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  1. Article ; Online: Epigallocatechin gallate regulates the myeloid-specific transcription factor PU.1 in macrophages.

    Karpurapu, Manjula / Kakarala, Kavita Kumari / Chung, Sangwoon / Nie, Yunjuan / Koley, Amritendu / Dougherty, Patrick / Christman, John W

    PloS one

    2024  Volume 19, Issue 4, Page(s) e0301904

    Abstract: Our previous research demonstrated that PU.1 regulates expression of the genes involved in inflammation in macrophages. Selective knockdown of PU.1 in macrophages ameliorated LPS-induced acute lung injury (ALI) in bone marrow chimera mice. Inhibitors ... ...

    Abstract Our previous research demonstrated that PU.1 regulates expression of the genes involved in inflammation in macrophages. Selective knockdown of PU.1 in macrophages ameliorated LPS-induced acute lung injury (ALI) in bone marrow chimera mice. Inhibitors that block the transcriptional activity of PU.1 in macrophages have the potential to mitigate the pathophysiology of LPS-induced ALI. However, complete inactivation of PU.1 gene disrupts normal myelopoiesis. Although the green tea polyphenol Epigallocatechin gallate (EGCG) has been shown to regulate inflammatory genes in various cell types, it is not known if EGCG alters the transcriptional activity of PU.1 protein. Using Schrodinger Glide docking, we have identified that EGCG binds with PU.1 protein, altering its DNA-binding and self-dimerization activity. In silico analysis shows that EGCG forms Hydrogen bonds with Glutamic Acid 209, Leucine 250 in DNA binding and Lysine 196, Tryptophan 193, and Leucine 182 in the self-dimerization domain of the PU.1 protein. Experimental validation using mouse bone marrow-derived macrophages (BMDM) confirmed that EGCG inhibits both DNA binding by PU.1 and self-dimerization. Importantly, EGCG had no impact on expression of the total PU.1 protein levels but significantly reduced expression of various inflammatory genes and generation of ROS. In summary, we report that EGCG acts as an inhibitor of the PU.1 transcription factor in macrophages.
    MeSH term(s) Catechin/analogs & derivatives ; Catechin/pharmacology ; Animals ; Trans-Activators/metabolism ; Trans-Activators/genetics ; Macrophages/metabolism ; Macrophages/drug effects ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins/genetics ; Mice ; Mice, Inbred C57BL ; Molecular Docking Simulation ; Protein Binding ; DNA/metabolism ; Gene Expression Regulation/drug effects ; Lipopolysaccharides/pharmacology
    Chemical Substances Catechin (8R1V1STN48) ; epigallocatechin gallate (BQM438CTEL) ; proto-oncogene protein Spi-1 ; Trans-Activators ; Proto-Oncogene Proteins ; DNA (9007-49-2) ; Lipopolysaccharides
    Language English
    Publishing date 2024-04-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0301904
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Long-Term Impact of Daily E-cigarette Exposure on the Lungs of Asthmatic Mice.

    Song, Min-Ae / Wold, Loren E / Aslaner, David M / Archer, Kellie J / Patel, Devki / Jeon, Hyeongseon / Chung, Dongjun / Shields, Peter G / Christman, John W / Chung, Sangwoon

    Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco

    2023  Volume 25, Issue 12, Page(s) 1904–1908

    Abstract: Introduction: Although the greater popularity of electronic cigarettes (EC) among asthmatics is alarming, there is limited knowledge of the long-term consequences of EC exposure in asthmatics.: Aims and methods: Mild asthmatic C57/BL6J adult male and ...

