LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 69

Search options

  1. Article: Vitamin D effects on lung immunity and respiratory diseases.

    Hansdottir, Sif / Monick, Martha M

    Vitamins and hormones

    2011  Volume 86, Page(s) 217–237

    Abstract: Our understanding of vitamin D metabolism and biological effects has grown exponentially in recent years and it has become clear that vitamin D has extensive immunomodulatory effects. The active vitamin D generating enzyme, 1α-hydroxylase, is expressed ... ...

    Abstract Our understanding of vitamin D metabolism and biological effects has grown exponentially in recent years and it has become clear that vitamin D has extensive immunomodulatory effects. The active vitamin D generating enzyme, 1α-hydroxylase, is expressed by the airway epithelium, alveolar macrophages, dendritic cells, and lymphocytes indicating that active vitamin D can be produced locally within the lungs. Vitamin D generated in tissues is responsible for many of the immunomodulatory actions of vitamin D. The effects of vitamin D within the lungs include increased secretion of the antimicrobial peptide cathelicidin, decreased chemokine production, inhibition of dendritic cell activation, and alteration of T-cell activation. These cellular effects are important for host responses against infection and the development of allergic lung diseases like asthma. Epidemiological studies do suggest that vitamin D deficiency predisposes to viral respiratory tract infections and mycobacterial infections and that vitamin D may play a role in the development and treatment of asthma. Randomized, placebo-controlled trials are lacking but ongoing.
    MeSH term(s) Animals ; Calcitriol/metabolism ; Humans ; Immunity ; Lung/immunology ; Lung/metabolism ; Respiratory Tract Diseases/etiology ; Respiratory Tract Diseases/immunology ; Respiratory Tract Diseases/metabolism ; Vitamin D/physiology ; Vitamin D Deficiency/physiopathology
    Chemical Substances Vitamin D (1406-16-2) ; Calcitriol (FXC9231JVH)
    Language English
    Publishing date 2011-03-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 201161-x
    ISSN 2162-2620 ; 0083-6729
    ISSN (online) 2162-2620
    ISSN 0083-6729
    DOI 10.1016/B978-0-12-386960-9.00009-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.238: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article: Vitamin D Effects on Lung Immunity and Respiratory Diseases

    Hansdottir, Sif / Monick, Martha M

    Vitamins and Hormones. 2011, v. 86

    2011  

    Abstract: Our understanding of vitamin D metabolism and biological effects has grown exponentially in recent years and it has become clear that vitamin D has extensive immunomodulatory effects. The active vitamin D generating enzyme, 1α-hydroxylase, is expressed ... ...

    Abstract Our understanding of vitamin D metabolism and biological effects has grown exponentially in recent years and it has become clear that vitamin D has extensive immunomodulatory effects. The active vitamin D generating enzyme, 1α-hydroxylase, is expressed by the airway epithelium, alveolar macrophages, dendritic cells, and lymphocytes indicating that active vitamin D can be produced locally within the lungs. Vitamin D generated in tissues is responsible for many of the immunomodulatory actions of vitamin D. The effects of vitamin D within the lungs include increased secretion of the antimicrobial peptide cathelicidin, decreased chemokine production, inhibition of dendritic cell activation, and alteration of T-cell activation. These cellular effects are important for host responses against infection and the development of allergic lung diseases like asthma. Epidemiological studies do suggest that vitamin D deficiency predisposes to viral respiratory tract infections and mycobacterial infections and that vitamin D may play a role in the development and treatment of asthma. Randomized, placebo-controlled trials are lacking but ongoing.
    Keywords T-lymphocytes ; asthma ; cathelicidins ; chemokines ; dendritic cells ; epidemiological studies ; epithelium ; immunomodulation ; lungs ; macrophages ; metabolism ; mycobacterial diseases ; secretion ; vitamin D ; vitamin D deficiency
    Language English
    Size p. 217-237.
    Publishing place Elsevier Science & Technology
    Document type Article
    ZDB-ID 201161-x
    ISSN 2162-2620 ; 0083-6729
    ISSN (online) 2162-2620
    ISSN 0083-6729
    DOI 10.1016/B978-0-12-386960-9.00009-5
    Database NAL-Catalogue (AGRICOLA)

    More links

    Kategorien

    In stock of ZB MED Bonn / Germany

    Z 55/42: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  3. Article ; Online: Effects of prenatal inhalation exposure to copper nanoparticles on murine dams and offspring.

