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Keywords = inflammatory skin mouse model

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17 pages, 4113 KiB  
Article
Protective Effect of Camellia japonica Extract on 2,4-Dinitrochlorobenzene (DNCB)-Induced Atopic Dermatitis in an SKH-1 Mouse Model
by Chaodeng Mo, Md. Habibur Rahman, Thu Thao Pham, Cheol-Su Kim, Johny Bajgai and Kyu-Jae Lee
Int. J. Mol. Sci. 2025, 26(15), 7286; https://doi.org/10.3390/ijms26157286 - 28 Jul 2025
Viewed by 217
Abstract
Atopic dermatitis (AD) is a common chronic inflammatory skin disorder characterized by immune dysregulation and skin barrier impairment. This study evaluated the anti-inflammatory and immunomodulatory effects of Camellia japonica extract in a 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model using SKH-1 hairless mice. Topical application [...] Read more.
Atopic dermatitis (AD) is a common chronic inflammatory skin disorder characterized by immune dysregulation and skin barrier impairment. This study evaluated the anti-inflammatory and immunomodulatory effects of Camellia japonica extract in a 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model using SKH-1 hairless mice. Topical application of Camellia japonica extract for four weeks significantly alleviated AD-like symptoms by reducing epidermal thickness, mast cell infiltration, and overall skin inflammation. Hematological analysis revealed a marked decrease in total white blood cell (WBC) and neutrophil counts. Furthermore, the Camellia japonica extract significantly decreased oxidative stress, as evidenced by reduced serum reactive oxygen species (ROS) and nitric oxide (NO) levels, while enhancing the activity of antioxidant enzymes such as catalase. Importantly, allergic response markers including serum immunoglobulin E (IgE), histamine, and thymic stromal lymphopoietin (TSLP), were also downregulated. At the molecular level, Camellia japonica extract suppressed the expression of key pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and T helper 2 (Th2)-type cytokines such as IL-4 and IL-5, while slightly upregulating the anti-inflammatory cytokine IL-10. Collectively, these findings suggest that Camellia japonica extract effectively modulates immune responses, suppresses allergic responses, attenuates oxidative stress, and promotes skin barrier recovery. Therefore, application of Camellia japonica extract holds the promising effect as a natural therapeutic agent for the prevention and treatment of AD-like skin conditions. Full article
(This article belongs to the Section Bioactives and Nutraceuticals)
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18 pages, 3083 KiB  
Article
Targeting Vascular and Inflammatory Crosstalk: Cannabigerol as a Dual-Pathway Modulator in Rosacea
by Suji Kim and Ji Hyun Lee
Int. J. Mol. Sci. 2025, 26(14), 6840; https://doi.org/10.3390/ijms26146840 - 16 Jul 2025
Viewed by 223
Abstract
Rosacea is a chronic inflammatory skin condition characterized by persistent erythema and abnormal vascular response. Although current treatments focus on symptomatic relief, they often provide only temporary improvement and may be associated with side effects or recurrence. Cannabigerol (CBG), a non-psychoactive cannabinoid, has [...] Read more.
Rosacea is a chronic inflammatory skin condition characterized by persistent erythema and abnormal vascular response. Although current treatments focus on symptomatic relief, they often provide only temporary improvement and may be associated with side effects or recurrence. Cannabigerol (CBG), a non-psychoactive cannabinoid, has recently garnered attention for its pharmacological activities, including anti-inflammatory, antioxidant, neuroprotective, and skin barrier–supportive effects. However, its role in modulating pathological responses in rosacea remains unclear. In this study, we investigated the therapeutic potential of topically applied CBG in an LL-37-induced rosacea-like mouse model. Clinical and histological assessments revealed that CBG markedly reduced erythema, epidermal hyperplasia, and mast cell infiltration. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) showed downregulation of Il1b, Il4, Il6, Il13, Il22, Il31, Tlr2, Vegfa, and Mmp9. Immunohistochemistry and Western blot analyses further demonstrated suppression of CD31, vascular endothelial growth factor (VEGF), and Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), along with reduced activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, including decreased levels of JAK1, STAT3, and phosphorylated STAT3. These findings suggest that topical CBG alleviates rosacea-like skin inflammation by targeting inflammatory and vascular pathways, including JAK/STAT and YAP/TAZ signaling. Full article
(This article belongs to the Special Issue Molecular Research Progress of Skin and Skin Diseases: 2nd Edition)
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15 pages, 10930 KiB  
Article
Leflunomide-Mediated Immunomodulation Inhibits Lesion Progression in a Vitiligo Mouse Model
by Fang Miao, Xiaohui Li, Liang Zhao, Shijiao Zhang, Mengmeng Geng, Chuhuan Ye, Ying Shi and Tiechi Lei
Int. J. Mol. Sci. 2025, 26(14), 6787; https://doi.org/10.3390/ijms26146787 - 15 Jul 2025
Viewed by 284
Abstract
Autoimmune CD8+ T cell-driven melanocyte destruction constitutes a key pathogenic mechanism in the development of vitiligo. Therefore, the pharmacological inhibition of CD8+ T cell effector functions and skin trafficking is a clinically viable therapeutic strategy. This study investigates leflunomide (LEF), an [...] Read more.
