSP and monitoring the progress. The underlying mechanisms of biomarkers were also discussed. Results: The pathogenesis of DSP is multifaceted, with various pathological mechanisms contributing to its development. Key mechanisms include aberrant glucose metabolism and induction of oxidative stress and inflammation. Several pathological processes, such as disrupted glucose metabolism, nerve damage, impaired microcirculation, genetic variants, and microRNA dysregulation, lead to molecular and protein changes that may be detectable in blood and other biological compartments, thus serving as potential biomarkers for DSP progression. However, the utility of a biomarker depends on its predictive accuracy, practicality, and ease of measurement. Conclusions: Most biomarkers for predicting DSP have demonstrated suboptimal predictive value, and many lack established accuracy in forecasting DSP progression. Consequently, the diagnostic utility of any single biomarker remains limited. A comprehensive combination of biomarkers from various categories may hold incredible promise for accurate detection. As artificial intelligence (AI) techniques, especially machine learning, rapidly advance, these technologies may offer significant potential for developing diagnostic platforms to integrate and interpret complex biomarker data for DSP. Full article
(This article belongs to the Special Issue Inflammation and Peripheral Nervous System)
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