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Molecular Mechanism in Inflammation and Immunity

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

Deadline for manuscript submissions: 31 July 2025 | Viewed by 6859

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Dr. Anella Saviano

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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

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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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13 pages, 3370 KiB

Open AccessArticle

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

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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 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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Figure 1

Figure 1
UDCA attenuates LPS-activated NF-κB expression. Expression of NF-κB p65, phospho-FN-κB p65, and farnesoid X receptors (NR1H4) (a) and the optical densities of the bands were quantified (b). HepG2 cells were treated with LPS in the presence and absence of UDCA. Control cells (Con) and UDCA alone determine the UDCA effect on LPS in HepG2 cells. The inflammation response of HepG2 cells was induced with the LPS (1 μg/mL) and under the UDCA (500 μM) for 24 h. Lysates were subjected to immunoblotting using anti-NF-κB/p65, anti-phospho-NF–κB/p65 antibodies. Protein expression was studied by Western blotting and GAPDH served as the control. * p < 0.001 Kruskal–Wallis test. Full article ">Figure 1 Cont.
UDCA attenuates LPS-activated NF-κB expression. Expression of NF-κB p65, phospho-FN-κB p65, and farnesoid X receptors (NR1H4) (a) and the optical densities of the bands were quantified (b). HepG2 cells were treated with LPS in the presence and absence of UDCA. Control cells (Con) and UDCA alone determine the UDCA effect on LPS in HepG2 cells. The inflammation response of HepG2 cells was induced with the LPS (1 μg/mL) and under the UDCA (500 μM) for 24 h. Lysates were subjected to immunoblotting using anti-NF-κB/p65, anti-phospho-NF–κB/p65 antibodies. Protein expression was studied by Western blotting and GAPDH served as the control. * p < 0.001 Kruskal–Wallis test. Full article ">Figure 2
UDCA regulates LPS-induced FN-κB and FXR target genes and proteins. UDCA regulates LPS-induced NF-κB target production of TNF-α, IL-6, and COX-2, and FXR target genes mRNA in HepG2 cells. HepG2 cells (1 × 106 cells/mL) were incubated with LPS (1 μg/mL) alone or in the presence of UDCA (500 μM) or the corresponding vehicle for 24 h. LPS could upregulate expression of TNFα (a), IL-6 (b), and COX-2 (c), which could be downregulated by co-treatment with UDCA. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as an internal control to normalize the target gene’s expression. UDCA decreases LPD-induced liver cyp7a1 mRNA expression (d) and increases liver shp mRNA expression (e). (f) The FN-κB regulated IL-6 is expressed at protein by ELISA * p < 0.05; ** p < 0.005; *** p < 0.0005: Kruskal–Wallis test. Full article ">Figure 2 Cont.
UDCA regulates LPS-induced FN-κB and FXR target genes and proteins. UDCA regulates LPS-induced NF-κB target production of TNF-α, IL-6, and COX-2, and FXR target genes mRNA in HepG2 cells. HepG2 cells (1 × 106 cells/mL) were incubated with LPS (1 μg/mL) alone or in the presence of UDCA (500 μM) or the corresponding vehicle for 24 h. LPS could upregulate expression of TNFα (a), IL-6 (b), and COX-2 (c), which could be downregulated by co-treatment with UDCA. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as an internal control to normalize the target gene’s expression. UDCA decreases LPD-induced liver cyp7a1 mRNA expression (d) and increases liver shp mRNA expression (e). (f) The FN-κB regulated IL-6 is expressed at protein by ELISA * p < 0.05; ** p < 0.005; *** p < 0.0005: Kruskal–Wallis test. Full article ">Figure 3
Effect of UDCA on the nuclear translocation of phospho-NF-κB p65 in LPS-induced HepG2 cells. Immunofluorescence assay and confocal microscopy image were applied to detect the distribution of phospho-NF-κB p65 in HepG2 cells treated with LPS alone or in combination with UDCA (LPS 1 µg/mL; ESO 25 µM). The images were captured at 200× magnification. Full article ">Figure 4
UDCA suppresses the NF-κB activity inside the nucleus of NF-κB in LPS-stimulated HepG2. Cells were treated with LPS (1 μg/mL) combined with/without UDCA (500 μM) for 24 h. EMSA was performed to determine the NF-κB activity in the nuclear fraction using a DNA probe specific to NF-κB. Full article ">Figure 5
UDCA down-regulates miR-21 level induced by LPS in HepG2 cells. The miR-21 expression was determined by qRT-PCR. Each reaction was performed in triplicate, and mean values were used for calculating the relative fold change. Black dot is preseted as every experimental relative expression of miR-21. * p < 0.001 Kruskal–Wallis test. ns: no significance. Full article ">

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21 pages, 2570 KiB

Open AccessSystematic 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

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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 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 KiB

Open AccessSystematic 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 1 | Viewed by 1723

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 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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