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Biomedicines
Special Issues
Inflammation, Immunity, and Tissue Regeneration: New Treatments and Future Directions
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Inflammation, Immunity, and Tissue Regeneration: New Treatments and Future Directions

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 5083

Special Issue Editor

Dr. Krisztina Nikovics

E-Mail Website
Guest Editor
Imagery Unit, Department of Platforms and Technology Research, French Armed Forces Biomedical Research Institute, 91223 Brétigny-sur-Orge, France
Interests: in situ macrophage characterization; in situ hybridization; cytokine expression
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Understanding the processes of inflammation, immunity and tissue regeneration after injury is of major scientific and clinical importance. Immune cells are a heterogeneous population of cells that acquire their functional specialization in response to micro-environmental alterations. For a long time, immune cells have been known to trigger inflammation and coordinate the efficient repair of damaged tissue. However, the mechanisms by which they exert their effects are mostly unknown. When repair is not coordinated, regeneration fails and fibrosis can take place. The investigation of immune cell sub-populations by different biological, molecular and cellular methods is essential in establishing new diagnostics for multiple diseases as well as therapeutic strategies for tissue repair.

The Special Issue aims to bring together original articles and reviews that highlight significant advances in the fields of "Inflammation, Immunity and Tissue Regeneration". We welcome submissions that provide novel insights into the complex interplay between immunity, inflammation and tissue regeneration and the development of their potential therapeutic agents.

Dr. Krisztina Nikovics
Guest Editor

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

  • inflammation
  • tissue regeneration
  • immune cells
  • cytokine

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Published Papers (5 papers)

