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  • 1
    Language: English
    In: The Journal of Allergy and Clinical Immunology, January 2015, Vol.135(1), pp.15-24
    Description: Chronic inflammatory diseases, including allergies and asthma, are the result of complex gene-environment interactions. One of the most challenging questions in this regard relates to the biochemical mechanism of how exogenous environmental trigger factors modulate and modify gene expression, subsequently leading to the development of chronic inflammatory conditions. Epigenetics comprises the umbrella of biochemical reactions and mechanisms, such as DNA methylation and chromatin modifications on histones and other structures. Recently, several lifestyle and environmental factors have been investigated in terms of such biochemical interactions with the gene expression–regulating machinery: allergens; microbes and microbial compounds; dietary factors, including vitamin B12, folic acid, and fish oil; obesity; and stress. This article aims to update recent developments in this context with an emphasis on allergy and asthma research.
    Keywords: Epigenetics ; Allergy ; Asthma ; DNA Methylation ; Histone Modifications ; Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 2
    Language: English
    In: The Journal of Allergy and Clinical Immunology, July 2015, Vol.136(1), pp.200-202
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jaci.2015.01.027 Byline: Hani Harb, Diana Raedler, Nikolaus Ballenberger, Andreas Bock, Dorthe A. Kesper, Harald Renz, Bianca Schaub Author Affiliation: (a) Institute of Laboratory Medicine, Pathobiochemistry and Molecular Diagnostics, Philipps University, Marburg, Germany (b) Department of Pulmonary and Allergy, University Children's Hospital Munich, LMU, Munich, Germany (c) German Center for Lung Research (DZL), Munich, Germany Article Note: (footnote) This study was funded by the Sonderforschungsbereich-Transregio 22 (SFB-TR22), Deutsche Forschungsgemeinschaft (DFG), Else-Kroner-Fresenius-Stiftung (EKFS), Universities of Giessen and Marburg Lung Center (UGMLC), and Deutsches Zentrum fur Lungenforschung (DZL)., Disclosure of potential conflict of interest: B. Schaub has received research support from the German Research Foundation (DFG SFB-TR22). The rest of the authors declare that they have no relevant conflicts of interest.
    Keywords: Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 3
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 10 September 2013, Vol.110(37), pp.15019-24
    Description: Robust cytotoxic CD8(+) T-cell response is important for immunity to intracellular pathogens. Here, we show that the transcription factor IFN Regulatory Factor 4 (IRF4) is crucial for the protective CD8(+) T-cell response to the intracellular bacterium Listeria monocytogenes. IRF4-deficient (Irf4(-/-)) mice could not clear L. monocytogenes infection and generated decreased numbers of L. monocytogenes-specific CD8(+) T cells with impaired effector phenotype and function. Transfer of wild-type CD8(+) T cells into Irf4(-/-) mice improved bacterial clearance, suggesting an intrinsic defect of CD8(+) T cells in Irf4(-/-) mice. Following transfer into wild-type recipients, Irf4(-/-) CD8(+) T cells became activated and showed initial proliferation upon L. monocytogenes infection. However, these cells could not sustain proliferation, produced reduced amounts of IFN-γ and TNF-α, and failed to acquire cytotoxic function. Forced IRF4 expression in Irf4(-/-) CD8(+) T cells rescued the defect. During acute infection, Irf4(-/-) CD8(+) T cells demonstrated diminished expression of B lymphocyte-induced maturation protein-1 (Blimp-1), inhibitor of DNA binding (Id)2, and T-box expressed in T cells (T-bet), transcription factors programming effector-cell generation. IRF4 was essential for expression of Blimp-1, suggesting that altered regulation of Blimp-1 contributes to the defects of Irf4(-/-) CD8(+) T cells. Despite increased levels of B-cell lymphoma 6 (BCL-6), Eomesodermin, and Id3, Irf4(-/-) CD8(+) T cells showed impaired memory-cell formation, indicating additional functions for IRF4 in this process. As IRF4 governs B-cell and CD4(+) T-cell differentiation, the identification of its decisive role in peripheral CD8(+) T-cell differentiation, suggests a common regulatory function for IRF4 in adaptive lymphocytes fate decision.
    Keywords: Interferon Regulatory Factors -- Immunology ; T-Lymphocytes, Cytotoxic -- Immunology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 4
    Language: English
    In: The Journal of Allergy and Clinical Immunology, February 2018, Vol.141(2), pp.AB283-AB283
    Description: Methods We employed in vitro cell culture assays using lung-derived antigen presenting cells and allergen-specific T cells, and in vivo mouse models of allergic airway inflammation that employed myeloid lineage-specific gene deletions, cellular reconstitution approaches and antibody inhibition studies. Furthermore, UFP promoted both Th2 and Th17 cell differentiation of allergen-specific T cells in a Jag1- and Notch4-dependent manner. [...]treatment of mice with an anti-Notch 4 antibody abrogated the exacerbation of allergic airway inflammation induced by UFP.