    Adamcakova-Dodd, Andrea / Monick, Martha M / Powers, Linda S / Gibson-Corley, Katherine N / Thorne, Peter S

    Particle and fibre toxicology

    2015  Volume 12, Page(s) 30

    Abstract: Background: Increasing numbers of individuals may be exposed to nanomaterials during pregnancy. The overarching goal of this investigation was to determine if prenatal inhalation exposure to copper nanoparticles (Cu NPs) has an effect on dams and ... ...

    Abstract Background: Increasing numbers of individuals may be exposed to nanomaterials during pregnancy. The overarching goal of this investigation was to determine if prenatal inhalation exposure to copper nanoparticles (Cu NPs) has an effect on dams and offspring, including an analysis of inflammatory markers (Th1/Th2 cytokine profiles).
    Methods: Physicochemical characterization of Cu NPs was performed. Pregnant and non-pregnant mice (C57Bl/6 J) were exposed to Cu NPs or laboratory air in the whole-body chamber for 4 hrs/day on gestation days (GD) 3-19 (3.5 mg/m(3)). Animals were euthanized on GD 19 (0 week) or 7 weeks later. Bronchoalveolar lavage (BAL) fluid was analyzed for total and differential cells. Cytokine/chemokine concentrations were determined in the BAL fluid and the plasma of dams/non-pregnant mice and pups. Cu content was determined in the lungs and the blood of dams/non-pregnant mice and pups, in the placentas as well as in the whole bodies of pups immediately after delivery. Lungs and placentas were evaluated for histopathological changes. Gene expression of the Th1/Th2 profiles were analyzed in spleens of pups.
    Results: The survival rate of 7 week old pups exposed to Cu NPs was significantly lower than control pups (73 vs. 97 %). The average litter size, male/female ratio, body weight and lenght at birth were not different between Cu NP-exposed and control mice. Both pregnant and non-pregnant mice exposed to Cu NPs had significant pulmonary inflammation with increased number of neutrophils in the BAL fluid compared to controls. Perivascular lymphoplasmacytic cuffing was found in the lungs of exposed mice and was more pronounced in the non-pregnant group. Similarly, levels of inflammatory cytokines/chemokines IL-12(p40), G-CSF, GM-CSF, KC, MCP-1, MIP-1α, MIP-1β, RANTES and TNF-α in BAL fluid were significantly higher in non-pregnant than pregnant exposed mice. Histopathology evaluation of placentas did not identify any pathological changes. No translocation of Cu into the placenta or the fetus was found by inductively coupled plasma-mass spectroscopy. Expression of several Th1/Th2 or other immune response genes in pups' spleens were found to be significantly up- or down-regulated.
    Conclusions: Prenatal exposure to Cu NPs caused a profound pulmonary inflammation in dams and strong immunomodulatory effects in offspring. There was no clear polarization of genes expressed in pups' spleens towards Th1 or Th2 type of response.
    MeSH term(s) Animals ; Bronchoalveolar Lavage Fluid ; Copper/toxicity ; Cytokines/blood ; Cytokines/metabolism ; Female ; Gene Expression Profiling ; Inhalation Exposure ; Maternal Exposure ; Mice ; Nanoparticles/toxicity ; Pregnancy
    Chemical Substances Cytokines ; Copper (789U1901C5)
    Language English
    Publishing date 2015-10-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2170936-1
    ISSN 1743-8977 ; 1743-8977
    ISSN (online) 1743-8977
    ISSN 1743-8977
    DOI 10.1186/s12989-015-0105-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article: Second messenger pathways in pulmonary host defense.

    Monick, Martha M / Hunninghake, Gary W

    Annual review of physiology

    2003  Volume 65, Page(s) 643–667

    Abstract: The alveolar macrophage responds to bacterial infection with the production of inflammatory mediators that include TNFalpha. Early production of TNFalpha results in increased bacterial clearance, whereas too much TNFalpha results in many of the hallmarks ...