Autoimmune CD8+ T cell-driven melanocyte destruction constitutes a key pathogenic mechanism in the development of vitiligo. Therefore, the pharmacological inhibition of CD8+ T cell effector functions and skin trafficking is a clinically viable therapeutic strategy. This study investigates leflunomide (LEF), an immunomodulatory drug with established safety in autoimmune diseases, for its therapeutic potential in a tyrosine-related protein (TRP) 2-180-induced vitiligo mouse model. Through flow cytometry, immunofluorescence, ELISA, and histopathological analyses, we systematically evaluated LEF’s effects on T cell regulation, chemokine expression, and cytokine profiles. Key findings demonstrated that LEF (20 mg/kg/day) significantly attenuated depigmentation by reducing CD8+ T cell infiltration and suppressing the IFN-γ-driven expression of CXCL9/10. Furthermore, LEF restored CD4+/CD8+ T cell homeostasis and rebalanced pro-inflammatory (IFN-γ, TNF-α, IL-2) and anti-inflammatory (IL-4, IL-10) cytokines, inducing a shift from Th1 to Th2. These results position LEF as an effective immunomodulator that disrupts the IFN-γ-CXCL9/10 axis and re-establishes immune balance, offering a promising repurposing strategy for halting vitiligo progression. Full article
(This article belongs to the Special Issue Advances in Vitiligo: From Mechanisms to Treatment Innovations)
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16 pages, 4613 KiB  
Article
Perfluorononanoic Acid (PFNA) Exacerbates Atopic Dermatitis by Inducing Inflammation in Mice
by Jiali Xiao, Junchao Wang, Nuo Xu, Xulong Huang, Farid Khalilov, Xianfeng Huang, Xiangyong Zheng, Xiashun Xu, Shisheng Lin, Wengang Zhao and Elchin Khalilov
Toxics 2025, 13(7), 585; https://doi.org/10.3390/toxics13070585 - 13 Jul 2025
Viewed by 452
Abstract
Perfluorononanoic acid (PFNA) is a ubiquitous persistent environmental pollutant, and several studies have found significant links between atopic dermatitis (AD) and prenatal exposure to PFNA. However, the relationship between PFNA and AD remains unclear. In this study, 2,4-dinitrochlorobenzene (DNCB)-treated female BALB/c mice were [...] Read more.
Perfluorononanoic acid (PFNA) is a ubiquitous persistent environmental pollutant, and several studies have found significant links between atopic dermatitis (AD) and prenatal exposure to PFNA. However, the relationship between PFNA and AD remains unclear. In this study, 2,4-dinitrochlorobenzene (DNCB)-treated female BALB/c mice were used as AD models to investigate the effects of PFNA and its potential mechanisms. These mice were topically applied with 5 mg/kg PFNA per day for 15 days. The results demonstrated that PFNA significantly increased AD lesion severity and clinical symptoms, including dermatitis score, ear thickness, and epidermal thickness. In addition, PFNA also increased the serum IgE level, splenic atrophy, and upregulated the expression of TNF-α, IL-6, and IL-, genes that are associated with skin inflammatory factors. In addition, Western blot results showed that PFNA treatment upregulated the expression of p-JNK protein. Additionally, cellular experiments indicated that RAW264.7 macrophages and mouse brain microvascular endothelial (bEnd.3) cells treated with PFNA at concentrations of 0.01–100 μM for 72 h showed no changes in cell viability. However, 100 μM PFNA upregulated the mRNA expression levels of the pro-inflammatory cytokines IL-1β and IL-6, as well as the protein expression of p-JNK, in RAW264.7 cells induced with 1 mg/mL LPS for 2 h. Similarly, PFNA increased TNF-α and IL-6 mRNA expression and p-JNK protein expression in bEnd.3 cells stimulated with 20 ng/mL TNF-α for 0.5 h. Based on these findings, we can conclude that PFNA may aggravate atopic dermatitis by promoting inflammation. Full article
(This article belongs to the Section Emerging Contaminants)
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21 pages, 4013 KiB  
Article
Taraxacum mongolicum Ameliorates DNCB-Induced Atopic Dermatitis-like Symptoms in Mice by Regulating Oxidative Stress, Inflammation, MAPK, and JAK/STAT/TSLP Signaling Pathways
by Wen-Ping Jiang, Hsi-Pin Hung, Jaung-Geng Lin, Ling-Huei Chang, Atsushi Inose and Guan-Jhong Huang
Int. J. Mol. Sci. 2025, 26(14), 6601; https://doi.org/10.3390/ijms26146601 - 9 Jul 2025
Viewed by 399
Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease stemming from genetic susceptibility and environmental factors. It is characterized by immune dysregulation, increased mast cell activity, elevated levels of immunoglobulin E (IgE), and excessive proinflammatory mediator expression. These factors contribute to hallmark symptoms [...] Read more.
