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American Journal of Respiratory Cell and Molecular Biology

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https://www.readbyqxmd.com/read/28535074/synchrotron-imaging-shows-effect-of-ventilator-settings-on-intra-breath-cyclic-changes-in-pulmonary-blood-volume
#1
Liisa Porra, Ludovic Broche, Loïc Dégrugilliers, Gergely Albu, Iliona Malaspinas, Camille Doras, Mats Wallin, Magnus Hallbäck, Walid Habre, Sam Bayat
RATIONALE: Despite the importance of dynamic changes in the regional distributions of gas and blood during the breathing cycle for lung function in the mechanically ventilated patient, no quantitative data on such cyclic changes is currently available. METHODS: We used a novel gated synchrotron CT-imaging to quantitatively image regional lung gas (Vg), tissue density and blood volume (Vb) in 6 anaesthetized, paralyzed and mechanically ventilated rabbits with normal lungs...
May 23, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28530121/glucocorticoids-retain-bi-potent-fibroblast-progenitors-during-alveolar-septation-in-mice
#2
Stephen E McGowan, Diann M McCoy
Glucocorticoids have been widely used and exert pleiotropic effects on alveolar structure and function, but do not improve the long-term clinical outcomes for patients with bronchopulmonary dysplasia, emphysema, or interstitial lung diseases. Treatments which foster alveolar regeneration could substantially improve the long-term outcomes for such patients. One approach to alveolar regeneration is to stimulate and guide intrinsic alveolar progenitors along developmental pathways used during secondary septation...
May 21, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28489455/micrornas-profiling-in-asthma-potential-biomarkers-and-therapeutic-targets
#3
Enrico Heffler, Alessandro Allegra, Giovanni Pioggia, Giuseppe Picardi, Caterina Musolino, Sebastiano Gangemi
Asthma is a heterogeneous chronic inflammatory disease in which different endotypes contribute to define clinical-inflammatory phenotypes. MicroRNAs (miRNAs) are a class of small, endogenous 22-25 nt RNA molecules that bind to specific mRNAs to inhibit translation and promote mRNA degradation. miRNAs function in post-transcriptional regulation and control physiological and pathological processes in various diseases. The purpose of this review is to summarize and discuss the current knowledge on the function of miRNAs in asthma, focusing the attention particularly on their biological properties, pathophysiologic roles, and potential use as biomarkers and/or therapies for asthma...
May 10, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28489415/hepatic-steatosis-accompanies-pulmonary-alveolar-proteinosis
#4
Alan N Hunt, Anagha Malur, Tual Monfort, Pavlos Lagoudakis, Sumeet Mahajan, Anthony D Postle, Mary Jane Thomassen
Maintenance of tissue-specific organ lipid compositions characterises mammalian lipid homeostasis. Lung and liver synthesise mixed phosphatidylcholine (PC) molecular species subsequently "tailored" for function. Lungs progressively enrich disaturated PC (DSPC) directed to lamellar body (LB) surfactant stores prior to secretion. Liver accumulates polyunsaturated PC directed to VLDL assembly and secretion, or triglyceride stores. In each tissue, selective PC species enrichment mechanisms lie at the heart of effective homeostasis...
May 10, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28481637/hydrogen-sulfide-a-novel-player-in-airway-development-pathophysiology-of-respiratory-diseases-and-antiviral-defenses
#5
Nikolay Bazhanov, Maria Ansar, Teodora Ivanciuc, Roberto P Garofalo, Antonella Casola
Hydrogen sulfide (H2S) is a biologically relevant signaling molecule in mammals. Together with the volatile substances nitric oxide (NO) and carbon monoxide (CO), H2S is defined as a gasotransmitter, playing a physiological role in a variety of functions such as synaptic transmission, vascular tone, angiogenesis, inflammation and cellular signaling. The generation of H2S is catalyzed by cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE) and 3 mercaptopyruvate sulfurtransferase (3-MST). The expression of CBS and CSE is tissue-specific with CBS being expressed predominantly in the brain and CSE in peripheral tissues, including lungs...