    Abstract The alveolar macrophage responds to bacterial infection with the production of inflammatory mediators that include TNFalpha. Early production of TNFalpha results in increased bacterial clearance, whereas too much TNFalpha results in many of the hallmarks of bacterial sepsis. TNFalpha production is regulated at many levels, including multiple signaling pathways, that lead to transcription, translation, and release of functional TNFalpha. Interactions of mitogen-activated protein (MAP) kinases, lipid signaling pathways, and oxidant-mediated mechanisms regulate the response of alveolar macrophages to infection. Animal models of sepsis support the central role played by macrophage-derived TNFalpha in sepsis.
    MeSH term(s) Animals ; Humans ; Lung/immunology ; Lung/metabolism ; Lung Diseases/immunology ; Lung Diseases/metabolism ; Lung Diseases/physiopathology ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/metabolism ; Second Messenger Systems/immunology ; Sepsis/immunology ; Sepsis/metabolism ; Sepsis/physiopathology
    Language English
    Publishing date 2003
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 207933-1
    ISSN 0066-4278
    ISSN 0066-4278
    DOI 10.1146/annurev.physiol.65.092101.142440
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.226: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: Inositol-requiring enzyme 1 inhibits respiratory syncytial virus replication.

    Hassan, Ihab / Gaines, Kayla S / Hottel, Wesley J / Wishy, Ryan M / Miller, Sara E / Powers, Linda S / Rutkowski, D Thomas / Monick, Martha M

    The Journal of biological chemistry

    2014  Volume 289, Issue 11, Page(s) 7537–7546

    Abstract: Despite being a major health problem, respiratory syncytial virus (RSV) infections remain without specific therapy. Identification of novel host cellular responses that play a role in the pathogenesis of RSV infection is needed for therapeutic ... ...

    Abstract Despite being a major health problem, respiratory syncytial virus (RSV) infections remain without specific therapy. Identification of novel host cellular responses that play a role in the pathogenesis of RSV infection is needed for therapeutic development. The endoplasmic reticulum (ER) stress response is an evolutionarily conserved cellular signaling cascade that has been implicated in multiple biological phenomena, including the pathogenesis of some viral infections. In this study, we investigate the role of the ER stress response in RSV infection using an in vitro A549 cell culture model. We found that RSV infection induces a non-canonical ER stress response with preferential activation of the inositol-requiring enzyme 1 (IRE1) and activated transcription factor 6 (ATF6) pathways with no concomitant significant activation of the protein kinase R-like ER kinase (PERK) pathway. Furthermore, we discovered that IRE1 has an inhibitory effect on RSV replication. Our data characterize, for the first time, the nature of the ER stress response in the setting of RSV infection and identify the IRE1 stress pathway as a novel cellular anti-RSV defense mechanism.
    MeSH term(s) Activating Transcription Factor 6/metabolism ; Animals ; Cell Line, Tumor ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress ; Endoribonucleases/metabolism ; Fibroblasts/metabolism ; Gene Expression Regulation, Viral ; Host-Pathogen Interactions ; Humans ; Mice ; Protein-Serine-Threonine Kinases/metabolism ; RNA Splicing ; Respiratory Syncytial Virus Infections/metabolism ; Respiratory Syncytial Viruses/physiology ; Signal Transduction ; Virus Replication
    Chemical Substances ATF6 protein, human ; Activating Transcription Factor 6 ; ERN1 protein, human (EC 2.7.11.1) ; Ern1 protein, mouse (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-)
    Keywords covid19
    Language English
    Publishing date 2014-02-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M113.510594
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article: Effects of vitamin D supplementation on alveolar macrophage gene expression: preliminary results of a randomized, controlled trial.

    Gerke, Alicia K / Pezzulo, Alejandro A / Tang, Fan / Cavanaugh, Joseph E / Bair, Thomas B / Phillips, Emily / Powers, Linda S / Monick, Martha M

    Multidisciplinary respiratory medicine

    2014  Volume 9, Issue 1, Page(s) 18

    Abstract: Background: Vitamin D deficiency has been implicated as a factor in a number of infectious and inflammatory lung diseases. In the lung, alveolar macrophages play a key role in inflammation and defense of infection, but there are little data exploring ... ...