    Abstract Introduction: Although the greater popularity of electronic cigarettes (EC) among asthmatics is alarming, there is limited knowledge of the long-term consequences of EC exposure in asthmatics.
    Aims and methods: Mild asthmatic C57/BL6J adult male and female mice were established by intranasal insufflation with three combined allergens. The asthmatic and age and sex-matched' naïve mice were exposed to air, nicotine-free (propylene glycol [PG]/vegetable glycerin [VG]-only), or PG/VG+Nicotine, 4 hours daily for 3 months. The effects of EC exposure were accessed by measuring cytokines in bronchoalveolar lavage, periodic acid-schiff (PAS) staining, mitochondrial DNA copy numbers (mtCN), and the transcriptome in the lung. Significance was false discovery rate <0.2 for transcriptome and 0.05 for the others.
    Results: In asthmatic mice, PG/VG+Nicotine increased PAS-positive cells and IL-13 compared to mice exposed to air and PG/VG-only. In naïve mice exposed to PG/VG+Nicotine and PG/VG-only, higher INF-γ was observed compared to mice exposed only to air. PG/VG-only and PG/VG+Nicotine had significantly higher mtCN compared to air exposure in asthmatic mice, while the opposite pattern was observed in non-asthmatic naïve mice. Different gene expression patterns were profoundly found for asthmatic mice exposed to PG/VG+Nicotine compared to PG/VG-only, including genes involved in mitochondrial dysfunction, oxidative phosphorylation, and p21-activated kinase (PAK) signaling.
    Conclusions: This study provides experimental evidence of the potential impact of nicotine enhancement on the long-term effects of EC in asthmatics compared to non-asthmatics.
    Implications: The findings from this study indicate the potential impact of EC in asthmatics by addressing multiple biological markers. The long-term health outcomes of EC in the susceptible group can be instrumental in supporting policymaking and educational campaigns and informing the public, healthcare providers, and EC users about the underlying risks of EC use.
    MeSH term(s) Male ; Mice ; Female ; Animals ; Nicotine/adverse effects ; Electronic Nicotine Delivery Systems ; Asthma/etiology ; Lung ; Propylene Glycol/pharmacology ; Glycerol/pharmacology ; Vegetables
    Chemical Substances Nicotine (6M3C89ZY6R) ; Propylene Glycol (6DC9Q167V3) ; Glycerol (PDC6A3C0OX)
    Language English
    Publishing date 2023-06-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 1452315-2
    ISSN 1469-994X ; 1462-2203
    ISSN (online) 1469-994X
    ISSN 1462-2203
    DOI 10.1093/ntr/ntad100
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Sex-specific lung inflammation and mitochondrial damage in a model of electronic cigarette exposure in asthma.

    Song, Min-Ae / Kim, Ji Young / Gorr, Matthew W / Miller, Roy A / Karpurapu, Manjula / Nguyen, Jackie / Patel, Devki / Archer, Kellie J / Pabla, Navjot / Shields, Peter G / Wold, Loren E / Christman, John W / Chung, Sangwoon

    American journal of physiology. Lung cellular and molecular physiology

    2023  Volume 325, Issue 5, Page(s) L568–L579

    Abstract: The prevalence of electronic cigarette (EC) use among adult with asthma has continued to increase over time, in part due to the belief of being less harmful than smoking. However, the extent of their toxicity and the involved mechanisms contributing to ... ...

    Abstract The prevalence of electronic cigarette (EC) use among adult with asthma has continued to increase over time, in part due to the belief of being less harmful than smoking. However, the extent of their toxicity and the involved mechanisms contributing to the deleterious impact of EC exposure on patients with preexisting asthma have not been delineated. In the present project, we tested the hypothesis that EC use contributes to respiratory damage and worsening inflammation in the lungs of patients with asthma. To define the consequences of EC exposure in established asthma, we used a mouse model with/without preexisting asthma for short-term exposure to EC aerosols. C57/BL6J mice were sensitized and challenged with a DRA (dust mite, ragweed,
    MeSH term(s) Humans ; Adult ; Male ; Female ; Mice ; Animals ; Electronic Nicotine Delivery Systems ; Nicotine/toxicity ; Respiratory Aerosols and Droplets ; Asthma/pathology ; Lung/pathology ; Pneumonia/pathology ; Inflammation/pathology ; Disease Models, Animal ; DNA, Mitochondrial
    Chemical Substances Nicotine (6M3C89ZY6R) ; DNA, Mitochondrial
    Language English
    Publishing date 2023-09-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00033.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mechanical Properties and Bioactivity of Polyetheretherketone/Hydroxyapatite/Carbon Fiber Composite Prepared by the Mechanofusion Process.

    Jeon, In Sung / Lee, Moon Hyun / Choi, Han-Hyeong / Lee, Sangwoon / Chon, Joon Woo / Chung, Dong June / Park, Jong Hyuk / Jho, Jae Young

    Polymers

    2021  Volume 13, Issue 12

    Abstract: The main obstacles in the melt-processing of hydroxyapatite (HA) and carbon fiber (CF) reinforced polyetheretherketone (PEEK) composite are the high melting temperature of PEEK, poor dispersion of HA nanofillers, and poor processability due to high ... ...