Atopic dermatitis (AD) is a chronic inflammatory skin disease stemming from genetic susceptibility and environmental factors. It is characterized by immune dysregulation, increased mast cell activity, elevated levels of immunoglobulin E (IgE), and excessive proinflammatory mediator expression. These factors contribute to hallmark symptoms such as pruritus, erythema, and skin barrier dysfunction. In this study, we investigated the antioxidant and anti-inflammatory effects of Taraxacum mongolicum (WTM) water extract, as well as its skin barrier regulation and immune functions in AD. In the present study, we explored the therapeutic efficacy and underlying mechanisms of WTM in a BALB/c mouse model of AD induced by 2,4-dinitrochlorobenzene (DNCB). Mice were administered WTM orally or topically for 14 consecutive days. The results demonstrated that WTM treatment significantly alleviated clinical severity, showing reductions in skin lesion scores, epidermal thickness, mast cell infiltration, and scratching behavior, compared to the DNCB-treated group. Mechanistically, WTM reduced serum levels of IgE and proinflammatory cytokines (IL-4, IL-6, IL-1β, TNF-α, and IL-31) while suppressing the expression of the JAK/STAT/TSLP signaling pathway in skin tissues. Furthermore, WTM inhibited the TLR4/NF-κB and MAPK pathways and enhanced antioxidant defense by elevating superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activities. These findings indicate that WTM attenuates DNCB-induced AD progression in mice, likely through the dual modulation of inflammatory signaling and oxidative stress. These findings suggest that WTM may modulate the immune response and alleviate AD symptoms by inhibiting the TLR4/NF-κB, MAPK, and JAK/STAT/TSLP pathways. Full article
(This article belongs to the Special Issue Molecular Research and Potential Effects of Medicinal Plants)
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43 pages, 25464 KiB  
Article
Exploring the Efficacy and Potential Mechanisms of Topical Periplaneta americana (L.) Extract in Treating Androgenetic Alopecia in a Mouse Model: A Systems Pharmacology and Skin Microbiome Analysis
by Tangfei Guan, Xin Yang, Canhui Hong, Peiyun Xiao, Yongshou Yang, Chenggui Zhang and Zhengchun He
Biology 2025, 14(7), 831; https://doi.org/10.3390/biology14070831 - 8 Jul 2025
Viewed by 538
Abstract
Androgenetic alopecia (AGA), the most prevalent form of hair loss worldwide, faces significant therapeutic challenges due to high costs and limited efficacy of current interventions, necessitating safer and more effective solutions. Periplaneta americana (L.)-derived PA-011, endowed with anti-inflammatory and antioxidant properties, has demonstrated [...] Read more.
