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Biomedicines
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Molecular Mechanism in Inflammation and Immunity
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Molecular Mechanism in Inflammation and Immunity

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 July 2025) | Viewed by 13925

Special Issue Editor

Dr. Anella Saviano

E-Mail Website
Guest Editor
ImmunoPharmaLab, Department of Pharmacy, University of Naples “Federico II”, Via Montesano 49, 80131 Naples, Italy
Interests: IL-17; inflammation; autoimmune-based diseases; Th17; Treg; natural compounds and nutraceuticals

Special Issue Information

Dear Colleagues,

Inflammation is a complex biological response to injury as a result of different stimuli, such
as pathogens, damaged cells, or irritants. Inflammatory injuries induce the release of a variety of systemic mediators, cytokines, and chemokines that orchestrate the cellular infiltration that consequentially brings about the resolution of inflammatory responses and the restoration of tissue integrity. However, persistent inflammatory stimuli or the dysregulation of mechanisms of the resolution phase can lead to chronic inflammation and inflammatory-based diseases.  

The recent and emerging scientific community slant is oriented towards novel mechanisms and mediators that could represent a boon for the discovery of new active molecules and for the development of new drugs and potentially useful therapeutic agents in different inflammatory and immune-mediated/related diseases. 

We cordially invite authors and investigators within this complex field of global interest to submit original research and/or review articles pertaining to this Special Issue.

Dr. Anella Saviano
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.

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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

  • adaptive immunity
  • autoimmune-based diseases
  • cyto/chemokines
  • inflammation
  • macrophages
  • natural compounds
  • nutraceuticals
  • signaling pathway in arachidonic acid cascade
  • T-cells
  • trained immunity

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Published Papers (6 papers)