    Abstract The main obstacles in the melt-processing of hydroxyapatite (HA) and carbon fiber (CF) reinforced polyetheretherketone (PEEK) composite are the high melting temperature of PEEK, poor dispersion of HA nanofillers, and poor processability due to high filler content. In this study, we prepared PEEK/HA/CF ternary composite using two different non-melt blending methods; suspension blending (SUS) in ethanol and mechanofusion process (MF) in dry condition. We compared the mechanical properties and bioactivity of the composite in a spinal cage application in the orthopedic field. Results showed that the PEEK/HA/CF composite made by the MF method exhibited higher flexural and compressive strengths than the composite prepared by the SUS method due to the enhanced dispersibility of HA nanofiller. On the basis of in vitro cell compatibility and cell attachment tests, PEEK/HA/CF composite by mechanofusion process showed an improvement in in vitro bioactivity and osteo-compatibility.
    Language English
    Publishing date 2021-06-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527146-5
    ISSN 2073-4360 ; 2073-4360
    ISSN (online) 2073-4360
    ISSN 2073-4360
    DOI 10.3390/polym13121978
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Targeting ETosis by miR-155 inhibition mitigates mixed granulocytic asthmatic lung inflammation.

    Kim, Ji Young / Stevens, Patrick / Karpurapu, Manjula / Lee, Hyunwook / Englert, Joshua A / Yan, Pearlly / Lee, Tae Jin / Pabla, Navjot / Pietrzak, Maciej / Park, Gye Young / Christman, John W / Chung, Sangwoon

    Frontiers in immunology

    2022  Volume 13, Page(s) 943554

    Abstract: Asthma is phenotypically heterogeneous with several distinctive pathological mechanistic pathways. Previous studies indicate that neutrophilic asthma has a poor response to standard asthma treatments comprising inhaled corticosteroids. Therefore, it is ... ...

    Abstract Asthma is phenotypically heterogeneous with several distinctive pathological mechanistic pathways. Previous studies indicate that neutrophilic asthma has a poor response to standard asthma treatments comprising inhaled corticosteroids. Therefore, it is important to identify critical factors that contribute to increased numbers of neutrophils in asthma patients whose symptoms are poorly controlled by conventional therapy. Leukocytes release chromatin fibers, referred to as extracellular traps (ETs) consisting of double-stranded (ds) DNA, histones, and granule contents. Excessive components of ETs contribute to the pathophysiology of asthma; however, it is unclear how ETs drive asthma phenotypes and whether they could be a potential therapeutic target. We employed a mouse model of severe asthma that recapitulates the intricate immune responses of neutrophilic and eosinophilic airway inflammation identified in patients with severe asthma. We used both a pharmacologic approach using miR-155 inhibitor-laden exosomes and genetic approaches using miR-155 knockout mice. Our data show that ETs are present in the bronchoalveolar lavage fluid of patients with mild asthma subjected to experimental subsegmental bronchoprovocation to an allergen and a severe asthma mouse model, which resembles the complex immune responses identified in severe human asthma. Furthermore, we show that miR-155 contributes to the extracellular release of dsDNA, which exacerbates allergic lung inflammation, and the inhibition of miR-155 results in therapeutic benefit in severe asthma mice. Our findings show that targeting dsDNA release represents an attractive therapeutic target for mitigating neutrophilic asthma phenotype, which is clinically refractory to standard care.
    MeSH term(s) Animals ; Asthma ; Disease Models, Animal ; Eosinophilia ; Granulocytes ; Humans ; Mice ; MicroRNAs/metabolism ; Neutrophils ; Pneumonia/drug therapy ; Pneumonia/metabolism
    Chemical Substances MIRN155 microRNA, human ; MicroRNAs ; Mirn155 microRNA, mouse
    Language English
    Publishing date 2022-07-26
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.943554
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Lipidomic Profiling of Bronchoalveolar Lavage Fluid Extracellular Vesicles Indicates Their Involvement in Lipopolysaccharide-Induced Acute Lung Injury

    Teja Srinivas Nirujogi / Sainath R. Kotha / Sangwoon Chung / Brenda F. Reader / Anita Yenigalla / Liwen Zhang / John P. Shapiro / Jon Wisler / John W. Christman / Krishnarao Maddipati / Narasimham L. Parinandi / Manjula Karpurapu

    Journal of Innate Immunity, Pp 1-

    2022  Volume 14

    Abstract: Emerging data support the pivotal role of extracellular vesicles (EVs) in normal cellular physiology and disease conditions. However, despite their abundance, there is much less information about the lipid mediators carried in EVs, especially in the ... ...