    Keywords: Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 5
    Language: English
    In: The Journal of Allergy and Clinical Immunology, October 2018, Vol.142(4), pp.1243-1256.e17
    Description: Exposure to traffic-related particulate matter promotes asthma and allergic diseases. However, the precise cellular and molecular mechanisms by which particulate matter exposure acts to mediate these effects remain unclear. We sought to elucidate the cellular targets and signaling pathways critical for augmentation of allergic airway inflammation induced by ambient ultrafine particles (UFP). We used cell-culture assays with lung-derived antigen-presenting cells and allergen-specific T cells and mouse models of allergic airway inflammation with myeloid lineage-specific gene deletions, cellular reconstitution approaches, and antibody inhibition studies. We identified lung alveolar macrophages (AM) as the key cellular target of UFP in promoting airway inflammation. Aryl hydrocarbon receptor–dependent induction of Jagged 1 (Jag1) expression in AM was necessary and sufficient for augmentation of allergic airway inflammation by UFP. UFP promoted T 2 and T 17 cell differentiation of allergen-specific T cells in a Jag1- and Notch 4–dependent manner. Treatment of mice with an anti–Notch 4 antibody abrogated exacerbation of allergic airway inflammation induced by UFP. UFP exacerbate allergic airway inflammation by promoting a Jag1-Notch 4–dependent interaction between AM and allergen-specific T cells, leading to augmented T cell differentiation.
    Keywords: Airway Hyperresponsiveness ; Allergic Airway Inflammation ; Alveolar Macrophages ; Aryl Hydrocarbon Receptor ; Asthma ; Jagged 1 ; Notch ; Notch 4 ; Traffic-Related Particulate Matter ; Ultrafine Particles ; Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 6
    Language: English
    In: FASEB journal : official publication of the Federation of American Societies for Experimental Biology, September 2014, Vol.28(9), pp.4068-76
    Description: Folate intake during pregnancy may affect the regulation of DNA methylation during fetal development. The genomic regions in the offspring that may be sensitive to folate exposure during in utero development have not been characterized. Using genome-scale profiling, we investigated DNA methylation in 2 immune cell types (CD4(+) and antigen-presenting cells) isolated from neonatal cord blood, selected on the basis of in utero folate exposure. High-folate (HF; n=11) and low-folate (LF; n=12) groups were selected from opposite extremes of maternal serum folate levels measured in the last trimester of pregnancy. A comparison of these groups revealed differential methylation at 7 regions across the genome. By far, the biggest effect observed was hypomethylation of a 923 bp region 3 kb upstream of the ZFP57 transcript, a regulator of DNA methylation during development, observed in both cell types. Levels of H3/H4 acetylation at ZFP57 promoter and ZFP57 mRNA expression were higher in CD4(+) cells in the HF group relative to the LF group. Hypomethylation at this region was replicated in an independent sample set. These data suggest that exposure to folate has effects on the regulation of DNA methylation during fetal development, and this may be important for health and disease.
    Keywords: T Cells ; Antigen-Presenting Cells ; Developmental Programming ; Epigenetics ; Neonate ; DNA Methylation ; Gene Expression Profiling ; Genome, Human ; Genomic Imprinting ; DNA-Binding Proteins -- Genetics ; Fetal Development -- Genetics ; Folic Acid -- Metabolism ; Transcription Factors -- Genetics
    ISSN: 08926638
    E-ISSN: 1530-6860
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  • 7
    Language: English
    In: The Journal of Allergy and Clinical Immunology, 2011, Vol.128(3), pp.618-625.e7
    Description: Bronchial asthma is a chronic inflammatory disease resulting from complex gene-environment interactions. Natural microbial exposure has been identified as an important environmental condition that provides asthma protection in a prenatal window of opportunity. Epigenetic regulation is an important mechanism by which environmental factors might interact with genes involved in allergy and asthma development. This study was designed to test whether epigenetic mechanisms might contribute to asthma protection conferred by early microbial exposure. Pregnant maternal mice were exposed to the farm-derived gram-negative bacterium F78. Epigenetic modifications in the offspring were analyzed in T 1- and T 2-relevant genes of CD4 T cells. Prenatal administration of F78 prevented the development of an asthmatic phenotype in the progeny, and this effect was IFN-γ dependent. Furthermore, the promoter of CD4 T cells in the offspring revealed a significant protection against loss of histone 4 (H4) acetylation, which was closely associated with IFN-γ expression. Pharmacologic inhibition of H4 acetylation in the offspring abolished the asthma-protective phenotype. Regarding T 2-relevant genes only at the promoter, a decrease could be detected for H4 acetylation but not at the promoter or the intergenic T 2 regulatory region conserved noncoding sequence 1 . These data support the hygiene concept and indicate that microbes operate by means of epigenetic mechanisms. This provides a new mechanism in the understanding of gene-environment interactions in the context of allergy protection.