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Research

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15 pages, 3163 KB  
Article
β-Casomorphin-7 as a Potential Inflammatory Marker: How β-Casomorphin-7 Induces Endothelial Dysfunction in HUVEC/TERT2 Cell Lines
by Judit Rita Homoki, Emese Szilágyi-Tolnai, Ildikó Kovács-Forgács, Georgina Pesti-Asbóth, Arnold Markovics, Attila Biró, Péter Dávid, János Lukács, László Stündl, Judit Remenyik and Attila Péter Kiss
Biomedicines 2025, 13(11), 2712; https://doi.org/10.3390/biomedicines13112712 - 5 Nov 2025
Viewed by 26
Abstract
Background/Objectives: Endothelial dysfunction plays a central role in the development of cardiovascular diseases. β-Casomorphin-7 (BCM-7), a biologically active peptide generated during the digestion of A1 β-casein, is presumed to contribute to this process; however, its direct effects on endothelial cells have not [...] Read more.
Background/Objectives: Endothelial dysfunction plays a central role in the development of cardiovascular diseases. β-Casomorphin-7 (BCM-7), a biologically active peptide generated during the digestion of A1 β-casein, is presumed to contribute to this process; however, its direct effects on endothelial cells have not been previously investigated. Here, we aimed to assess whether BCM-7 treatment induces endothelial cell dysfunction through inflammatory cytokines and reactive oxygen species (ROS). Methods: In our study, we analyzed the effects of BCM-7 (5 µg/mL) in combination with lipopolysaccharide (LPS, 100 ng/mL) on human umbilical vein endothelial cells (HUVECs/TERT2). The cell viability, apoptosis, necrosis, and intracellular reactive oxygen species were measured. Furthermore, proinflammatory cytokines and enzymes involved in the regulation of inflammation were assessed with quantitative real-time PCR. The gene and protein expression of enzymes that regulate inflammation and vascular function, thus maintaining endothelial homeostasis were assessed. Results: BCM-7 enhanced intracellular ROS production p ≤ 0.001, increased the expression of interleukin-6 (IL-6) and interleukin-8 (IL-8) p ≤ 0.001, and was more effective when used in combination with LPS p ≤ 0.001. It decreased the expression of cyclooxygenase-1 (COX-1) p ≤ 0.05, during 4 h of exposure, whereas it increased the expression of cyclooxygenase-2 (COX-2) p ≤ 0.001, lipoxygenase-5 (LOX-5) p ≤ 0.01, and nitric oxide synthase 3 (NOS3) p ≤ 0.001; prostaglandin D2 synthase (PTGDS) (p ≤ 0.05), expression was also increased after short treatment. Conclusions: Our results suggest that BCM-7 may contribute to the development of endothelial dysfunction, especially in the presence of LPS, by enhancing oxidative stress and inflammatory response. Full article
(This article belongs to the Special Issue Molecular Mechanism in Inflammation and Immunity)
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19 pages, 5052 KB  
Article
Hydrogen Sulfide Attenuates Cisplatin-Induced Acute Kidney Injury via Dual Inhibition of Apoptosis and Pyroptosis
by Zhenyuan Han, Yutao Jia, Dechao Yan, Ying Xue, Tianyu Deng, Ping Wang, Leijuan Xiao and Xiaoyan Wang
Biomedicines 2025, 13(11), 2696; https://doi.org/10.3390/biomedicines13112696 - 3 Nov 2025
Viewed by 227
Abstract
Purpose: Cisplatin chemotherapy is complicated by acute kidney injury (cis-AKI), driven by regulated cell death pathways, including apoptosis and pyroptosis. However, the temporal relationship between apoptosis and pyroptosis in cis-AKI remains unclear. This study investigated the roles of these pathways and evaluated the [...] Read more.
Purpose: Cisplatin chemotherapy is complicated by acute kidney injury (cis-AKI), driven by regulated cell death pathways, including apoptosis and pyroptosis. However, the temporal relationship between apoptosis and pyroptosis in cis-AKI remains unclear. This study investigated the roles of these pathways and evaluated the renoprotective effect of the hydrogen sulfide (H2S) donor GYY4137. Method: Cis-AKI was modeled in mice and HK2 cells, divided into control, cisplatin, and cisplatin + GYY groups. Kidney function parameters, histopathology, and cell death were evaluated. Markers of apoptosis and pyroptosis, along with the H2S-producing enzyme, were analyzed. Results: Renal impairment progressed from BUN elevation to increased Scr, coupled with aggravated renal tissue damage. Apoptotic signaling peaked at 24 h, evidenced by a raised Bax/Bcl-2 ratio and caspase-3 cleavage. Pyroptosis pathways, via both NLRP3/caspase-1/GSDMD and caspase-3/GSDME axes, were activated later at 72 h, with concurrent rises in IL-1β and IL-18. GYY4137 treatment significantly ameliorated renal dysfunction, reducing serum creatinine and BUN levels by 22.64% and 22.5%, respectively. It suppressed both the early apoptotic and delayed pyroptosis cascades without reversing CBS downregulation. Conclusions: GYY4137 mitigated both apoptosis and pyroptosis, offering a promising multi-targeted therapy for cis-AKI. Full article
(This article belongs to the Special Issue Molecular Mechanism in Inflammation and Immunity)
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13 pages, 3370 KB  
Article
Ursodeoxycholic Acid Modulates the Interaction of miR-21 and Farnesoid X Receptor and NF-κB Signaling
by Chi-Yi Peng, Yi-Chun Liao, Yi-Chin Yang, Yi-Wen Hung, Lan-Ru Huang and Yen-Chun Peng
Biomedicines 2024, 12(6), 1236; https://doi.org/10.3390/biomedicines12061236 - 2 Jun 2024
Cited by 2 | Viewed by 5268
Abstract
(1) Background: This study investigates the effects of Ursodeoxycholic acid (UDCA) on NF-κB signaling, farnesoid X receptor (FXR) singling, and microRNA-21 in HepG2 cells. (2) Methods: HepG2 cells were treated with lipopolysaccharide (LPS) to simulate hepatic inflammation. The investigation focused on the expression [...] Read more.
(1) Background: This study investigates the effects of Ursodeoxycholic acid (UDCA) on NF-κB signaling, farnesoid X receptor (FXR) singling, and microRNA-21 in HepG2 cells. (2) Methods: HepG2 cells were treated with lipopolysaccharide (LPS) to simulate hepatic inflammation. The investigation focused on the expression of NF-κB activation, which was analyzed using Western blot, confocal microscopy, and Electrophoretic Mobility-shift Assays (EMSA). Additionally, NF-κB and farnesoid X receptor (FXR) singling expressions of micro-RNA-21, COX-2, TNF-α, IL-6, cyp7A1, and shp were assessed by RT-PCR. (3) Results: UDCA effectively downregulated LPS-induced expressions of NF-κB/65, p65 phosphorylation, and also downregulated FXR activity by Western blot. Confocal microscopy and EMSA results confirmed UDCA’s role in modulating NF-κB signaling. UDCA reduced the expressions of LPS-induced COX-2, TNF-α, and IL-6, which were related to NF-κB signaling. UDCA downregulated LPS-induced cyp7A1 gene expression and upregulated shp gene expression, demonstrating selective gene regulation via FXR. UDCA also significantly decreased micro-RNA 21 levels. (4) Conclusions: This study demonstrates UDCA’s potent anti-inflammatory effects on NF-κB and FXR signaling pathways, and thus its potential to modulate hepatic inflammation and carcinogenesis through interactions with NF-κB and FXR. The decrease in micro-RNA 21 expression further underscores its therapeutic potential. Full article
(This article belongs to the Special Issue Molecular Mechanism in Inflammation and Immunity)
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Review