    Abstract Emerging data support the pivotal role of extracellular vesicles (EVs) in normal cellular physiology and disease conditions. However, despite their abundance, there is much less information about the lipid mediators carried in EVs, especially in the context of acute lung injury (ALI). Our data demonstrate that C57BL/6 mice subjected to intranasal Escherichia coli lipopolysaccharide (LPS)-induced ALI release, a higher number of EVs into the alveolar space, compared to saline-treated controls. EVs released during ALI originated from alveolar epithelial cells, macrophages, and neutrophils and carry a diverse array of lipid mediators derived from ω-3 and ω-6 polyunsaturated fatty acids (PUFA). The eicosanoids in EVs correlated with cellular levels of arachidonic acid, expression of cytosolic phospholipase A2, cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome epoxygenase p450 proteins in pulmonary macrophages. Furthermore, EVs from LPS-toll-like receptor 4 knockout (TLR4-/-) mice contained significantly lower amounts of COX and LOX catalyzed eicosanoids and ω-3 PUFA metabolites. More importantly, EVs from LPS-treated wild-type mice increased TNF-α release by macrophages and reduced alveolar epithelial monolayer barrier integrity compared to EVs from LPS-treated TLR4−/− mice. In summary, our study demonstrates for the first time that the EV carried PUFA metabolite profile in part depends on the inflammatory status of the lung macrophages and modulates pulmonary macrophage and alveolar epithelial cell function during LPS-induced ALI.
    Keywords acute lung injury ; inflammation ; extracellular vesicles ; polyunsaturated fatty acids ; macrophage ; Medicine ; R ; Internal medicine ; RC31-1245
    Subject code 610
    Language English
    Publishing date 2022-04-01T00:00:00Z
    Publisher Karger Publishers
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Lung mitochondrial DNA copy number, inflammatory biomarkers, gene transcription and gene methylation in vapers and smokers.

    Mori, Kellie M / McElroy, Joseph P / Weng, Daniel Y / Chung, Sangwoon / Fadda, Paolo / Reisinger, Sarah A / Ying, Kevin L / Brasky, Theodore M / Wewers, Mark D / Freudenheim, Jo L / Shields, Peter G / Song, Min-Ae

    EBioMedicine

    2022  Volume 85, Page(s) 104301

    Abstract: Background: Mitochondrial DNA copy number (mtCN) maintains cellular function and homeostasis, and is linked to nuclear DNA methylation and gene expression. Increased mtCN in the blood is associated with smoking and respiratory disease, but has received ... ...

    Abstract Background: Mitochondrial DNA copy number (mtCN) maintains cellular function and homeostasis, and is linked to nuclear DNA methylation and gene expression. Increased mtCN in the blood is associated with smoking and respiratory disease, but has received little attention for target organ effects for smoking or electronic cigarette (EC) use.
    Methods: Bronchoscopy biospecimens from healthy EC users, smokers (SM), and never-smokers (NS) were assessed for associations of mtCN with mtDNA point mutations, immune responses, nuclear DNA methylation and gene expression using linear regression. Ingenuity pathway analysis was used for enriched pathways. GEO and TCGA respiratory disease datasets were used to explore the involvement of mtCN-associated signatures.
    Findings: mtCN was higher in SM than NS, but EC was not statistically different from either. Overall there was a negative association of mtCN with a point mutation in the D-loop but no difference within groups. Positive associations of mtCN with IL-2 and IL-4 were found in EC only. mtCN was significantly associated with 71,487 CpGs and 321 transcripts. 263 CpGs were correlated with nearby transcripts for genes enriched in the immune system. EC-specific mtCN-associated-CpGs and genes were differentially expressed in respiratory diseases compared to controls, including genes involved in cellular movement, inflammation, metabolism, and airway hyperresponsiveness.
    Interpretation: Smoking may elicit a lung toxic effect through mtCN. While the impact of EC is less clear, EC-specific associations of mtCN with nuclear biomarkers suggest exposure may not be harmless. Further research is needed to understand the role of smoking and EC-related mtCN on lung disease risks.
    Funding: The National Cancer Institute, the National Heart, Lung, and Blood Institute, the Food and Drug Administration Center for Tobacco Products, the National Center For Advancing Translational Sciences, and Pelotonia Intramural Research Funds.
    MeSH term(s) Humans ; DNA, Mitochondrial/genetics ; Smokers ; DNA Copy Number Variations ; Electronic Nicotine Delivery Systems ; Biomarkers ; DNA Methylation ; Lung ; Transcription, Genetic
    Chemical Substances DNA, Mitochondrial ; Biomarkers
    Language English
    Publishing date 2022-10-07
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2022.104301
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Lipidomic Profiling of Bronchoalveolar Lavage Fluid Extracellular Vesicles Indicates Their Involvement in Lipopolysaccharide-Induced Acute Lung Injury.

