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Pharmaceuticals
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Inflammatory Cytokines as New Therapeutic Targets
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Inflammatory Cytokines as New Therapeutic Targets

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 6009

Special Issue Editors

Prof. Dr. Jae Seung Kang

E-Mail Website
Guest Editor
Department of Anatomy and Cell Biology, Institute of Allergy and Clinical Immunology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
Interests: antioxidant; vitamin C; inflammation; interleukin-22; NK cells; immune regulation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Yejin Kim

E-Mail Website
Guest Editor
Laboratory of Vitamin C and Antioxidant Immunology, Department of Anatomy and Cell Biology, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
Interests: antioxidant; vitamin C; cancer; inflammation

Special Issue Information

Dear Colleagues,

It is generally known that inflammatory responses are accompanied by the regulation of autoimmune diseases, infectious diseases, and cancers by the immune system. In this process, excessive production of inflammatory cytokine by inflammatory immune cells that mediate inflammatory reactions is known to make the disease get worse. Therefore, research regarding immunomodulating molecules, including monoclonal antibodies and small chemical compounds, is needed to regulate the production and function of inflammatory cytokines in this regard. 

Cytokines, or immune-cytokines, are a type of immune-modulatory proteins, also known as immune-transmitters, that are predominantly produced by T helper cells and macrophages, including interleukin-1 (IL-1), IL-6, IL-12, and IL-18, tumor necrosis factor alpha (TNF-α), interferon gamma (IFNγ), and granulocyte-macrophage colony-stimulating factor (GM-CSF). 

In this Special Issue, we will deal with research on the regulation of inflammatory immune cells and various kinds of inflammatory cytokines produced by these cells. Reviews and original papers discussing these points are welcome.

Prof. Dr. Jae Seung Kang
Prof. Dr. Yejin Kim
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. Pharmaceuticals 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 2900 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
  • inflammatory immune cells
  • cytokines
  • autoimmune diseases
  • infectious diseases
  • cancer

Published Papers (5 papers)