May 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28481622/cardiomyocytes-of-the-heart-and-pulmonary-veins-novel-contributors-to-asthma
#6
Stephen Sai Folmsbee, Cara J Gottardi
Recent genome-wide association studies have implicated both cardiac and pulmonary vein-related genes in the pathogenesis of asthma. Since cardiac cells are not present in lung airways or viewed to affect the immune system, interpretation of these findings in the context of more well-established contributors to asthma has remained challenging. However, cardiomyocytes are present in the lung, specifically along pulmonary veins, and recent murine models suggest that cardiac cells lining pulmonary veins may contribute to allergic airway disease...
May 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28481620/ifn%C3%AE-influences-epithelial-anti-viral-responses-via-histone-methylation-of-the-rig-i-promoter
#7
C Mirella Spalluto, Akul Singhania, Doriana Cellura, Christopher H Woelk, Tilman Sanchez-Elsner, Karl J Staples, Tom M A Wilkinson
The asthmatic lung is prone to respiratory viral infections that exacerbate the symptoms of the underlying disease. Recent work has suggested that a deficient Th1 response in early life may lead to these aberrant anti-viral responses. We investigated whether the inflammatory environment of the airway epithelium could modulate anti-viral gene expression via epigenetic mechanisms, in order to study the development of a long-term dysregulation of innate responses, which are a hallmark of asthma. We primed AALEB, a human bronchial epithelial cell line, with IFNγ and IL13 and subsequently infected cells with Respiratory Syncytial Virus (RSV) and innate anti-viral genes expression and their epigenetic markers were analysed...
May 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28463086/vitamin-d-counteracts-an-il-23-dependent-il-17a-ifn%C3%AE-response-driven-by-urban-particulate-matter
#8
Elizabeth H Mann, Tzer-Ren Ho, Paul E Pfeffer, Nick C Matthews, Elfy Chevretton, Ian Mudway, Frank J Kelly, Catherine M Hawrylowicz
Urban particulate matter (UPM) air pollution and vitamin D deficiency are detrimentally associated with respiratory health; this is hypothesised to be due in part to regulation of IL-17A, which UPM is reported to promote. Here we use a myeloid (m)DC-memory CD4+ T cell co-culture system to characterize UPM-driven IL-17A+ cells, investigate the mechanism by which UPM-primed DCs promote this phenotype and address evidence for cross-regulation by vitamin D. CD1c+ mDCs were cultured overnight with or without a reference source of UPM and/or active vitamin D (1,25(OH)2D3) before co-culturing with autologous memory CD4+ T cells...
May 2, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28459279/integrative-genomics-of-emphysema-associated-genes-reveals-potential-disease-biomarkers
#9
Ma'en Obeidat, Yunlong Nie, Nick Fishbane, Xuan Li, Yohan Bossé, Philippe Joubert, David C Nickle, Ke Hao, Dirkje S Postma, Wim Timens, Marc A Sze, Casey P Shannon, Zsuzsanna Hollander, Raymond T Ng, Bruce McManus, Bruce E Miller, Stephen Rennard, Avrum Spira, Tillie Louise Hackett, Wan Lam, Stephen Lam, Rosa Faner, Alvar Agusti, James C Hogg, Don D Sin, Peter D Paré
RATIONALE: Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. Gene expression profiling across multiple regions of the same lung identified genes significantly related to emphysema. OBJECTIVE: To determine whether the lung and epithelial expression of 127 emphysema-related genes is also related to lung function in independent cohorts and whether any of these genes could be used as biomarkers in the peripheral blood of COPD patients...
May 1, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28445073/plasminogen-activator-inhibitor-1-is-critical-in-alcohol-enhanced-acute-lung-injury-in-mice
#10
Lauren G Poole, Veronica L Massey, Deanna L Siow, Edilson Torres-González, Nikole L Warner, James P Luyendyk, Jeffrey D Ritzenthaler, Jesse Roman, Gavin E Arteel
RATIONALE: Chronic alcohol exposure is a clinically important risk factor for development of acute respiratory distress syndrome, the most severe form of acute lung injury (ALI). However, the mechanisms by which alcohol sensitizes the lung to development of this disease are poorly understood. OBJECTIVES: We determined the role of the anti-fibrinolytic protein plasminogen activator inhibitor-1 (PAI-1) in alcohol enhancement of experimental endotoxin-induced ALI. METHODS: Wild-type (WT), PAI-1(-/-) and Integrin β3(-/-) mice were fed ethanol-containing Lieber-DeCarli liquid or control diet for 6 weeks followed by systemic lipopolysaccharide (LPS) challenge...