Androgenetic alopecia (AGA), the most prevalent form of hair loss worldwide, faces significant therapeutic challenges due to high costs and limited efficacy of current interventions, necessitating safer and more effective solutions. Periplaneta americana (L.)-derived PA-011, endowed with anti-inflammatory and antioxidant properties, has demonstrated notable hair growth-promoting effects in AGA mouse models. This study employed LC-MS/MS, peptidomics, and network pharmacology to characterize PA-011’s chemical composition and predict its potential targets in AGA pathogenesis. Using Western blot and RT-qPCR, PA-011 intervention significantly inhibited inflammatory responses and oxidative stress levels in mouse skin tissues. Concurrently, PA-011 activated the proliferative potential of hair follicle stem cells, as demonstrated by upregulated expression of the cell proliferation marker Ki67, and activated the Wnt/β-catenin signaling pathway in DHT-induced AGA mice. Transcriptomic and metabolomic analyses revealed multi-target effects of PA-011, including modulation of PI3K-Akt/MAPK pathways, pentose phosphate metabolism, and amino acid biosynthesis. 16S rRNA sequencing and metagenomic analysis showed that AGA disrupts skin microbial homeostasis, while PA-011 intervention normalized the microbiota composition. Topical application of PA-011 promoted robust hair regrowth without detectable toxicity in safety assessments. This preclinical study establishes PA-011 as a promising candidate for AGA therapy, warranting further translational investigation. Full article
(This article belongs to the Section Medical Biology)
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24 pages, 5180 KiB  
Article
Resolvin D2 Reduces UVB Skin Pathology by Targeting Cytokines, Oxidative Stress, and NF-κB Activation
by Ingrid C. Pinto, Priscila Saito, Camilla C. A. Rodrigues, Renata M. Martinez, Cristina P. B. Melo, Maiara Piva, Clovis M. Kumagai, David L. Vale, Telma Saraiva-Santos, Allan J. C. Bussmann, Marcela M. Baracat, Sandra R. Georgetti, Fabiana T. M. C. Vicentini, Waldiceu A. Verri and Rubia Casagrande
Antioxidants 2025, 14(7), 830; https://doi.org/10.3390/antiox14070830 - 6 Jul 2025
Viewed by 584
Abstract
UVB skin pathology is initiated by reactive oxygen species (ROS), differentiating this condition from other inflammatory diseases involving first the immune cell activation by danger or pathogen molecular patterns followed by oxidative stress. Resolvin D2 (RvD2) has been found to reduce inflammation in [...] Read more.
UVB skin pathology is initiated by reactive oxygen species (ROS), differentiating this condition from other inflammatory diseases involving first the immune cell activation by danger or pathogen molecular patterns followed by oxidative stress. Resolvin D2 (RvD2) has been found to reduce inflammation in preclinical models. However, whether or not RvD2 reduces skin pathology caused by UVB irradiation is not yet known. Therefore, the efficacy of RvD2 on skin pathology triggered by UVB irradiation in female hairless mice was assessed. RvD2 (0.3, 1 or 3 ng/mouse, i.p.) was found to protect the skin against UVB inflammation, as observed in the reduction in edema (46%), myeloperoxidase activity (77%), metalloproteinase-9 activity (39%), recruitment of neutrophils/macrophages (lysozyme+ cells, 76%) and mast cells (106%), epidermal thickening (93%), sunburn cell formation (68%), collagen fiber breakdown (55%), and production of cytokines such as TNF-α (100%). Considering the relevance of oxidative stress to UVB irradiation skin pathologies, an important observation was that the skin antioxidant capacity was recovered by RvD2 according to the results that show the ferric reducing antioxidant power (68%), cationic radical scavenges (93%), catalase activity (74%), and the levels of reduced glutathione (48%). Oxidative damage was also attenuated, as observed in the reduction in superoxide anion production (69%) and lipid hydroperoxides (71%). The RvD2 mechanism involved the inhibition of NF-κB activation, as observed in the diminished degradation of IκBα (48%) coupled with a reduction in its downstream targets that are involved in inflammation and oxidative stress, such as COX-2 (66%) and gp91phox (77%) mRNA expression. In conclusion, RvD2 mitigates the inflammatory and oxidative pathologic skin aggression that is triggered by UVB. Full article
(This article belongs to the Special Issue Antioxidants for Skin Health)
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14 pages, 2464 KiB  
Article
Salvia miltiorrhiza Root Extract as a Potential Therapeutic Agent for IgE/Ag-Induced Allergic Reactions and Atopic Dermatitis via the Syk/MAPK Pathway
by Min-ah Kim, Jin-Ho Lee, Keunjung Woo, Eunwoo Jeong and Tack-Joong Kim
Biomedicines 2025, 13(7), 1547; https://doi.org/10.3390/biomedicines13071547 - 25 Jun 2025
Viewed by 386
Abstract
Background/Objectives: Allergens can trigger severe immune responses in hypersensitive individuals, with mast cells releasing inflammatory mediators via IgE-FcɛRI signaling. Spleen tyrosine kinase (Syk) is a key regulator in this pathway, making it a promising therapeutic target. Natural modulators of Syk-mediated mast cell [...] Read more.