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Research

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10 pages, 3177 KiB  
Article
The Role of α-Enolase on the Production of Interleukin (IL)-32 in Con A-Mediated Inflammation and Rheumatoid Arthritis (RA)
by Hyejung Jo, Seulgi Shin, Tomoyo Agura, Seoyoun Jeong, Hyovin Ahn, Junmyung Lee, Yejin Kim and Jae Seung Kang
Pharmaceuticals 2024, 17(4), 531; https://doi.org/10.3390/ph17040531 - 20 Apr 2024
Viewed by 290
Abstract
Interleukin (IL)-32 is produced by T lymphocytes, natural killer cells, monocytes, and epithelial cells. IL-32 induces the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, IL-1β, IL-6, and IL-8, and IL-32 expression is highly increased in rheumatoid arthritis (RA) patients. Enolase-1 [...] Read more.
Interleukin (IL)-32 is produced by T lymphocytes, natural killer cells, monocytes, and epithelial cells. IL-32 induces the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, IL-1β, IL-6, and IL-8, and IL-32 expression is highly increased in rheumatoid arthritis (RA) patients. Enolase-1 (ENO1) is a glycolytic enzyme and the stimulation of ENO1 induces high levels of pro-inflammatory cytokines in concanavalin A (Con A)-activated peripheral blood mononuclear cells (PBMCs) and macrophages in RA patients. In addition, there are many reports that anti-ENO1 antibody is correlated with the disease progression of RA. It implies that ENO1 could regulate IL-32 production during inflammation related to the pathogenesis of RA. Therefore, we investigated the role of ENO1 in IL-32 production using Con A-activated PBMCs and RA PBMCs. IL-32 expression is increased by ENO1 stimulation using real-time PCR and ELISA. In addition, we confirmed that IL-32 production was decreased in Con A-activated PBMCs and RA PBMCs pre-treated with NF-κB or p38 MAPK pathway inhibitors. Taken together, these results suggest that ENO1 plays an important role in inflammation through the induction of IL-32 production by the activation of the NF-κB and p38 MAPK pathways. Full article
(This article belongs to the Special Issue Inflammatory Cytokines as New Therapeutic Targets)
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16 pages, 5727 KiB  
Article
The Analgesia Effect of Aucubin on CFA-Induced Inflammatory Pain by Inhibiting Glial Cells Activation-Mediated Inflammatory Response via Activating Mitophagy
by Dandan Yao, Yongjie Wang, Yeru Chen and Gang Chen
Pharmaceuticals 2023, 16(11), 1545; https://doi.org/10.3390/ph16111545 - 01 Nov 2023
Viewed by 1301
Abstract
Background: Inflammatory pain, characterized by sustained nociceptive hypersensitivity, represents one of the most prevalent conditions in both daily life and clinical settings. Aucubin, a natural plant iridoid glycoside, possesses potent biological effects, encompassing anti-inflammatory, antioxidant, and neuroprotective properties. However, its impact on inflammatory [...] Read more.
Background: Inflammatory pain, characterized by sustained nociceptive hypersensitivity, represents one of the most prevalent conditions in both daily life and clinical settings. Aucubin, a natural plant iridoid glycoside, possesses potent biological effects, encompassing anti-inflammatory, antioxidant, and neuroprotective properties. However, its impact on inflammatory pain remains unclear. The aim of this study is to investigate the therapeutic effects and underlying mechanism of aucubin in addressing inflammatory pain induced by complete Freund’s adjuvant (CFA). Methods: The CFA-induced inflammatory pain model was employed to assess whether aucubin exerts analgesic effects and its potential mechanisms. Behavioral tests evaluated mechanical and thermal hyperalgesia as well as anxiety-like behaviors in mice. The activation of spinal glial cells and the expression of pro-inflammatory cytokines were examined to evaluate neuroinflammation. Additionally, RNA sequencing was utilized for the identification of differentially expressed genes (DEGs). Molecular biology experiments were conducted to determine the levels of the PINK1 gene and autophagy-related genes, along with PINK1 distribution in neural cells. Furthermore, mitophagy induced by carbonyl cyanide m-chlorophenylhydrazone (CCCP) was employed to examine the roles of PINK1 and mitophagy in pain processing. Results: Aucubin significantly ameliorated pain and anxiety-like behaviors induced by CFA in mice and reduced spinal inflammation. RNA sequencing indicated PINK1 as a pivotal gene, and aucubin treatment led to a significant downregulation of PINK1 expression. Further GO and KEGG analyses suggested the involvement of mitochondrial function in the therapeutic regulation of aucubin. Western blotting revealed that aucubin markedly decreased PINK1, Parkin, and p62 levels while increasing LC3B expression. Immunofluorescence showed the predominant co-localization of PINK1 with neuronal cells. Moreover, CCCP-induced mitophagy alleviated mechanical and thermal hyperalgesia caused by CFA and reversed CFA-induced mitochondrial dysfunction. Conclusions: In summary, our data suggest that aucubin effectively alleviates CFA-induced inflammatory pain, potentially through triggering the PINK1 pathway, promoting mitophagy, and suppressing inflammation. These results provide a novel theoretical foundation for addressing the treatment of inflammatory pain. Full article
(This article belongs to the Special Issue Inflammatory Cytokines as New Therapeutic Targets)
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18 pages, 3575 KiB  
Article
Therapeutic Outcomes of High Dose-Dexamethasone versus Prednisolone + Azathioprine, Rituximab, Eltrombopag, and Romiplostim Strategies in Persistent, Chronic, Refractory, and Relapsed Immune Thrombocytopenia Patients
by Eman Mostafa Hamed, Ahmed R. N. Ibrahim, Mohamed Hussein Meabed, Ahmed M. Khalaf, Doaa Mohamed El Demerdash, Marwa O. Elgendy, Haitham Saeed, Heba F. Salem and Hoda Rabea
Pharmaceuticals 2023, 16(9), 1215; https://doi.org/10.3390/ph16091215 - 29 Aug 2023
Cited by 1 | Viewed by 1382
Abstract
Background: Primary immune thrombocytopenia (ITP) is an inflammatory autoimmune disease that can be managed with several treatment options. However, there is a lack of comparative data on the efficacy of these options in different phases of the disease. Aim of the study: This [...] Read more.
Background: Primary immune thrombocytopenia (ITP) is an inflammatory autoimmune disease that can be managed with several treatment options. However, there is a lack of comparative data on the efficacy of these options in different phases of the disease. Aim of the study: This study aimed to evaluate the efficacy of high-dose Dexamethasone (HD-DXM), Prednisolone + Azathioprine, Rituximab, Eltrombopag, and Romiplostim schedules in persistent, chronic refractory or relapsed Egyptian ITP patients with a platelet count ≤30 × 109/L. The primary outcome measure was a sustained increase in platelet counts over 50 × 109/L for an additional 12 months without additional ITP regimens. The study also aimed to identify a suitable treatment regimen with a long remission duration for each phase of ITP. Results: Prednisolone + Azathioprine was significantly more effective in achieving an overall response in persistent patients than Romiplostim, high-dose Dexamethasone, and Rituximab. (90.9% vs. 66.6, [Odds ratio, OR: 5; confidence interval, CI 95% (0.866–28.86)], 45%, [OR: 0.082, CI 95% (0.015–0.448)] and, 25%, [OR: 30, CI 95% (4.24–211.8)], respectively, p-value < 0.01). Eltrombopag was significantly more effective in achieving a durable response in refractory ITP than HD-DXM, Rituximab, and Prednisolone; (80% compared to 32.2% [OR: 0.119, CI 95% (0.035–0.410)], 22.2% [OR:0.071, CI 95% (0.011–0.455)], and 18.1% [OR: 0.056, CI 95% (0.009–0.342)], respectively, p-value < 0.01). Conclusions: Finally, Eltrombopag following HD-DXM showed the highest percentage of patients with complete treatment-free survival times of at least 330 days. These findings could help clinicians choose the most appropriate treatment for their patients with ITP based on the phase of the disease. This trial is registered in clinicaltrials.gov with registration number NCT05861297. Full article
(This article belongs to the Special Issue Inflammatory Cytokines as New Therapeutic Targets)
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13 pages, 2364 KiB  
Article
Dulaglutide Ameliorates Intrauterine Adhesion by Suppressing Inflammation and Epithelial–Mesenchymal Transition via Inhibiting the TGF-β/Smad2 Signaling Pathway
by Yifan Wang, Yixiang Wang, Yang Wu and Yiqing Wang
Pharmaceuticals 2023, 16(7), 964; https://doi.org/10.3390/ph16070964 - 05 Jul 2023
Viewed by 1450
Abstract
Intrauterine adhesion (IUA) is a common gynecological disease with limited therapeutic options. Dulaglutide is a long-acting glucagon-like peptide-1 (GLP-1) analog with some anti-fibrotic and anti-inflammatory properties; however, its action on IUA remains uncertain. The purpose of the experiments in this study was to [...] Read more.
Intrauterine adhesion (IUA) is a common gynecological disease with limited therapeutic options. Dulaglutide is a long-acting glucagon-like peptide-1 (GLP-1) analog with some anti-fibrotic and anti-inflammatory properties; however, its action on IUA remains uncertain. The purpose of the experiments in this study was to explore the effect of dulaglutide on IUA and to elucidate its mechanism to provide new ideas for the clinical treatment of IUA. An IUA mouse model was established via mechanical curettage and inflammation induction; mice received subcutaneous injection with three doses of dulaglutide once a day for two weeks (treatment) or equal amounts of sterile ddH2O (control), and sham-operated mice were treated similarly to the control mice. Mice were sacrificed, and uterine tissues were subjected to hematoxylin and eosin (H&E) and Masson’s trichrome staining for histomorphological and pathological analyses and real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting (WB) for gene and protein expression analyses. Dulaglutide improved the shape of the uterine cavity, increased endometrial thickness and the number of glands, and significantly reduced the area of collagen fiber deposition in the endometrium. It significantly reduced collagen type I A 1 (COL1A1), interleukin-1beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), C-C motif chemokine ligand 2 (CCL2), F4/80 (macrophage), vimentin and transforming growth factor-beta (TGF-β) mRNA levels and COL1A1, IL-1β, IL-6, TNF-α, F4/80, vimentin, E-cadherin, TGF-β, and p-Smad2 protein expression levels. This study demonstrates that dulaglutide reduces inflammatory responses by inhibiting M1 macrophage polarization and inflammatory factor release and may ameliorate fibrosis by inhibiting epithelial–mesenchymal transition (EMT) via TGF-β/Smad2 signaling. Full article
(This article belongs to the Special Issue Inflammatory Cytokines as New Therapeutic Targets)
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Review