April 26, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28443685/lymphatic-changes-in-respiratory-diseases-more-than-just-remodeling-of-the-lung
#11
Benjamin Stump, Ye Cui, Pranav Kidambi, Anthony M Lamattina, Souheil El-Chemaly
Advances in our ability to identify lymphatic endothelial cells and differentiate them from blood endothelial cells have led to important progress in the study of lymphatic biology. Over the past decade, pre-clinical and clinical studies have shown that there are changes to the lymphatic vasculature in nearly all lung diseases. Efforts to understand the contribution of lymphatics and their growth factors to disease initiation, progression and resolution have led to seminal findings establishing critical roles for lymphatics in lung biology spanning from the first breath after birth to asthma, tuberculosis, and lung transplantation...
April 26, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28443674/perinatal-bacterial-exposure-contributes-to-il-13-aeroallergen-response
#12
Benjamin A Turturice, Ravi Ranjan, Brian Nguyen, Lauren M Hughes, Kalista E Andropolis, Diane R Gold, Augusto A Litonjua, Emily Oken, David L Perkins, Patricia W Finn
There is a high prevalence of aeroallergen sensitivity in asthmatic populations, and seroreactivity to aeroallergens early in infancy is associated with increased risk of developing asthma later in life. In addition to allergen sensitivity, asthma development has been associated with differential microbial exposure and infection in early life. We have has previously shown that cord blood mononuclear cells respond to common aeroallergens (i.e., house dust mite (Der f1), cockroach (Bla g2)) as assayed by lymphoproliferation and cytokine (IL-13, IFN-γ) production...
April 26, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28441029/variable-susceptibility-to-cigarette-smoke-induced-emphysema-in-34-inbred-strains-of-mice-implicates-abi3bp-in-emphysema-susceptibility
#13
Josiah E Radder, Alyssa D Gregory, Adriana S Leme, Michael H Cho, Yanxia Chu, Neil J Kelly, Per Bakke, Amund Gulsvik, Augusto A Litonjua, David Sparrow, Terri H Beaty, James D Crapo, Edwin K Silverman, Yingze Zhang, Annerose Berndt, Steven D Shapiro
RATIONALE: Chronic obstructive pulmonary disease (COPD) is caused by a complex interaction of environmental exposures, most commonly cigarette smoke, and genetic factors. Chronic cigarette smoke exposure in the mouse is a commonly used animal model of COPD. We aimed to expand our knowledge of the variable susceptibility of inbred strains to this model and test for genetic variants associated with this trait. OBJECTIVE: To measure differential susceptibility to cigarette smoke-induced emphysema in the mouse, identify genetic loci associated with this quantitative trait, and find homologous human genes associated with COPD...
April 25, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28421819/il-4-induces-the-il17rb-gene-transcription-in-monocytic-cells-with-coordinate-autocrine-il-25-signaling
#14
Nathaniel M Weathington, Shreya S Kanth, Qiaoke Gong, James Londino, Akihiko Hoji, Mauricio Rojas, John Trudeau, Sally Wenzel, Rama K Mallampalli
IL-25 and IL-4 signaling in the setting of infection or allergic responses can drive Type 2 inflammation. IL-25 requires the IL-17 receptor B (IL-17Rb) to mediate signaling through nuclear factor kappa B transcriptional activation. Despite the known coexistence of these two cytokines in the Type 2 inflammatory environment, collaborative signaling between the IL-4 and IL-25 axes is poorly explored. Here we demonstrate IL-4 induction of both IL-25 and IL-17Rb protein in human lung tissue culture, primary alveolar macrophages, and the THP-1 monocytic cell line...
April 19, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28421818/cell-origin-dictates-programming-of-resident-versus-recruited-macrophages-during-acute-lung-injury
#15
Kara J Mould, Lea Barthel, Michael P Mohning, Stacey M Thomas, Alexandra L McCubbrey, Thomas Danhorn, Sonia M Leach, Tasha E Fingerlin, Brian P O'Connor, Julie A Reisz, Angelo D'Alessandro, Donna L Bratton, Claudia V Jakubzick, William J Janssen
Two populations of alveolar macrophages (AMs) co-exist in the inflamed lung: resident AMs that arise during embryogenesis, and recruited AMs that originate postnatally from circulating monocytes. The objective of this study was to determine whether origin or environment dictates the transcriptional, metabolic, and functional programming of these two ontologically distinct populations over the time course of acute inflammation. RNA sequencing demonstrated marked transcriptional differences between resident and recruited AMs affecting three main areas: proliferation, inflammatory signaling, and metabolism...