    Nirujogi, Teja Srinivas / Kotha, Sainath R / Chung, Sangwoon / Reader, Brenda F / Yenigalla, Anita / Zhang, Liwen / Shapiro, John P / Wisler, Jon / Christman, John W / Maddipati, Krishnarao / Parinandi, Narasimham L / Karpurapu, Manjula

    Journal of innate immunity

    2022  Volume 14, Issue 5, Page(s) 555–568

    Abstract: Emerging data support the pivotal role of extracellular vesicles (EVs) in normal cellular physiology and disease conditions. However, despite their abundance, there is much less information about the lipid mediators carried in EVs, especially in the ... ...

    Abstract Emerging data support the pivotal role of extracellular vesicles (EVs) in normal cellular physiology and disease conditions. However, despite their abundance, there is much less information about the lipid mediators carried in EVs, especially in the context of acute lung injury (ALI). Our data demonstrate that C57BL/6 mice subjected to intranasal Escherichia coli lipopolysaccharide (LPS)-induced ALI release, a higher number of EVs into the alveolar space, compared to saline-treated controls. EVs released during ALI originated from alveolar epithelial cells, macrophages, and neutrophils and carry a diverse array of lipid mediators derived from ω-3 and ω-6 polyunsaturated fatty acids (PUFA). The eicosanoids in EVs correlated with cellular levels of arachidonic acid, expression of cytosolic phospholipase A2, cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome epoxygenase p450 proteins in pulmonary macrophages. Furthermore, EVs from LPS-toll-like receptor 4 knockout (TLR4-/-) mice contained significantly lower amounts of COX and LOX catalyzed eicosanoids and ω-3 PUFA metabolites. More importantly, EVs from LPS-treated wild-type mice increased TNF-α release by macrophages and reduced alveolar epithelial monolayer barrier integrity compared to EVs from LPS-treated TLR4-/- mice. In summary, our study demonstrates for the first time that the EV carried PUFA metabolite profile in part depends on the inflammatory status of the lung macrophages and modulates pulmonary macrophage and alveolar epithelial cell function during LPS-induced ALI.
    MeSH term(s) Acute Lung Injury/chemically induced ; Acute Lung Injury/metabolism ; Animals ; Bronchoalveolar Lavage Fluid ; Extracellular Vesicles/metabolism ; Lipidomics ; Lipopolysaccharides/pharmacology ; Lung/metabolism ; Mice ; Mice, Inbred C57BL ; Toll-Like Receptor 4/metabolism
    Chemical Substances Lipopolysaccharides ; Toll-Like Receptor 4
    Language English
    Publishing date 2022-04-01
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2454158-8
    ISSN 1662-8128 ; 1662-811X
    ISSN (online) 1662-8128
    ISSN 1662-811X
    DOI 10.1159/000522338
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Scavenger receptor BI attenuates oxidized phospholipid-induced pulmonary inflammation.