    Abstract Background: Vitamin D deficiency has been implicated as a factor in a number of infectious and inflammatory lung diseases. In the lung, alveolar macrophages play a key role in inflammation and defense of infection, but there are little data exploring the immunomodulatory effects of vitamin D on innate lung immunity in humans. The objective of this study was to determine the effects of vitamin D supplementation on gene expression of alveolar macrophages.
    Methods: We performed a parallel, double-blind, placebo-controlled, randomized trial to determine the effects of vitamin D on alveolar macrophage gene expression. Vitamin D3 (1000 international units/day) or placebo was administered to adults for three months. Bronchoscopy was performed pre- and post-intervention to obtain alveolar macrophages. Messenger RNA was isolated from the macrophages and subjected to whole genome exon array analysis. The primary outcome was differential gene expression of the alveolar macrophage in response to vitamin D supplementation. Specific genes underwent validation by polymerase chain reaction methods.
    Results: Fifty-eight subjects were randomized to vitamin D (n = 28) or placebo (n = 30). There was a marginal overall difference between treatment group and placebo group in the change of 25-hydroxyvitaminD levels (4.43 ng/ml vs. 0.2 ng/ml, p = 0.10). Whole genome exon array analysis revealed differential gene expression associated with change in serum vitamin D levels in the treated group. CCL8/MCP-2 was the top-regulated cytokine gene and was further validated.
    Conclusions: Although only a non-significant increased trend was seen in serum vitamin D levels, subjects treated with vitamin D supplementation had immune-related differential gene expression in alveolar macrophages.
    Trial registration: ClinicalTrials.org: NCT01967628.
    Language English
    Publishing date 2014-03-26
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 2677839-7
    ISSN 2049-6958 ; 1828-695X
    ISSN (online) 2049-6958
    ISSN 1828-695X
    DOI 10.1186/2049-6958-9-18
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  7. Article: Human alveolar macrophages are deficient in PTEN. The role of endogenous oxidants.

    Flaherty, Dawn M / Monick, Martha M / Hinde, Sara L

    The Journal of biological chemistry

    2005  Volume 281, Issue 8, Page(s) 5058–5064

    Abstract: Human alveolar macrophages play a critical role in host defense and in the development of inflammation and fibrosis in the lung. Unlike their precursor cells, blood monocytes, alveolar macrophages are long-lived and tend to be resistant to apoptotic ... ...

    Abstract Human alveolar macrophages play a critical role in host defense and in the development of inflammation and fibrosis in the lung. Unlike their precursor cells, blood monocytes, alveolar macrophages are long-lived and tend to be resistant to apoptotic stimuli. In this study, we examined the role of differentiation in altering baseline phosphatidylinositol (PI) 3-kinase/Akt activity. We found that differentiation increased activity of pro-survival PI 3-kinase/Akt while decreasing amounts of the negative PI 3-kinase regulator, PTEN. PTEN is a lipid phosphatase with activity against phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3), the major bioactive product of PI 3-kinase. Examining in vivo differentiation of alveolar macrophages (by comparing blood monocytes to alveolar macrophages from single donors), we found that differentiation resulted in increased baseline reactive oxygen species (ROS) in the alveolar macrophages. This led to a deficiency in PTEN, increased activity of Akt, and prolonged survival of alveolar macrophages. These data support the hypothesis that alterations in ROS levels contribute to macrophage homeostasis by altering the balance between PI 3-kinase/Akt and the phosphatase, PTEN.
    MeSH term(s) Adenoviridae/genetics ; Blotting, Western ; Cell Differentiation ; Cell Survival ; Cells, Cultured ; Down-Regulation ; Electron Spin Resonance Spectroscopy ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Genetic Vectors ; Humans ; Lung/metabolism ; Macrophages/metabolism ; Macrophages, Alveolar/metabolism ; Monocytes/metabolism ; Oxidants/chemistry ; Oxidants/metabolism ; PTEN Phosphohydrolase/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Messenger/metabolism ; Reactive Oxygen Species ; Reverse Transcriptase Polymerase Chain Reaction
    Chemical Substances Enzyme Inhibitors ; Oxidants ; RNA, Messenger ; Reactive Oxygen Species ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67)
    Language English
    Publishing date 2005-12-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M508997200
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  8. Article ; Online: Interferons increase cell resistance to Staphylococcal alpha-toxin.