Background/Objectives: Allergens can trigger severe immune responses in hypersensitive individuals, with mast cells releasing inflammatory mediators via IgE-FcɛRI signaling. Spleen tyrosine kinase (Syk) is a key regulator in this pathway, making it a promising therapeutic target. Natural modulators of Syk-mediated mast cell activation remain underexplored. This study investigated the anti-allergic effects of a 70% ethanol extract of Salvia miltiorrhiza (SME) using in vitro and in vivo models. Methods: SME was evaluated using IgE-sensitized RBL-2H3 cells, a passive cutaneous anaphylaxis model, and a DNCB-induced atopic dermatitis-like mouse model. Allergic responses were assessed via degranulation assays, histopathology, serum IgE levels, and the spleen index. Results: SME significantly inhibited mast cell degranulation by 44.4 ± 1.6% in RBL-2H3 cells at 100 µg/mL following 30 min of treatment compared to the untreated control. Western blot analysis demonstrated dose-dependent suppression of protein kinase B (PKB, also known as AKT), c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and spleen tyrosine kinase (Syk) phosphorylation, indicating inhibition of key allergic signaling pathways. In an IgE/Ag-induced passive cutaneous anaphylaxis model in ICR mice, SME (100 mg/kg, orally) significantly attenuated vascular permeability, as evidenced by a 20.6 ± 9.7% reduction in Evans blue extravasation relative to the Ag-treated group. In a 1-chloro-2,4-dinitrobenzene (DNCB)-induced atopic dermatitis (AD)-like model, six treatments of SME significantly improved the skin condition, reduced spleen enlargement associated with allergic inflammation, and decreased serum IgE levels by 43.3 ± 11.2% compared to the DNCB group. Conclusions: These findings suggest that SME may help to alleviate allergic responses and AD by modulating key immune signaling pathways. Full article
(This article belongs to the Section Cell Biology and Pathology)
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20 pages, 6373 KiB  
Article
An Elucidation of the Anti-Photoaging Efficacy and Molecular Mechanisms of Epigallocatechin Gallate Nanoparticles in a Balb/c Murine Model
by Fangzhi Xia, Fei Wang, Liangchun Kuo, Pengyu Huang, Anyi Liu, Gao Wang, Xiaomin Tang, Kun Guan, Ying Xie and Junbo Wang
Foods 2025, 14(13), 2150; https://doi.org/10.3390/foods14132150 - 20 Jun 2025
Viewed by 429
Abstract
With the increasing frequency of ultraviolet (UV) exposure in daily life and the exploration of anti-photoaging strategies, natural plant-derived compounds with anti-skin-aging properties have garnered significant attention. This study aimed to evaluate the efficacy of zein-chitosan-based nanocarriers in enhancing the bioavailability of epigallocatechin [...] Read more.
With the increasing frequency of ultraviolet (UV) exposure in daily life and the exploration of anti-photoaging strategies, natural plant-derived compounds with anti-skin-aging properties have garnered significant attention. This study aimed to evaluate the efficacy of zein-chitosan-based nanocarriers in enhancing the bioavailability of epigallocatechin gallate (EGCG) and to elucidate its mechanisms in ameliorating skin photoaging. Utilizing a Balb/c mouse model of photoaging, we monitored skin conditions, analyzed skin barrier function parameters, and observed changes in skin tissue structure and collagen fibers through hematoxylin–eosin (H&E) and Masson staining. Immunohistochemical staining was employed to assess COL1A1 levels in the skin, while enzyme-linked immunosorbent assay (ELISA) was used to measure antioxidant enzymes, inflammatory cytokines, matrix metalloproteinases (MMPs), and NF-kB levels. The effects of orally administered EGCG nanoparticles on UV-induced skin aging were investigated. UV exposure significantly increased skin roughness, impaired skin barrier function, thickened the epidermis, reduced collagen content, decreased antioxidant enzyme activity, and elevated levels of inflammatory cytokines, MMPs, and NF-kB in the model group compared to the normal control group. EGCG nanoparticles markedly ameliorated these photoaging manifestations, with some indicators showing superior improvement compared to free EGCG. These findings suggest that EGCG nanoparticles exhibit enhanced anti-photoaging effects over free EGCG, highlighting the potential of nanocarriers as a promising strategy to improve the bioavailability of EGCG. Full article
(This article belongs to the Section Nutraceuticals, Functional Foods, and Novel Foods)
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14 pages, 2941 KiB  
Article
Oxidative-Inflammatory Modulation of Skin Lipid Metabolism by Squalane, Oleic Acid, and Linoleic Acid
by Wen-Rong Zhang, Qi-Rong Zhang, Zi-Yan Zhou, Yi-Fan Zhang, Xue-Wan Li, Hai-Yang Shen, Li-Feng Tang and Qi Xiang
Cosmetics 2025, 12(4), 130; https://doi.org/10.3390/cosmetics12040130 - 20 Jun 2025
Viewed by 953
Abstract
Squalane (SQ, a saturated, sebum-mimetic hydrocarbon), oleic acid (OA, a monounsaturated fatty acid), and linoleic acid (LA, a polyunsaturated essential fatty acid) belong to the category of “lipids and fats” in cosmetic materials, and are widely employed as skin-conditioning emollients. However, they present [...] Read more.
