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Pro- and Anti-inflammation Signaling Pathways and Development of Anti-inflammatory Drugs

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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 (31 July 2021) | Viewed by 35751

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Special Issue Editor

Prof. Dr. Sayeon Cho

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Guest Editor

College of Pharmacy, Chung-Ang University, 84 Heukseok-ro, Dongjak-gu, Seoul 06974, Korea
Interests: inflammation; apoptosis; cancer; metastasis; anti-inflammatory drugs; anti-metastasis drugs; signal transduction

Special Issue Information

Dear Colleagues,

The inflammatory response defends the host from harmful external factors, such as bacteria and fungi, and works to eliminate the harmful external factors and injured cells through the regulation of several inflammatory mechanisms. However, excessive inflammatory responses, which result in overproduction of inflammatory mediators, may lead to various inflammatory diseases, such as arthritis, asthma, multiple sclerosis, inflammatory bowel disease, and atherosclerosis. Therefore, the balance between pro-and anti-inflammation is critical for homeostasis. Until now, research has been intensively conducted to identify the inflammatory signaling pathways and anti-inflammatory drugs. Many novel synthetic or natural compounds showing anti-inflammatory activity will be discovered, and research on the efficacy evaluation, mechanism of action, and molecular target identification of these compounds will be of great help in the development of anti-inflammatory drugs.

This Special Issue aims to cover original and review articles on pro- and anti-inflammatory signaling pathways and the development of new synthetic or natural anti-inflammatory drugs. Therefore, we welcome research or review papers to expand our knowledge of pro- inflammatory and anti-inflammatory signaling pathways as well as to learn the latest information on novel synthetic or natural compounds with anti-inflammatory activity.

Prof. Dr. Sayeon Cho
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
pro-inflammatory mediator
anti-inflammatory mediator
anti-inflammatory compound
signal transduction
mechanism of action
molecular target
efficacy

Published Papers (5 papers)

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Research

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14 pages, 3241 KiB

Open AccessArticle

Activation of Nrf2/HO-1 by Peptide YD1 Attenuates Inflammatory Symptoms through Suppression of TLR4/MYyD88/NF-κB Signaling Cascade

by Md Saifur Rahman, Md Badrul Alam, Young Kyun Kim, Mst Hur Madina, Ismail Fliss, Sang Han Lee and Jin Cheol Yoo

Int. J. Mol. Sci. 2021, 22(10), 5161; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105161 - 13 May 2021

Cited by 14 | Viewed by 2383

Abstract

In this study, we investigate the immunomodulatory effects of a novel antimicrobial peptide, YD1, isolated from Kimchi, in both in vitro and in vivo models. We establish that YD1 exerts its anti-inflammatory effects via up-regulation of the Nrf2 pathway, resulting in the production of HO-1, which suppresses activation of the NF-κB pathway, including the subsequent proinflammatory cytokines IL-1β, IL-6, and TNF-α. We also found that YD1 robustly suppresses nitric oxide (NO) and prostaglandin E2 (PGE₂) production by down-regulating the expression of the upstream genes, iNOS and COX-2, acting as a strong antioxidant. Collectively, YD1 exhibits vigorous anti-inflammatory and antioxidant activity, presenting it as an interesting potential therapeutic agent. Full article

(This article belongs to the Special Issue Pro- and Anti-inflammation Signaling Pathways and Development of Anti-inflammatory Drugs)

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26 pages, 2936 KiB

Open AccessArticle

High-Throughput Screening for CEBPD-Modulating Compounds in THP-1-Derived Reporter Macrophages Identifies Anti-Inflammatory HDAC and BET Inhibitors

by Tatjana Ullmann, Sonja Luckhardt, Markus Wolf, Michael J. Parnham and Eduard Resch

Int. J. Mol. Sci. 2021, 22(6), 3022; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063022 - 16 Mar 2021

Cited by 8 | Viewed by 3118

Abstract

This study aimed to identify alternative anti-inflammatory compounds that modulate the activity of a relevant transcription factor, CCAAT/enhancer binding protein delta (C/EBPδ). C/EBPδ is a master regulator of inflammatory responses in macrophages (Mϕ) and is mainly regulated at the level of CEBPD gene transcription initiation. To screen for CEBPD-modulating compounds, we generated a THP-1-derived reporter cell line stably expressing secreted alkaline phosphatase (SEAP) under control of the defined CEBPD promoter (CEBPD::SEAP). A high-throughput screening of LOPAC^®1280 and ENZO^®774 libraries on LPS- and IFN-γ-activated THP-1 reporter Mϕ identified four epigenetically active hits: two bromodomain and extraterminal domain (BET) inhibitors, I-BET151 and Ro 11-1464, as well as two histone deacetylase (HDAC) inhibitors, SAHA and TSA. All four hits markedly and reproducibly upregulated SEAP secretion and CEBPD::SEAP mRNA expression, confirming screening assay reliability. Whereas BET inhibitors also upregulated the mRNA expression of the endogenous CEBPD, HDAC inhibitors completely abolished it. All hits displayed anti-inflammatory activity through the suppression of IL-6 and CCL2 gene expression. However, I-BET151 and HDAC inhibitors simultaneously upregulated the mRNA expression of pro-inflammatory IL-1ß. The modulation of CEBPD gene expression shown in this study contributes to our understanding of inflammatory responses in Mϕ and may offer an approach to therapy for inflammation-driven disorders. Full article