    Yarovinsky, Timur O / Monick, Martha M / Husmann, Matthias / Hunninghake, Gary W

    Infection and immunity

    2007  Volume 76, Issue 2, Page(s) 571–577

    Abstract: Many bacterial pathogens, including Staphylococcus aureus, use a variety of pore-forming toxins as important virulence factors. Staphylococcal alpha-toxin, a prototype beta-barrel pore-forming toxin, triggers the release of proinflammatory mediators and ... ...

    Abstract Many bacterial pathogens, including Staphylococcus aureus, use a variety of pore-forming toxins as important virulence factors. Staphylococcal alpha-toxin, a prototype beta-barrel pore-forming toxin, triggers the release of proinflammatory mediators and induces primarily necrotic death in susceptible cells. However, whether host factors released in response to staphylococcal infections may increase cell resistance to alpha-toxin is not known. Here we show that prior exposure to interferons (IFNs) prevents alpha-toxin-induced membrane permeabilization, the depletion of ATP, and cell death. Moreover, pretreatment with IFN-alpha decreases alpha-toxin-induced secretion of interleukin 1beta (IL-1beta). IFN-alpha, IFN-beta, and IFN-gamma specifically protect cells from alpha-toxin, whereas tumor necrosis factor alpha (TNF-alpha), IL-6, and IL-4 have no effects. Furthermore, we show that IFN-alpha-induced protection from alpha-toxin is not dependent on caspase-1 or mitogen-activated protein kinases, but requires protein synthesis and fatty acid synthase activity. Our results demonstrate that IFNs may increase cell resistance to staphylococcal alpha-toxin via the regulation of lipid metabolism and suggest that interferons play a protective role during staphylococcal infections.
    MeSH term(s) Adenosine Triphosphate/metabolism ; Bacterial Toxins/immunology ; Bacterial Toxins/toxicity ; Cell Death ; Cell Line ; Cell Membrane Permeability/drug effects ; Epithelial Cells/drug effects ; Fatty Acid Synthases/metabolism ; Hemolysin Proteins/immunology ; Hemolysin Proteins/toxicity ; Humans ; Interferons/immunology ; Interleukin-1beta/metabolism ; Protein Biosynthesis ; Staphylococcus aureus/immunology ; Staphylococcus aureus/metabolism
    Chemical Substances Bacterial Toxins ; Hemolysin Proteins ; Interleukin-1beta ; staphylococcal alpha-toxin ; Adenosine Triphosphate (8L70Q75FXE) ; Interferons (9008-11-1) ; Fatty Acid Synthases (EC 2.3.1.85)
    Language English
    Publishing date 2007-12-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    DOI 10.1128/IAI.01088-07
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 684: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  9. Article ; Online: Respiratory syncytial virus limits alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) phosphorylation to maintain translation and viral replication.

    Groskreutz, Dayna J / Babor, Ellen C / Monick, Martha M / Varga, Steven M / Hunninghake, Gary W

    The Journal of biological chemistry

    2010  Volume 285, Issue 31, Page(s) 24023–24031

    Abstract: The impact of respiratory syncytial virus (RSV) on morbidity and mortality is significant in that it causes bronchiolitis in infants, exacerbations in patients with obstructive lung disease, and pneumonia in immunocompromised hosts. RSV activates protein ...