Squalane (SQ, a saturated, sebum-mimetic hydrocarbon), oleic acid (OA, a monounsaturated fatty acid), and linoleic acid (LA, a polyunsaturated essential fatty acid) belong to the category of “lipids and fats” in cosmetic materials, and are widely employed as skin-conditioning emollients. However, they present differences in UV stress. In this study, we compared their effects on UV-induced oxidative damage, inflammation, and lipid metabolism using a mouse model and human sebaceous gland cells (SZ95). Results showed that 10% SQ did not worsen oxidative damage or inflammation after 6 weeks of UV exposure. In contrast, the 5% and 10% OA/LA groups showed increased skin wrinkling (p < 0.01), epidermal thickening (p < 0.05), and sebaceous gland atrophy. Transcriptome analysis indicated OA/LA upregulated arachidonic acid-related cytokine pathways (PTGS2/IL-1β; p < 0.001). In SZ95 cells, 0.006% OA/LA significantly increased lipid droplet formation (p < 0.001), free fatty acid (FFA) levels (p < 0.001), and pro-inflammatory gene expression (p < 0.001). Conversely, SQ neither promoted lipid droplet/FFA secretion nor induced oxidative stress. These findings suggest that high concentrations of unsaturated fatty acids in skincare may worsen lipid dysregulation and inflammation, while formulations based on saturated hydrocarbons like SQ could provide superior photoaging management by stabilizing skin barrier function. Full article
(This article belongs to the Section Cosmetic Dermatology)
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17 pages, 3567 KiB  
Article
Tripterhyponoid A from Tripterygium hypoglaucum Inhibiting MRSA by Multiple Mechanisms
by Yan-Yan Zhu, Qiong Jin, Zhao-Jie Wang, Mei-Zhen Wei, Wen-Biao Zu, Zhong-Shun Zhou, Bin-Yuan Hu, Yun-Li Zhao, Xu-Jie Qin and Xiao-Dong Luo
Molecules 2025, 30(12), 2539; https://doi.org/10.3390/molecules30122539 - 10 Jun 2025
Viewed by 515
Abstract
The emergence of methicillin-resistant Staphylococcus aureus (MRSA) and its biofilm-forming ability underscore the limitations of current antibiotics. In this study, a new compound named tripterhyponoid A was found to effectively combat MRSA, with an MIC of 2.0 μg/mL. It inhibited biofilm formation by [...] Read more.
The emergence of methicillin-resistant Staphylococcus aureus (MRSA) and its biofilm-forming ability underscore the limitations of current antibiotics. In this study, a new compound named tripterhyponoid A was found to effectively combat MRSA, with an MIC of 2.0 μg/mL. It inhibited biofilm formation by downregulating genes related to the quorum sensing (QS) pathway (sarA, agrA, agrB, agrC, agrD, and hld) and eradicated mature biofilms. Furthermore, it induced DNA damage by binding to bacterial DNA, enhancing its efficiency against MRSA. Therefore, its anti-MRSA properties with multiple mechanisms of action make it less prone to developing resistance over 20 days. In addition, it reduced the bacterial load and regulated the levels of inflammatory cytokines IL-6 and IL-10 at the wound site in a mouse skin infection model. This paper provides the first in-depth investigation of the mechanisms of triterpenoids against MRSA by inhibiting the expression of QS system genes and binding to DNA. Full article
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18 pages, 15349 KiB  
Article
Enhanced Innate Immunity Mediated by IL-36α in Atopic Dermatitis and Differences in Cytokine Profiles of Lymphocytes in the Skin and Draining Lymph Nodes
by Ayaka Ichikawa, Mai Nishimura, Masako Ichishi, Yasutomo Imai, Yoshiaki Matsushima, Yoichiro Iwakura, Masatoshi Watanabe, Kiyofumi Yamanishi and Keiichi Yamanaka
Biomolecules 2025, 15(6), 817; https://doi.org/10.3390/biom15060817 - 4 Jun 2025
Viewed by 979
Abstract
(1) Background: The IL-36 cytokines have been identified as key contributors to pustular psoriasis, and their inhibitor is already in clinical use. However, few studies have explored them in atopic dermatitis. (2) Methods: The role of IL-36α was investigated in various atopic dermatitis [...] Read more.