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22 pages, 7188 KiB  
Review
Interleukins in Platelet Biology: Unraveling the Complex Regulatory Network
by Miao Huang, Long Wang, Qianhui Zhang, Ling Zhou, Rui Liao, Anguo Wu, Xinle Wang, Jiesi Luo, Feihong Huang, Wenjun Zou and Jianming Wu
Pharmaceuticals 2024, 17(1), 109; https://doi.org/10.3390/ph17010109 - 13 Jan 2024
Viewed by 1143
Abstract
Interleukins, a diverse family of cytokines produced by various cells, play crucial roles in immune responses, immunoregulation, and a wide range of physiological and pathological processes. In the context of megakaryopoiesis, thrombopoiesis, and platelet function, interleukins have emerged as key regulators, exerting significant [...] Read more.
Interleukins, a diverse family of cytokines produced by various cells, play crucial roles in immune responses, immunoregulation, and a wide range of physiological and pathological processes. In the context of megakaryopoiesis, thrombopoiesis, and platelet function, interleukins have emerged as key regulators, exerting significant influence on the development, maturation, and activity of megakaryocytes (MKs) and platelets. While the therapeutic potential of interleukins in platelet-related diseases has been recognized for decades, their clinical application has been hindered by limitations in basic research and challenges in drug development. Recent advancements in understanding the molecular mechanisms of interleukins and their interactions with MKs and platelets, coupled with breakthroughs in cytokine engineering, have revitalized the field of interleukin-based therapeutics. These breakthroughs have paved the way for the development of more effective and specific interleukin-based therapies for the treatment of platelet disorders. This review provides a comprehensive overview of the effects of interleukins on megakaryopoiesis, thrombopoiesis, and platelet function. It highlights the potential clinical applications of interleukins in regulating megakaryopoiesis and platelet function and discusses the latest bioengineering technologies that could improve the pharmacokinetic properties of interleukins. By synthesizing the current knowledge in this field, this review aims to provide valuable insights for future research into the clinical application of interleukins in platelet-related diseases. Full article
(This article belongs to the Special Issue Inflammatory Cytokines as New Therapeutic Targets)
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