    Dunigan-Russell, Katelyn / Yaeger, Michael J / Hodge, Myles X / Kilburg-Basnyat, Brita / Reece, Sky W / Birukova, Anastasiya / Guttenberg, Marissa A / Novak, Caymen / Chung, Sangwoon / Ehrmann, Brandie Michelle / Wallace, E Diane / Tokarz, Debra / Majumder, Nairrita / Xia, Li / Christman, John W / Shannahan, Jonathan / Ballinger, Megan N / Hussain, Salik / Shaikh, Saame Raza /
    Tighe, Robert M / Gowdy, Kymberly M

    Toxicology and applied pharmacology

    2023  Volume 462, Page(s) 116381

    Abstract: Damage associated molecular patterns (DAMPs) are molecules released from dead/dying cells following toxicant and/or environmental exposures that activate the immune response through binding of pattern recognition receptors (PRRs). Excessive production of ...

    Abstract Damage associated molecular patterns (DAMPs) are molecules released from dead/dying cells following toxicant and/or environmental exposures that activate the immune response through binding of pattern recognition receptors (PRRs). Excessive production of DAMPs or failed clearance leads to chronic inflammation and delayed inflammation resolution. One category of DAMPs are oxidized phospholipids (oxPLs) produced upon exposure to high levels of oxidative stress, such as following ozone (O
    MeSH term(s) Animals ; Female ; Mice ; Carrier Proteins ; Inflammation/chemically induced ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Phospholipids ; Pneumonia/chemically induced ; Pneumonia/prevention & control ; Receptors, Scavenger/genetics ; Receptors, Scavenger/metabolism ; Toll-Like Receptor 4/metabolism
    Chemical Substances Carrier Proteins ; NF-kappa B ; Phospholipids ; Receptors, Scavenger ; Toll-Like Receptor 4 ; Cd36 protein, mouse
    Language English
    Publishing date 2023-01-19
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 204477-8
    ISSN 1096-0333 ; 0041-008X
    ISSN (online) 1096-0333
    ISSN 0041-008X
    DOI 10.1016/j.taap.2023.116381
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Donor protection: Iron supplementation for frequent blood donors in Korea.

    Lee, Seok Joon / Min, Hyuk Ki / Jang, Jin Sung / Lee, Sangwoon / Chung, Yousun / Kim, Moon Jung

    Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis

    2019  Volume 59, Issue 1, Page(s) 102611

    Abstract: Objective: This study aimed to evaluate the effect of oral iron supplementation in frequent donors in Korea, based solely on donation history.: Study design: The hemoglobin (Hb) level, ferritin level, soluble transferrin receptor (sTfR), total iron ... ...

    Abstract Objective: This study aimed to evaluate the effect of oral iron supplementation in frequent donors in Korea, based solely on donation history.
    Study design: The hemoglobin (Hb) level, ferritin level, soluble transferrin receptor (sTfR), total iron binding capacity (TIBC), and transferrin saturation of frequent donors at high risk for iron deficiency were compared to those of first donors. The frequent donors took iron supplements for 4 weeks and the same tests were repeated after 2 and 4 weeks to evaluate their effects.
    Result: A total of 53 male and 57 female frequent donors were recruited. After 4-week iron supplementation, among the men, the prevalence of a: low Hb level (<13.0 g/dL) decreased from 25% to 2%; low ferritin level (<15.0 ng/mL) decreased from 58% to 4%; iron deficient erythropoiesis (IDE) (log(sTfR/ferritin) ≥ 2.07) decreased from 77% to 33%. Among the women, the percentage of a: low Hb level (<12.0 g/dL) decreased from 44% to 9%; low ferritin level decreased from 79% to 11%; IDE decreased from 95% to 47%. In total, 15 male (28.3%) and 29 female (56.9%) blood donors reported undesirable side effects related to iron supplementation. No serious adverse events were reported.
    Conclusion: Ferritin level, a reliable indicator of iron status, increased and IDE decreased significantly after four-week iron supplementation in the female, but not in the male, donor group, compared to those of control donors. Four-week oral iron supplement was not enough to restore iron storage level in the male donor group.
    MeSH term(s) Adult ; Blood Donors/statistics & numerical data ; Female ; Humans ; Iron/pharmacology ; Iron/therapeutic use ; Male ; Republic of Korea
    Chemical Substances Iron (E1UOL152H7)
    Language English
    Publishing date 2019-07-09
    Publishing country England
    Document type Journal Article
    ZDB-ID 2046795-3
    ISSN 1878-1683 ; 1473-0502
    ISSN (online) 1878-1683
    ISSN 1473-0502
    DOI 10.1016/j.transci.2019.07.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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