    Abstract The impact of respiratory syncytial virus (RSV) on morbidity and mortality is significant in that it causes bronchiolitis in infants, exacerbations in patients with obstructive lung disease, and pneumonia in immunocompromised hosts. RSV activates protein kinase R (PKR), a cellular kinase relevant to limiting viral replication (Groskreutz, D. J., Monick, M. M., Powers, L. S., Yarovinsky, T. O., Look, D. C., and Hunninghake, G. W. (2006) J. Immunol. 176, 1733-1740). It is activated by autophosphorylation, likely triggered by a double-stranded RNA intermediate during replication of the virus. In most instances, ph-PKR targets the alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) protein via phosphorylation, leading to an inhibition of translation of cellular and viral protein. However, we found that although ph-PKR increases in RSV infection, significant eIF2alpha phosphorylation is not observed, and inhibition of protein translation does not occur. RSV infection attenuates eIF2alpha phosphorylation by favoring phosphatase rather than kinase activity. Although PKR is activated, RSV sequesters PKR away from eIF2alpha by binding of the kinase to the RSV N protein. This occurs in conjunction with an increase in the association of the phosphatase, PP2A, with eIF2alpha following PKR activation. The result is limited phosphorylation of eIF2alpha and continued translation of cellular and viral proteins.
    MeSH term(s) Cell Line, Tumor ; Epithelial Cells ; Eukaryotic Initiation Factor-2/metabolism ; Humans ; Immunity, Innate ; Models, Biological ; Phosphorylation ; Poly I-C/chemistry ; Protein Biosynthesis ; RNA, Double-Stranded/genetics ; RNA, Viral/genetics ; Respiratory Syncytial Viruses/metabolism ; Signal Transduction ; Time Factors ; Virus Replication/genetics
    Chemical Substances Eukaryotic Initiation Factor-2 ; RNA, Double-Stranded ; RNA, Viral ; Poly I-C (O84C90HH2L)
    Keywords covid19
    Language English
    Publishing date 2010-06-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M109.077321
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  10. Article: Integrin receptors are crucial for the restimulation of activated T lymphocytes.

    Yarovinsky, Timur O / Monick, Martha M / Hunninghake, Gary W

    American journal of respiratory cell and molecular biology

    2003  Volume 28, Issue 5, Page(s) 607–615

    Abstract: Stimulation via the T-cell receptor results in proliferation of naive T cells and activation-induced death of activated T cells. The expression of Fas ligand and activation-induced cell death are major mechanisms by which immune responses are modulated ... ...

    Abstract Stimulation via the T-cell receptor results in proliferation of naive T cells and activation-induced death of activated T cells. The expression of Fas ligand and activation-induced cell death are major mechanisms by which immune responses are modulated in the lung. Although it is known that the binding of integrin receptors to extracellular matrix proteins provides co-stimulatory signals to naive T cells, it is not clear whether these signals are critical for activated T cells. The activation and differentiation of T cells is marked by significant changes in integrin expression and affinity. To determine the role of integrin signaling in restimulation of activated T cells, we blocked integrin receptors with RGD peptides. Using murine activated CD4+ T cells and the T-cell hybridoma DO11.10, we found that RGD peptides inhibit tyrosine phosphorylation of CD3 epsilon-chain and ZAP-70, clustering of T-cell receptors, extracellular signal-regulated kinase mitogen-activated protein-kinase activation, and Fas ligand expression and prevent activation-induced cell death. We demonstrate that activated T cells are sensitive to integrin co-stimulation and that integrin receptors are required for the successful restimulation of activated T cells. This indicates that matrix proteins may play a major role in regulating T-cell-mediated immune responses in the lung.
    MeSH term(s) Animals ; Antibodies/immunology ; Antibodies/metabolism ; CD3 Complex/immunology ; Cell Adhesion/physiology ; Cell Death/physiology ; Cells, Cultured ; Enterotoxins/pharmacology ; Female ; Focal Adhesion Kinase 1 ; Focal Adhesion Protein-Tyrosine Kinases ; Integrins/metabolism ; Lymphocyte Activation/physiology ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinases/metabolism ; Oligopeptides/metabolism ; Phosphorylation ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Receptors, Cell Surface/metabolism ; Signal Transduction/physiology ; T-Lymphocytes/cytology ; T-Lymphocytes/drug effects ; T-Lymphocytes/metabolism
    Chemical Substances Antibodies ; CD3 Complex ; Enterotoxins ; Integrins ; Oligopeptides ; Receptors, Antigen, T-Cell ; Receptors, Cell Surface ; enterotoxin B, staphylococcal (39424-53-8) ; arginyl-glycyl-aspartic acid (78VO7F77PN) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Focal Adhesion Kinase 1 (EC 2.7.10.2) ; Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2) ; Ptk2 protein, mouse (EC 2.7.10.2) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2003-05
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2002-0105OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top