(1) Background: The IL-36 cytokines have been identified as key contributors to pustular psoriasis, and their inhibitor is already in clinical use. However, few studies have explored them in atopic dermatitis. (2) Methods: The role of IL-36α was investigated in various atopic dermatitis models using wild-type, keratin 14-specific IL-33 transgenic, IL-18 transgenic, caspase-1 transgenic, and caspase-1 transgenic mice with IL-17AF deletion, reflecting diverse aspects of human skin inflammation. IL-36α was administered subcutaneously in five doses on alternate days across the five strains to examine cellular infiltration patterns and cytokine expression levels. (3) Results: The skin phenotype was exacerbated, accompanied by worsening edema and skin thickness in all mouse groups upon IL-36α administration. An increase in infiltrating cells was observed among innate immune cells, while lymphocyte counts, including T cells and innate lymphoid cells, did not rise. Additionally, anti-inflammatory cytokines were induced simultaneously with inflammatory cytokines and downstream cytokines of IL-36α as well. Infiltrating lymphocytes in the skin displayed a distinct Type 2 cytokine-dominant profile for innate lymphoid cells and a Type 3 cytokine-dominant profile for T helper cells and γδ T cells, contrasting with the Type 1-dominant cell profile in draining lymph nodes. Type 1, Type 2, and Type 3 cytokine dominance patterns were not affected by the administration of IL-36α. (4) Conclusions: IL-36α triggers inflammatory responses in atopic dermatitis by activating innate immunity. The infiltrating lymphocytes in the skin have different cytokine production profiles between innate lymphoid cells and T cells, as well as different patterns of cytokine production in their draining lymph nodes. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms in Skin Disorders)
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16 pages, 2816 KiB  
Article
Zinc-Enriched Bifidobacterium longum subsp. longum CCFM1195 Alleviates Cutibacterium acnes-Induced Skin Lesions in Mice by Mitigating Inflammatory Responses and Oxidative Stress
by Xiangyue Gu, Botao Wang, Tianmeng Zhang, Qiuxiang Zhang, Bingyong Mao, Xin Tang, Jianxin Zhao and Shumao Cui
Nutrients 2025, 17(11), 1803; https://doi.org/10.3390/nu17111803 - 26 May 2025
Viewed by 798
Abstract
Background: Acne vulgaris, a prevalent inflammatory skin disorder, stems from factors like Cutibacterium acnes overgrowth, inflammation dysregulation, and immune dysfunction. Clinically, acne severity inversely correlates with serum zinc (Zn) levels, and oral Zn supplementation shows efficacy. Lactic acid bacteria are capable of converting [...] Read more.
Background: Acne vulgaris, a prevalent inflammatory skin disorder, stems from factors like Cutibacterium acnes overgrowth, inflammation dysregulation, and immune dysfunction. Clinically, acne severity inversely correlates with serum zinc (Zn) levels, and oral Zn supplementation shows efficacy. Lactic acid bacteria are capable of converting inorganic Zn into organic forms via biological transformation, potentially generating Zn-enriched bacteria as superior Zn delivery vehicles. Methods: In this study, a Zn-deficient acne mouse model was established through dietary Zn restriction combined with intradermal C. acnes injection. The therapeutic effects of orally administered Zn-containing supplements, including Zn-enriched Bifidobacterium longum subsp. longum CCFM1195 (Zn-CCFM1195), were systematically evaluated through multiple parameters: histopathological evaluation of skin lesions, cutaneous inflammatory and oxidative stress markers, serum Zn concentration, and gene expression levels of pathway-associated proteins. Results: Induction of C. acnes led to decreased serum Zn levels (14.98 μmol/L in Control vs. 9.71 μmol/L in Model) and skin metallothionein content, causing Zn imbalance. Zn deficiency caused increased levels of lesion elevation (9.23 in Model vs. 10.53 in Zn-deficient Model), IL-17A, TNF-α, and MMP9 in skin, thereby exacerbating the inflammatory response in C. acnes-induced mice. Zn supplementation alleviated inflammatory responses and oxidative stress in Zn-deficient acne-like mice. Notably, inactivated Zn-CCFM1195 exhibited superior efficacy to ZnSO4, significantly reducing lesion diameter and decreasing cutaneous levels of IL-1β, IL-17A, and MDA while enhancing GSH-Px activity. Similarly, viable Zn-CCFM1195 treatment significantly decreased IL-17A and enhanced GSH-Px activity compared with ZnSO4 treatment. Furthermore, Zn supplementation downregulated the expression of TLR2, IκBα, and IKKβ, which may exert its anti-acne effect by regulating related pathways. Conclusions: Zn deficiency exacerbates skin inflammation, whereas Zn supplementation, particularly with Zn-CCFM1195, alleviates acne vulgaris through anti-inflammatory and antioxidant effects. Full article
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16 pages, 7796 KiB  
Article
Glycine soja Leaf and Stem Extract Ameliorates Atopic Dermatitis-like Skin Inflammation by Inhibiting JAK/STAT Signaling
by Yoon-Young Sung, Misun Kim, Dong-Seon Kim and Eunjung Son
Int. J. Mol. Sci. 2025, 26(10), 4560; https://doi.org/10.3390/ijms26104560 - 9 May 2025
Viewed by 754
Abstract
Wild soybean (Glycine soja, GS) is a traditional medicine used to treat inflammation. In this study, the anti-atopic properties of GS leaf and stem extract on skin inflammation were evaluated in the Dermatophagoides farinae-extract-induced mouse model and keratinocytes. Oral administration [...] Read more.