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22 pages, 672 KB  
Review
Chronic Inflammation and Immune Dysregulation in Metabolic-Dysfunction-Associated Steatotic Liver Disease Progression: From Steatosis to Hepatocellular Carcinoma
by Young-Min Jee, Jeong-Yoon Lee and Tom Ryu
Biomedicines 2025, 13(5), 1260; https://doi.org/10.3390/biomedicines13051260 - 21 May 2025
Cited by 5 | Viewed by 2592
Abstract
Background/Objectives: Metabolic-dysfunction-associated steatotic liver disease (MASLD) progresses from hepatic steatosis to hepatocellular carcinoma (HCC) as a result of systemic immunometabolic dysfunction. This review summarizes the key roles of the innate and adaptive immune mechanisms driving hepatic injury, fibrogenesis, and carcinogenesis in MASLD. [...] Read more.
Background/Objectives: Metabolic-dysfunction-associated steatotic liver disease (MASLD) progresses from hepatic steatosis to hepatocellular carcinoma (HCC) as a result of systemic immunometabolic dysfunction. This review summarizes the key roles of the innate and adaptive immune mechanisms driving hepatic injury, fibrogenesis, and carcinogenesis in MASLD. Methods: A comprehensive literature review was performed using PubMed to identify relevant published studies. Eligible articles included original research and clinical studies addressing immunological and metabolic mechanisms in MASLD, as well as emerging therapeutic strategies. Results: We highlight the roles of cytokine networks, the gut–liver axis, and immune cell reprogramming. Emerging therapeutic strategies, including cytokine inhibitors, anti-fibrotic agents, metabolic modulators, and nutraceuticals, offer several indications for attenuating MASLD progression and reducing the prevalence of extrahepatic manifestations. Conclusions: Given the heterogeneity of MASLD, personalized combination-based approaches targeting both inflammation and metabolic stress are essential for effective disease management and the prevention of systemic complications. Full article
(This article belongs to the Special Issue Molecular Mechanism in Inflammation and Immunity)
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Other