    Keywords: Asthma ; Allergy ; Epigenetics ; Histone Acetylation ; Hygiene Hypothesis ; T Cells ; Medicine
    ISSN: 0091-6749
    E-ISSN: 1097-6825
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  • 8
    Language: English
    In: Arabian Journal for Science and Engineering, 2014, Vol.39(12), pp.8793-8810
    Description: This paper presents a practical PC-based speed and direction controller (PC-SDC) for controlling DC motors. Developing PC-SDC is dependent on open architecture and intelligence features. Open architecture feature refers to apply the same firmware components of this PC-SDC with different types of DC motors and sensory systems. Intelligence feature is achieved by applying the collect-process-decide-deliver-instructions (CPDDI) model. The suggested CPDDI model is the real software implementation of moment perspective of a new intelligence model called “Accumulative Intelligence”. CPDDI can control DC motor via bi-directional communication channels with two practical in-house designed firmware systems. The first system is μC-based feedback speed monitoring module (FSMM) system which collects speed data (i.e., pulses count) for this DC motor by using a PIC μC-based encoder sensory system. The second system is μC-based motor control module (MCM) to control this DC motor via different intelligent rules. These rules control DC motors according to previous moving state and next required moving state. Real-time feature is investigated via two performance metrics; ART and SMT. Also, the effectiveness of the proposed PC-SDC system is investigated by a comparison between pulses count that is measured practically by FSMM system and real pulses count that is gathered from an oscilloscope.
    Keywords: DC motor ; Speed control ; Direction control ; Accumulative intelligence model ; Microcontroller
    ISSN: 1319-8025
    E-ISSN: 2191-4281
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  • 9
    Language: English
    In: Current opinion in pediatrics, December 2016, Vol.28(6), pp.754-763
    Description: The goal of this review was to systematically analyze recent studies updating our knowledge on the role of epigenetic mechanisms in childhood asthma. A systematic literature search was conducted that identified 23 fresh articles published within the last 5 years reporting the results of human studies on the relationships between epigenetic modifications and childhood asthma or its/related phenotypes. In almost all these studies, meaningful associations between levels of epigenetic marks (DNA methylation and/or histone modifications) and pediatric asthma or its/related phenotypes have been observed. In addition, many studies identified by our screening analyzed those associations in the context of environmental factors, such as pollution, tobacco smoke, farming, or diet, showing in a huge majority a modifying effect of those exposures. The results of our systematic literature search provide a strong support for the role of epigenetic mechanisms in (mediating the effects of environmental exposure on) pediatric asthma. This knowledge may possibly be translated into diagnostic and/or therapeutic approaches.
    Keywords: Epigenesis, Genetic ; Asthma -- Genetics
    E-ISSN: 1531-698X
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 10
    In: Journal of Diabetes Mellitus, 2012, Vol.02(01), pp.47-51
    Description: Background: Systemic thrombin activity (F2a), i.e. thrombin protected and transported by a2- macroglobulin, is a new biomarker for the activation state of coagulation in vivo. F2a 〉 120% of normal diagnoses a pathologic disseminated intravascular coagulation (PIC) in humans, either acute or chronic. Since glucose triggers intrinsic coagulation, the present work aimed to quantify systemic thrombin generation induced by glucose in vivo in mice. Material and Methods: Balb/c mice were i.p. injected with different concentrations of glucose (0 - 0.3 mmoles). After 0 - 3 h EDTA-blood was withdrawn, centrifuged, and the plasma was stabilized 1 + 1 with 2.5 M arginine, pH 8.6, and analyzed for systemically circulating F2a (that is F2a.α2M). The F2a.α2M activity in mice without glucose injection was defined as 100% of murine norm. Results: 1 h after i.p. injection 0.1 - 0.3 mmoles glucose resulted in about 1.4 fold increase of plasmatic glucose and in about 2.5 fold increase of systemic F2a activity. At the 45 min time interval between i.p. injection of 0.038 mmoles glucose and blood withdrawing an approximately 1.5fold increase of plasma glucose caused a 4fold increase in systemic F2a. Discussion: When systemic F2a reaches 120% of the normal, the normal human intravascular coagulation (NIC) turns to the pre-phase of pathologic plasmatic intravascular coagulation (PIC-0 also defined as pre-PIC). At 150% systemic F2a, the PIC-0 changes to PIC-1 which is the common pathologic plasmatic intravascular coagulation (typical PIC). At 200% systemic F2a, PIC-1 changes to PIC-2 (consumption PIC). The present assay technique seems to be suitable in judging the coagulation activation state of any mammalian blood. Diabetic patients should be monitored for the new biomarker systemic F2a similarly as for the old biomarker glycated hemoglobin (HbA1c). The target systemic F2a range should be NIC, preferably around 100% of normal.
    Keywords: Medicine;
    ISSN: 2160-5831
    E-ISSN: 2160-5858
    Source: CrossRef
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