(This article belongs to the Special Issue Pro- and Anti-inflammation Signaling Pathways and Development of Anti-inflammatory Drugs)

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Review

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19 pages, 1477 KiB

Open AccessReview

Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis

by Yoshitaka Kimura, Daisuke Tsukui and Hajime Kono

Int. J. Mol. Sci. 2021, 22(22), 12394; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212394 - 17 Nov 2021

Cited by 96 | Viewed by 14011

Abstract

Hyperuricemia is a common metabolic syndrome. Elevated uric acid levels are risk factors for gout, hypertension, and chronic kidney diseases. Furthermore, various epidemiological studies have also demonstrated an association between cardiovascular risks and hyperuricemia. In hyperuricemia, reactive oxygen species (ROS) are produced simultaneously with the formation of uric acid by xanthine oxidases. Intracellular uric acid has also been reported to promote the production of ROS. The ROS and the intracellular uric acid itself regulate several intracellular signaling pathways, and alterations in these pathways may result in the development of atherosclerotic lesions. In this review, we describe the effect of uric acid on various molecular signals and the potential mechanisms of atherosclerosis development in hyperuricemia. Furthermore, we discuss the efficacy of treatments for hyperuricemia to protect against the development of atherosclerosis. Full article

(This article belongs to the Special Issue Pro- and Anti-inflammation Signaling Pathways and Development of Anti-inflammatory Drugs)

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20 pages, 1071 KiB

Open AccessReview

Oxidative Stress, Testicular Inflammatory Pathways, and Male Reproduction

by Sulagna Dutta, Pallav Sengupta, Petr Slama and Shubhadeep Roychoudhury

Int. J. Mol. Sci. 2021, 22(18), 10043; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221810043 - 17 Sep 2021

Cited by 104 | Viewed by 10376

Abstract

Inflammation is among the core causatives of male infertility. Despite male infertility being a serious global issue, “bits and pieces” of its complex etiopathology still remain missing. During inflammation, levels of proinflammatory mediators in the male reproductive tract are greater than usual. According to epidemiological research, in numerous cases of male infertility, patients suffer from acute or chronic inflammation of the genitourinary tract which typically occurs without symptoms. Inflammatory responses in the male genital system are inextricably linked to oxidative stress (OS). OS is detrimental to male fertility parameters as it causes oxidative damage to reproductive cells and intracellular components. Multifarious male infertility causative factors pave the way for impairing male reproductive functions via the common mechanisms of OS and inflammation, both of which are interlinked pathophysiological processes, and the occurrence of any one of them induces the other. Both processes may be simultaneously found in the pathogenesis of male infertility. Thus, the present article aims to explain the role of inflammation and OS in male infertility in detail, as well as to show the mechanistic pathways that link causative factors of male reproductive tract inflammation, OS induction, and oxidant-sensitive cellular cascades leading to male infertility. Full article

(This article belongs to the Special Issue Pro- and Anti-inflammation Signaling Pathways and Development of Anti-inflammatory Drugs)

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16 pages, 791 KiB

Open AccessReview

Inflammatory Mechanisms in COVID-19 and Atherosclerosis: Current Pharmaceutical Perspectives

by Marios Sagris, Panagiotis Theofilis, Alexios S. Antonopoulos, Costas Tsioufis, Evangelos Oikonomou, Charalambos Antoniades, Filippo Crea, Juan Carlos Kaski and Dimitris Tousoulis

Int. J. Mol. Sci. 2021, 22(12), 6607; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22126607 - 21 Jun 2021

Cited by 51 | Viewed by 4964

Abstract

Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been associated with excess mortality worldwide. The cardiovascular system is the second most common target of SARS-CoV-2, which leads to severe complications, including acute myocardial injury, myocarditis, arrhythmias, and venous thromboembolism, as well as other major thrombotic events because of direct endothelial injury and an excessive systemic inflammatory response. This review focuses on the similarities and the differences of inflammatory pathways involved in COVID-19 and atherosclerosis. Anti-inflammatory agents and immunomodulators have recently been assessed, which may constitute rational treatments for the reduction of cardiovascular events in both COVID-19 and atherosclerotic heart disease. Full article

(This article belongs to the Special Issue Pro- and Anti-inflammation Signaling Pathways and Development of Anti-inflammatory Drugs)

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