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Research

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19 pages, 2606 KiB  
Article
Pro-Resolving Inflammatory Effects of a Marine Oil Enriched in Specialized Pro-Resolving Mediators (SPMs) Supplement and Its Implication in Patients with Post-COVID Syndrome (PCS)
by Asun Gracia Aznar, Fernando Moreno Egea, Rafael Gracia Banzo, Rocio Gutierrez, Jose Miguel Rizo, Pilar Rodriguez-Ledo, Isabel Nerin and Pedro-Antonio Regidor
Biomedicines 2024, 12(10), 2221; https://doi.org/10.3390/biomedicines12102221 - 29 Sep 2024
Viewed by 811
Abstract
Objectives: This study aimed to evaluate the eicosanoid and pro-resolutive parameters in patients with Post-COVID Syndrome (PCS) during a 12-week supplementation with a marine oil enriched in specialized pro-resolving mediators (SPMs). Patient and methods: This study was conducted on 53 adult patients with [...] Read more.
Objectives: This study aimed to evaluate the eicosanoid and pro-resolutive parameters in patients with Post-COVID Syndrome (PCS) during a 12-week supplementation with a marine oil enriched in specialized pro-resolving mediators (SPMs). Patient and methods: This study was conducted on 53 adult patients with PCS. The subjects included must have had a positive COVID-19 test (PCR, fast antigen test, or serologic test) and persistent symptoms related to COVID-19 at least 12 weeks before their enrolment in the study. The following parameters were evaluated: polyunsaturated fatty acids EPA, DHA, ARA, and DPA; specialized pro-resolving mediators (SPMs), 17-HDHA, 18-HEPE, 14-HDHA, resolvins, maresins, protectins, and lipoxins. The eicosanoids group included prostaglandins, thromboxanes, and leukotrienes. The development of the clinical symptoms of fatigue and dyspnea were evaluated using the Fatigue Severity Scale (FSS) and the Modified Medical Research Council (mMRC) Dyspnea Scale. Three groups with different intake amounts were evaluated (daily use of 500 mg, 1500 mg, and 3000 mg) and compared to a control group not using the product. Results: In the serum from patients with PCS, an increase in 17-HDHA, 18-HEPE, and 14-HDHA could be observed, and a decrease in the ratio between the pro-inflammatory and pro-resolutive lipid mediators was detected; both differences were significant (p < 0.05). There were no differences found between the three treatment groups. Fatigue and dyspnea showed a trend of improvement after supplementation in all groups. Conclusions: A clear enrichment in the serum of the three monohydroxylated SPMs could be observed at a dosage of 500 mg per day. Similarly, a clear improvement in fatigue and dyspnea was observed with this dosage. Full article
(This article belongs to the Special Issue Inflammation, Immunity, and Tissue Regeneration: New Treatments and Future Directions)
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11 pages, 3583 KiB  
Article
Anti-Allergic and Anti-Inflammatory Effects of Lidocaine-Derived Organic Compounds in a House Dust Mite-Induced Allergic Rhinitis Mouse Model
by Seung-Heon Shin, Mi-Kyung Ye, Mi-Hyun Chae, Sang-Yen Geum, Ahmed S. Aboraia, Abu-Baker M. Abdel-Aal, Wesam S. Qayed, Hend A. A. Abd El-wahab, Ola F. Abou-Ghadir and Tarek Aboul-Fadl
Biomedicines 2024, 12(9), 1965; https://doi.org/10.3390/biomedicines12091965 - 29 Aug 2024
Viewed by 878
Abstract
Allergic rhinitis (AR) is a common chronic disease that significantly impacts the quality of life. Lidocaine is known to have anti-inflammatory and immunomodulatory effects. This study evaluated the effect of lidocaine analogs in a Dermatophagoides pteronyssinus (DP)-induced AR mouse model. An AR model [...] Read more.
Allergic rhinitis (AR) is a common chronic disease that significantly impacts the quality of life. Lidocaine is known to have anti-inflammatory and immunomodulatory effects. This study evaluated the effect of lidocaine analogs in a Dermatophagoides pteronyssinus (DP)-induced AR mouse model. An AR model was developed using BALB/c mice via intraperitoneal sensitization with DP and intranasal challenge with DP. One hour before stimulation with DP, lidocaine analogs, EI137 and EI341 (at a dose of 0.5 or 5 ug/g), were administered intranasally. Nasal symptoms and serum total IgE, interleukin (IL)-4, IL-10, interferon (IFN)-γ, and tumor necrosis factor (TNF)-α levels were evaluated. Reverse-transcription polymerase chain reaction was used to determine IL-4, IL-10, and IFN-γ, as well as the expression of their mRNA transcription factors in the sinonasal mucosa. Histologic changes were evaluated using hematoxylin and eosin and periodic acid–Schiff staining. The DP-induced AR mouse model had increased serum levels of total IgE and cytokines. EI137 and EI341 significantly suppressed the levels of total IgE, IL-4, and TNF-α. Intranasal instillation of EI137 and EI341 significantly inhibited IL-4, IL-10, and IFN-γ mRNA expression, as well as inflammatory cells and mucus-producing goblet cells. Lidocaine analogs also suppressed DP-stimulated IL-4, IFN-γ, and IFN-γ production by splenocytes. Intranasal instillation of EI137 and EI341 exhibited anti-allergic and anti-inflammatory effects, influenced by Th1 and Th2 inflammatory cytokines. These lidocaine analogs suppressed DP-induced sinonasal mucosal inflammation, inflammatory cell infiltration, and mucus hypersecretion. Full article
(This article belongs to the Special Issue Inflammation, Immunity, and Tissue Regeneration: New Treatments and Future Directions)
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11 pages, 2725 KiB  
Article
Hyperglycemia in a NOD Mice Model of Type-I Diabetes Aggravates Collagenase-Induced Intracerebral Hemorrhagic Injury
by Qasim M. Alhadidi, Kevin M. Nash, Ghaith A. Bahader, Emily Zender, Marcia F. McInerney and Zahoor A. Shah
Biomedicines 2024, 12(8), 1867; https://doi.org/10.3390/biomedicines12081867 - 15 Aug 2024
Viewed by 930
Abstract
Background: Intracerebral hemorrhage (ICH) is a severe type of stroke with high mortality. Persistent hyperglycemia following ICH is linked to deteriorated neurological functions and death. However, the exacerbating effect of hyperglycemia on ICH injury at the molecular level is still unclear. Therefore, this [...] Read more.
Background: Intracerebral hemorrhage (ICH) is a severe type of stroke with high mortality. Persistent hyperglycemia following ICH is linked to deteriorated neurological functions and death. However, the exacerbating effect of hyperglycemia on ICH injury at the molecular level is still unclear. Therefore, this study explores the impact of diabetes on ICH injury using a non-obese diabetic (NOD) mouse model of type I diabetes mellitus. Methods: NOD and non-diabetic (non-obese resistant) mice subjected to ICH by intrastriatal injection of collagenase were sacrificed three days following the ICH. Brains were collected for hematoma volume measurement and immunohistochemistry. Neurobehavioral assays were conducted 24 h before ICH and then repeated at 24, 48 and 72 h following ICH. Results: NOD mice showed increased hematoma volume and impairment in neurological function, as revealed by rotarod and grip strength analyses. Immunohistochemical staining showed reduced glial cell activation, as indicated by decreased GFAP and Iba1 staining. Furthermore, the expression of oxidative/nitrosative stress markers represented by 3-nitrotyrosine and inducible nitric oxide synthase was reduced in the diabetic group. Conclusions: Overall, our findings support the notion that hyperglycemia exacerbates ICH injury and worsens neurological function and that the mechanism of injury varies depending on the type of diabetes model used. Full article
(This article belongs to the Special Issue Inflammation, Immunity, and Tissue Regeneration: New Treatments and Future Directions)
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Review

