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Molecular Insight into Pharmacological Research on Anti-inflammatory Immunity
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Molecular Insight into Pharmacological Research on Anti-inflammatory Immunity

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

Deadline for manuscript submissions: closed (20 March 2025) | Viewed by 7014

Special Issue Editor

Dr. Elisabetta Caiazzo

E-Mail Website
Guest Editor
Department of Pharmacy, University of Naples Federico II, Naples, Italy
Interests: the role of adenosine signaling in the modulation of inflammatory processes; the identification of molecular and cellular mechanisms underlying hemostasis alteration in inflammation; the study of medicinal plants and active ingredients with anti-inflammatory effects; the study of cellular and molecular mechanisms involved in the pathophysiology of cardiovascular inflammation at the translational level
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce a Special Issue of International Journal of Molecular Sciences focused on “Molecular Insight into Pharmacological Research on Anti-inflammatory Immunity”.

Inflammation is a protective process involving immune cells to eliminate pathogens and promote tissue repair and recovery. The failure of resolution results in prolonged or chronic inflammation, contributing to a vicious cycle leading to chronic diseases.

This Special Issue aims to cover the current state of the art of preclinical and clinical studies, including original research articles, systematic reviews, and meta-analyses on drugs, immune-mediated diseases, molecular pathways, and future therapeutic targets to better understand molecular mechanisms of anti-inflammatory immunity and contribute to the development of new effective therapies for many different immune-mediated diseases.

We look forward to your contributions to this exciting Special Issue.

Dr. Elisabetta Caiazzo
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. 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

  • inflammation
  • immunity
  • pharmacology
  • anti-inflammatory drugs
  • immune-mediated diseases
  • anti-inflammatory immunity
  • immunopharmacology

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Published Papers (3 papers)

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Research

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19 pages, 6514 KiB  
Article
bFGF-like Activity Supported Tissue Regeneration, Modulated Neuroinflammation, and Rebalanced Ca2+ Homeostasis following Spinal Cord Injury
by Alessio Ardizzone, Valentina Bova, Giovanna Casili, Alessia Filippone, Marika Lanza, Alberto Repici, Emanuela Esposito and Irene Paterniti
Int. J. Mol. Sci. 2023, 24(19), 14654; https://doi.org/10.3390/ijms241914654 - 27 Sep 2023
Cited by 2 | Viewed by 2139
Abstract
A spinal cord injury (SCI) is a well-defined debilitating traumatic event to the spinal cord that usually triggers permanent changes in motor, sensory, and autonomic functions. Injured tissue becomes susceptible to secondary mechanisms caused by SCIs, which include pro-inflammatory cytokine release, the activation [...] Read more.
A spinal cord injury (SCI) is a well-defined debilitating traumatic event to the spinal cord that usually triggers permanent changes in motor, sensory, and autonomic functions. Injured tissue becomes susceptible to secondary mechanisms caused by SCIs, which include pro-inflammatory cytokine release, the activation of astrocytes and microglia, and increased neuronal sensibility. As a consequence, the production of factors such as GFAP, IBA-1, TNF-α, IL-1β, IFN-γ, and S100-β slow down or inhibit central nervous system (CNS) regeneration. In this regard, a thorough understanding of the mechanisms regulating the CNS, and specifically SCI, is essential for the development of new therapeutic strategies. It has been demonstrated that basic fibroblast growth factor (bFGF) was successful in the modulation of neurotrophic activity, also promoting neurite survival and tissue repair, thus resulting in the valuable care of CNS disorders. However, bFGF therapeutic use is limited due to the undesirable effects developed following its administration. Therefore, the synthetic compound mimetic of bFGF, SUN11602 (with chemical name 4-[[4-[[2-[(4-Amino-2,3,5,6-tetramethylphenyl)amino]acetyl]methylamino]-1-piperidinyl]methyl]benzamide), has been reported to show neuroprotective activities similar to those of bFGF, also demonstrating a good pharmacokinetic profile. Here, we aimed to investigate the neuroprotective activity of this bFGF-like compound in modulating tissue regeneration, neuroinflammation, and Ca2+ overload by using a subacute mouse model of SCI. SUN11602 (1, 2.5, and 5 mg/kg) was administered orally to mice for 72 h daily following the in vivo model of SCI, which was generated by the extradural compression of the spinal cord. The data obtained demonstrated that SUN11602 treatment considerably decreased motor alteration and diminished the neuroinflammatory state through the regulation of glial activation, the NF-κB pathway, and kinases. Additionally, by controlling Ca2+-binding proteins and restoring neurotrophin expression, we showed that SUN11602 therapy restored the equilibrium of the neuronal circuit. Because of these findings, bFGF-like compounds may be an effective tool for reducing inflammation in SCI patients while enhancing their quality of life. Full article
(This article belongs to the Special Issue Molecular Insight into Pharmacological Research on Anti-inflammatory Immunity)
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Review