Wild soybean (Glycine soja, GS) is a traditional medicine used to treat inflammation. In this study, the anti-atopic properties of GS leaf and stem extract on skin inflammation were evaluated in the Dermatophagoides farinae-extract-induced mouse model and keratinocytes. Oral administration of the GS extract reduced scratching, dermatitis score, transepidermal water loss, thickness of epidermis, inflammatory cell accumulation, and serum concentrations of thymic stromal lymphopoietin and immunoglobulin E. GS downregulated the expression of inflammatory gene markers of atopic dermatitis (AD), including interleukin (IL)-6; regulated on activation, normal T cell expressed and secreted (RANTES); thymus- and activation-regulated chemokine (TARC); and macrophage-derived chemokine (MDC) and upregulated the expression of filaggrin, a keratinocyte differentiation marker, in skin tissue. GS downregulated Janus kinase 1, signal transducer and activation of transcription (STAT) 1, and STAT3 pathways. Using ultra-performance liquid chromatography, we identified seven flavonoids in GS extract, including apigenin, epicatechin, genistein, genistin, daidzin, daidzein, and soyasaponin Bb. GS, apigenin, and genistein reduced the expression of IL-6, MDC, TARC, and RANTES and increased filaggrin via the downregulation of STAT3 phosphorylation in interferon-γ/tumor necrosis factor-α-stimulated keratinocytes. Our results suggest that GS leaf and stem extract ameliorates AD-like skin inflammation by regulating the immune response and restoring skin barrier function. Full article
(This article belongs to the Special Issue Anti-Inflammatory and Anti-Oxidant Effects of Extracts from Plants)
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Article
A Tea Polyphenol-Infused Sprayable Thermosensitive Liposomal Hydrogel for Enhanced Anti-Inflammatory and Antibacterial Psoriasis Treatment
by Wei Shen, Qilian Ye, Hongbo Zhang, Shenghong Xie, Shiqi Xie, Cailian Chen, Jinying Liu, Zhengwei Huang, Hai-Bin Luo and Ling Guo
J. Funct. Biomater. 2025, 16(4), 124; https://doi.org/10.3390/jfb16040124 - 1 Apr 2025
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Abstract
Psoriasis is a chronic and recurrent inflammatory disease driven not only by intrinsic factors such as immune system dysregulation but also by external factors, including bacterial infections. In contrast to the control of a single pathogenic pathway, combination therapies addressing both the immune [...] Read more.
Psoriasis is a chronic and recurrent inflammatory disease driven not only by intrinsic factors such as immune system dysregulation but also by external factors, including bacterial infections. In contrast to the control of a single pathogenic pathway, combination therapies addressing both the immune and infectious components of psoriasis pathogenesis may offer a more effective strategy for controlling its progression. In this study, we developed a sprayable hydrogel incorporating tea polyphenol-loaded lauric acid liposomes (TP@LA-Lipo gel) to investigate its anti-inflammatory and antibacterial role in psoriasis. Our results demonstrated that TP@LA-Lipo modulated macrophage activity, reduced the expression of iNOS and TNF-α, and remodeled the immune microenvironment. Meanwhile, TP@LA-Lipo effectively eliminated Staphylococcus aureus and Escherichia coli through membrane disruption, mitigating the provoked inflammatory response. More importantly, TP@LA-Lipo gel, when sprayed onto the psoriasis lesions, provided sustained drug release over three days, enabling deeper penetration through the thickened stratum corneum to reach the inflamed layers beneath. Furthermore, in an imiquimod-induced psoriasis mouse model, TP@LA-Lipo gel effectively restored the damaged skin, alleviated histopathological changes, and reduced the systemic immune response. In summary, these findings indicate that TP@LA-Lipo gel offers a comprehensive strategy for effective disease management and improving the quality of life for psoriasis patients. Full article
(This article belongs to the Special Issue Controlled Release Technologies for Localized Drug Delivery)
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