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21 pages, 2570 KB  
Systematic Review
Systematic Review and Meta-Analysis of Inflammatory Biomarkers in Individuals Exposed to Radon
by Anel Lesbek, Yasutaka Omori, Meirat Bakhtin, Polat Kazymbet, Shinji Tokonami, Nursulu Altaeva, Danara Ibrayeva and Yerlan Kashkinbayev
Biomedicines 2025, 13(2), 499; https://doi.org/10.3390/biomedicines13020499 - 17 Feb 2025
Cited by 2 | Viewed by 2018
Abstract
Background/Objectives: Radon is a significant carcinogen, particularly as a leading cause of lung cancer among non-smokers. While its carcinogenic effects are well documented, the relationship between radon exposure and inflammatory reactions remains underexplored. This systematic review investigates inflammatory biomarkers in individuals exposed [...] Read more.
Background/Objectives: Radon is a significant carcinogen, particularly as a leading cause of lung cancer among non-smokers. While its carcinogenic effects are well documented, the relationship between radon exposure and inflammatory reactions remains underexplored. This systematic review investigates inflammatory biomarkers in individuals exposed to chronic radon exposure and conducts a meta-analysis on serum C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α) levels. Methods: A systematic search was conducted in PubMed, Scopus, Web of Science, ScienceDirect, and Google Scholar using the keywords “radon” AND “inflammation biomarkers” following established guidelines. Studies reporting inflammatory biomarker levels in biological fluids of human participants exposed to residential or occupational radon were included. Statistical analyses, including pooled mean estimates, influence analysis, publication bias, and meta-regression, were performed in RStudio. Results: Ten studies involving 33,099 individuals met the inclusion criteria. Eight studies focused on residential radon exposure, and two examined occupational exposure among uranium miners. Inflammatory biomarkers were analyzed in serum, bronchoalveolar lavage fluid, and saliva. Among individuals exposed to high residential radon levels, serum CRP and TNF-α were the most frequently assessed biomarkers, with pooled mean levels of 2.11 mg/L (95% CI, 1.32–2.89) and 2.20 pg/mL (95% CI, 0.25–4.64), respectively. Conclusions: Serum CRP and TNF-α levels appear lower in adults with chronic radon exposure, suggesting potential anti-inflammatory effects despite radon’s established carcinogenicity. Future longitudinal studies using standardized methods are crucial to elucidate the long-term health impacts of radon exposure. Full article
(This article belongs to the Special Issue Molecular Mechanism in Inflammation and Immunity)
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20 pages, 894 KB  
Systematic Review
The Pharmacological Effect of Hemin in Inflammatory-Related Diseases: A Systematic Review
by João Estarreja, Gonçalo Caldeira, Inês Silva, Priscila Mendes and Vanessa Mateus
Biomedicines 2024, 12(4), 898; https://doi.org/10.3390/biomedicines12040898 - 18 Apr 2024
Cited by 4 | Viewed by 2670
Abstract
Background: Hemin is clinically used in acute attacks of porphyria; however, recent evidence has also highlighted its capability to stimulate the heme oxygenase enzyme, being associated with cytoprotective, antioxidant, and anti-inflammatory effects. Indeed, current preclinical evidence emphasizes the potential anti-inflammatory role of hemin [...] Read more.
Background: Hemin is clinically used in acute attacks of porphyria; however, recent evidence has also highlighted its capability to stimulate the heme oxygenase enzyme, being associated with cytoprotective, antioxidant, and anti-inflammatory effects. Indeed, current preclinical evidence emphasizes the potential anti-inflammatory role of hemin through its use in animal models of disease. Nevertheless, there is no consensus about the underlying mechanism(s) and the most optimal therapeutic regimens. Therefore, this review aims to summarize, analyze, and discuss the current preclinical evidence concerning the pharmacological effect of hemin. Methods: Following the application of the search expression and the retrieval of the articles, only nonclinical studies in vivo written in English were considered, where the potential anti-inflammatory effect of hemin was evaluated. Results: Forty-nine articles were included according to the eligibility criteria established. The results obtained show the preference of using 30 to 50 mg/kg of hemin, administered intraperitoneally, in both acute and chronic contexts. This drug demonstrates significant anti-inflammatory and antioxidant activities considering its capacity for reducing the expression of proinflammatory and oxidative markers. Conclusions: This review highlighted the significant anti-inflammatory and antioxidant effects of hemin, providing a clearer vision for the medical community about the use of this drug in several human diseases. Full article
(This article belongs to the Special Issue Molecular Mechanism in Inflammation and Immunity)
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