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12 pages, 454 KiB  
Review
Idiosyncratic Hepatocellular Drug-Induced Liver Injury by Flucloxacillin with Evidence Based on Roussel Uclaf Causality Assessment Method and HLA B*57:01 Genotype: From Metabolic CYP 3A4/3A7 to Immune Mechanisms
by Rolf Teschke
Biomedicines 2024, 12(10), 2208; https://doi.org/10.3390/biomedicines12102208 - 27 Sep 2024
Viewed by 621
Abstract
Idiosyncratic drug-induced liver injury (iDILI) by flucloxacillin presents as both cholestatic and hepatocellular injury. Its mechanistic steps are explored in the present analysis as limited data exist on the cascade of events leading to iDILI in patients with an established diagnosis assessed for [...] Read more.
Idiosyncratic drug-induced liver injury (iDILI) by flucloxacillin presents as both cholestatic and hepatocellular injury. Its mechanistic steps are explored in the present analysis as limited data exist on the cascade of events leading to iDILI in patients with an established diagnosis assessed for causality by the Roussel Uclaf Causality Assessment Method (RUCAM). Studies with human liver microsomes showed that flucloxacillin is a substrate of cytochrome P450 (CYP) with ist preferred isoforms CYP 3A4/3A7 that toxified flucloxacillin toward 5′-hydroxymethylflucloxacillin, which was cytotoxic to human biliary epithelial cell cultures, simulating human cholestatic injury. This provided evidence for a restricted role of the metabolic CYP-dependent hypothesis. In contrast, 5′-hydroxymethylflucloxacillin generated metabolically via CYP 3A4/3A7 was not cytotoxic to human hepatocytes due to missing genetic host features and a lack of non-parenchymal cells, including immune cells, which commonly surround the hepatocytes in the intact liver in abundance. This indicated a mechanistic gap regarding the clinical hepatocellular iDILI, now closed by additional studies and clinical evidence based on HLA B*57:01-positive patients with iDILI by flucloxacillin and a verified diagnosis by the RUCAM. Naïve T-cells from volunteers expressing HLA B*57:01 activated by flucloxacillin when the drug antigen was presented by dendritic cells provided the immunological basis for hepatocellular iDILI caused by flucloxacillin. HLA B*57:01-restricted activation of drug-specific T-cells caused covalent binding of flucloxacillin to albumin acting as a hapten. Following drug stimulation, T-cell clones expressing CCR4 and CCR9 migrated toward CCL17 and CCL25 and secreted interferon-γ and cytokines. In conclusion, cholestatic injury can be explained metabolically, while hepatocellular injury requires both metabolic and immune activation. Full article
(This article belongs to the Special Issue Inflammation, Immunity, and Tissue Regeneration: New Treatments and Future Directions)
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32 pages, 2806 KiB  
Review
The Categorization of Perinatal Derivatives for Orthopedic Applications
by Amol H. Trivedi, Vicki Z. Wang, Edward J. McClain IV, Praveer S. Vyas, Isaac R. Swink, Edward D. Snell, Boyle C. Cheng and Patrick J. DeMeo
Biomedicines 2024, 12(7), 1544; https://doi.org/10.3390/biomedicines12071544 - 11 Jul 2024
Viewed by 1008
Abstract
Musculoskeletal (MSK) pathology encompasses an array of conditions that can cause anything from mild discomfort to permanent injury. Their prevalence and impact on disability have sparked interest in more effective treatments, particularly within orthopedics. As a result, the human placenta has come into [...] Read more.
Musculoskeletal (MSK) pathology encompasses an array of conditions that can cause anything from mild discomfort to permanent injury. Their prevalence and impact on disability have sparked interest in more effective treatments, particularly within orthopedics. As a result, the human placenta has come into focus within regenerative medicine as a perinatal derivative (PnD). These biologics are sourced from components of the placenta, each possessing a unique composition of collagens, proteins, and factors believed to aid in healing and regeneration. This review aims to explore the current literature on PnD biologics and their potential benefits for treating various MSK pathologies. We delve into different types of PnDs and their healing effects on muscles, tendons, bones, cartilage, ligaments, and nerves. Our discussions highlight the crucial role of immune modulation in the healing process for each condition. PnDs have been observed to influence the balance between anti- and pro-inflammatory factors and, in some cases, act as biologic scaffolds for tissue growth. Additionally, we assess the range of PnDs available, while also addressing gaps in our understanding, particularly regarding biologic processing methods. Although certain PnD biologics have varying levels of support in orthopedic literature, further clinical investigations are necessary to fully evaluate their impact on human patients. Full article
(This article belongs to the Special Issue Inflammation, Immunity, and Tissue Regeneration: New Treatments and Future Directions)
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