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16 pages, 1458 KiB  
Review
Advancing Inflammatory Bowel Disease Treatment by Targeting the Innate Immune System and Precision Drug Delivery
by Kat F. Kiilerich, Trine Andresen, Behrooz Darbani, Laura H. K. Gregersen, Anette Liljensøe, Tue B. Bennike, René Holm, Jesper B. Moeller and Vibeke Andersen
Int. J. Mol. Sci. 2025, 26(2), 575; https://doi.org/10.3390/ijms26020575 - 11 Jan 2025
Cited by 1 | Viewed by 2073
Abstract
Inflammatory bowel disease (IBD), encompassing Crohn’s disease and ulcerative colitis, involves chronic inflammation of the gastrointestinal tract. Current immune-modulating therapies are insufficient for 30–50% of patients or cause significant side effects, emphasizing the need for new treatments. Targeting the innate immune system and [...] Read more.
Inflammatory bowel disease (IBD), encompassing Crohn’s disease and ulcerative colitis, involves chronic inflammation of the gastrointestinal tract. Current immune-modulating therapies are insufficient for 30–50% of patients or cause significant side effects, emphasizing the need for new treatments. Targeting the innate immune system and enhancing drug delivery to inflamed gut regions are promising strategies. Neutrophils play a central role in IBD by releasing reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) —DNA-based structures with cytotoxic proteins—that contribute to mucosal damage and inflammation. Recent studies linking ROS production, DNA repair, and NET formation have identified NETs as potential therapeutic targets, with preclinical models showing positive outcomes from NET inhibition. Innovative oral drug delivery systems designed to target gut inflammation directly—without systemic absorption—could improve treatment precision and reduce side effects. Advanced formulations utilize properties such as particle size, surface modifications, and ROS-triggered release to selectively target the distal ileum and colon. A dual strategy that combines a deeper understanding of IBD pathophysiology to identify inflammation-related therapeutic targets with advanced drug delivery systems may offer significant promise. For instance, pairing NET inhibition with ROS-responsive nanocarriers could enhance treatment efficacy, though further research is needed. This synergistic approach has the potential to greatly improve outcomes for IBD patients. Full article
(This article belongs to the Special Issue Molecular Insight into Pharmacological Research on Anti-inflammatory Immunity)
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Other

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6 pages, 465 KiB  
Case Report
Decrease in Mycophenolate Mofetil Plasma Concentration in the Presence of Antibiotics: A Case Report in a Cystic Fibrosis Patient with Lung Transplant
by Giuliano Ponis, Giuliana Decorti, Egidio Barbi, Gabriele Stocco and Massimo Maschio
Int. J. Mol. Sci. 2024, 25(4), 2358; https://doi.org/10.3390/ijms25042358 - 17 Feb 2024
Cited by 1 | Viewed by 1910
Abstract
Immunosuppression management in transplant recipients is a critical component of pharmacotherapy. This becomes particularly crucial when patients are exposed to multiple medications that may lead to pharmacological interactions, potentially compromising the effectiveness of immunosuppression. We present the case of a 46-year-old patient diagnosed [...] Read more.
Immunosuppression management in transplant recipients is a critical component of pharmacotherapy. This becomes particularly crucial when patients are exposed to multiple medications that may lead to pharmacological interactions, potentially compromising the effectiveness of immunosuppression. We present the case of a 46-year-old patient diagnosed with cystic fibrosis in childhood at our hospital, who underwent bilateral lung transplantation and is undergoing immunosuppressive therapy. The patient was hospitalized due to an acute pulmonary exacerbation. During the hospitalization, the patient was administered various classes of antibiotics while continuing the standard antirejection regimen of everolimus and mycophenolate. Plasma concentrations of immunosuppressants, measured after antibiotic therapy, revealed significantly lower levels than the therapeutic thresholds, providing the basis for formulating the hypothesis of a drug–drug interaction phenomenon. This hypothesis is supported by the rationale of antibiotic-induced disruption of the intestinal flora, which directly affects the kinetics of mycophenolate. These levels increased after discontinuation of the antimicrobials. Patients with CF undergoing lung transplantation, especially prone to pulmonary infections due to their medical condition, considering the enterohepatic circulation of mycophenolate mediated by intestinal bacteria, necessitate routine monitoring of mycophenolate concentrations during and immediately following the cessation of antibiotic therapies, that could potentially result in insufficient immunosuppression. Full article
(This article belongs to the Special Issue Molecular Insight into Pharmacological Research on Anti-inflammatory Immunity)
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