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Anti-inflammatory Molecules
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Anti-inflammatory Molecules

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2002

Special Issue Editor

Dr. Simona Dedoni

E-Mail Website
Guest Editor
Laboratory of Cellular and Molecular Pharmacology, Section of Neurosciences, University of Cagliari, 09042 Monserrato, Italy
Interests: cell signaling; apoptosis; neurotrophins; cytokines; neuroscience
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The infection causes inflammation, which weakens both the innate and adaptive immune systems while also affecting the microbiota, which is thought to represent our second brain.

Inflammation represents the physiological goal of restoring tissue homeostasis. Uncontrolled or unresolved inflammation, on the other hand, can cause tissue damage, giving birth to a slew of chronic inflammatory disorders. If ignored, this can lead to autoimmune or autoinflammatory disorders, neurological disease, or cancer. Cytokines that deliver proinflammatory cytokines include, among others, IL-1, IL-6, IL-18, tumor necrosis factor, and IFNs. The goal of this Special Issue is to investigate the function of these molecules alone in pre-clinical human and animal studies, as well as in vitro, in order to describe the pathways involved in their harmful effects and how to counteract them.

The Special Issue “Anti-inflammatory Molecules” will concentrate on novel and unique signaling pathways and mechanisms for new anti-inflammatory medications to minimize the "inflammatory cascade." The purpose of this Special Issue is to examine the current mechanistic methodologies and the development of next-generation anti-inflammatory natural and synthetic medicines that can also work together.

Dr. Simona Dedoni
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. Molecules is an international peer-reviewed open access semimonthly 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 2700 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

  • chemokines
  • citokines
  • dead receptors
  • interleukin
  • TNF alpha
  • lipids

Published Papers (2 papers)

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Research

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17 pages, 4096 KiB  
Article
Oleoylethanolamide and Palmitoylethanolamide Enhance IFNβ-Induced Apoptosis in Human Neuroblastoma SH-SY5Y Cells
by Chiara Camoglio, Jihane Balla, Paola Fadda and Simona Dedoni
Molecules 2024, 29(7), 1592; https://doi.org/10.3390/molecules29071592 - 02 Apr 2024
Viewed by 681
Abstract
Oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) are endogenous lipids that act as agonists of the peroxisome proliferator-activated receptor α (PPARα). Recently, an interest in the role of these lipids in malignant tumors has emerged. Nevertheless, the effects of OEA and PEA on human neuroblastoma [...] Read more.
Oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) are endogenous lipids that act as agonists of the peroxisome proliferator-activated receptor α (PPARα). Recently, an interest in the role of these lipids in malignant tumors has emerged. Nevertheless, the effects of OEA and PEA on human neuroblastoma cells are still not documented. Type I interferons (IFNs) are immunomodulatory cytokines endowed with antiviral and anti-proliferative actions and are used in the treatment of various pathologies such as different cancer forms (i.e., non-Hodgkin’s lymphoma, melanoma, leukemia), hepatitis B, hepatitis C, multiple sclerosis, and many others. In this study, we investigated the effect of OEA and PEA on human neuroblastoma SH-SY5Y cells treated with IFNβ. We focused on evaluating cell viability, cell proliferation, and cell signaling. Co-exposure to either OEA or PEA along with IFNβ leads to increased apoptotic cell death marked by the cleavage of caspase 3 and poly-(ADP ribose) polymerase (PARP) alongside a decrease in survivin and IKBα levels. Moreover, we found that OEA and PEA did not affect IFNβ signaling through the JAK-STAT pathway and the STAT1-inducible protein kinase R (PKR). OEA and PEA also increased the phosphorylation of p38 MAP kinase and programmed death-ligand 1 (PD-L1) expression both in full cell lysate and surface membranes. Furthermore, GW6471, a PPARα inhibitor, and the genetic silencing of the receptor were shown to lower PD-L1 and cleaved PARP levels. These results reveal the presence of a novel mechanism, independent of the IFNβ-prompted pathway, by which OEA and PEA can directly impair cell survival, proliferation, and clonogenicity through modulating and potentiating the intrinsic apoptotic pathway in human SH-SY5Y cells. Full article
(This article belongs to the Special Issue Anti-inflammatory Molecules)
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Review

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27 pages, 2504 KiB  
Review
Uncovering the Power of GPR18 Signalling: How RvD2 and Other Ligands Could Have the Potential to Modulate and Resolve Inflammation in Various Health Disorders
by Ewelina Honkisz-Orzechowska, Dorota Łażewska, Grzegorz Baran and Katarzyna Kieć-Kononowicz
Molecules 2024, 29(6), 1258; https://doi.org/10.3390/molecules29061258 - 12 Mar 2024
Cited by 1 | Viewed by 940
Abstract
The resolution of inflammation is the primary domain of specialised pro-resolving mediators (SPMs), which include resolvins, protectins, and their forms synthesised under the influence of aspirin and the maresins. The role of these SPMs has been discussed by many authors in the literature, [...] Read more.
The resolution of inflammation is the primary domain of specialised pro-resolving mediators (SPMs), which include resolvins, protectins, and their forms synthesised under the influence of aspirin and the maresins. The role of these SPMs has been discussed by many authors in the literature, with particular reference to neuroinflammation and significant neurological disorders. This review discusses the role of G protein-coupled receptor 18 (GPR18), resolvin D2 (RvD2) activity, and the GPR18-RvD2 signalling axis, as well as the role of small molecule ligands of GPR18 in inflammation in various health disorders (brain injuries, neuropathic pain, neurodegenerative/cardiometabolic/cardiovascular/gastrointestinal diseases, peritonitis, periodontitis, asthma and lung inflammation, Duchenne muscular dystrophy, SARS-CoV-2-induced inflammation, and placenta disorders. The idea of biological intervention through modulating GPR18 signalling is attracting growing attention because of its great therapeutic potential. With this paper, we aimed to present a comprehensive review of the most recent literature, perform a constructive view of data, and point out research gaps. Full article
(This article belongs to the Special Issue Anti-inflammatory Molecules)
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