April 19, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28421813/hemin-causes-lung-microvascular-endothelial-barrier-dysfunction-by-necroptotic-cell-death
#16
Sunit Singla, Justin R Sysol, Benjamin Dille, Nicole Jones, Jiwang Chen, Roberto F Machado
Hemin, the oxidized prosthetic moiety of hemoglobin, has been implicated in the pathogenesis of acute chest syndrome (ACS) in sickle cell patients by virtue of its endothelial-activating properties. In this study, we examined whether hemin can cause lung microvascular endothelial barrier dysfunction. By assessing transendothelial resistance using electrical cell impedance sensing, and by directly measuring trans-monolayer FITC-dextran flux, we found that hemin does cause endothelial barrier dysfunction in a concentration-dependent manner...
April 19, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28398769/potential-involvement-of-the-epidermal-growth-factor-receptor-ligand-epiregulin-and-matrix-metalloproteinase-1-in-pathogenesis-of-chronic-rhinosinusitis
#17
Tetsuya Homma, Atsushi Kato, Masafumi Sakashita, Tetsuji Takabayashi, James E Norton, Lydia A Suh, Roderick G Carter, Kathleen E Harris, Anju T Peters, Leslie C Grammer, Jin-Young Min, Stephanie Shintani-Smith, Bruce K Tan, Kevin Welch, David B Conley, Robert C Kern, Robert P Schleimer
RATIONALE: Chronic rhinosinusitis (CRS) is a heterogeneous chronic inflammatory disease of the nose and paranasal sinuses that presents without (CRSsNP) or with nasal polyps (CRSwNP). Features of CRSwNP are the frequent presence of type 2 allergic inflammation and high prevalence of Staphylococcus aureus (SA) colonization. As inflammation persists, sinus tissue undergoes epithelial damage and repair along with polyp growth. Since one feature of damaged tissue is enhancement of growth factor signaling, we evaluated the presence of EGFR ligands and MMPs in CRS...
April 11, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28398760/nicotine-impairs-macrophage-control-of-mycobacterium-tuberculosis
#18
Xiyuan Bai, Jerry A Stitzel, An Bai, Cristian A Zambrano, Matthew Phillips, Philippa Marrack, Edward D Chan
Pure nicotine impairs macrophage killing of Mycobacterium tuberculosis (MTB) but it is not known whether the nicotine component in cigarette smoke (CS) plays a role. Moreover, the mechanisms by which nicotine impairs macrophage immunity against MTB have not been explored. To neutralize the effects of nicotine in CS extract, we utilized a competitive inhibitor to the nicotinic acetylcholine receptor (nAChR) - mecamylamine - as well as macrophages derived from mice with genetic disruption of specific subunits of nAChR...
April 11, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28379718/sonic-hedgehog-signaling-regulates-myofibroblast-function-during-alveolar-septum-formation-in-murine-postnatal-lung
#19
Matthias C Kugler, Cynthia A Loomis, Zhicheng Zhao, Jennifer C Cushman, Li Liu, John S Munger
Sonic Hedgehog (Shh) signaling regulates mesenchymal proliferation and differentiation during embryonic lung development. In the adult lung, Shh signaling maintains mesenchymal quiescence and is dysregulated in diseases such as IPF and COPD. Our previous data implicated a role for Shh in postnatal lung development. Here we report a detailed analysis of Shh signaling during murine postnatal lung development. We show that Shh pathway expression and activity during alveolarization (P0-P14) are distinct from those during maturation (P14-P24)...
April 5, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28375666/glucocorticoid-receptor-chip-seq-identifies-plcd1-as-a-klf15-target-that-represses-airway-smooth-muscle-hypertrophy
#20
Sarah K Sasse, Vineela Kadiyala, Thomas Danhorn, Reynold A Panettieri, Tzu L Phang, Anthony N Gerber
Glucocorticoids exert important therapeutic effects on airway smooth muscle (ASM), yet few direct targets of glucocorticoid signaling in ASM have been definitively identified. Here, we show that the transcription factor, KLF15, is directly induced by glucocorticoids in primary human ASM and that KLF15 represses ASM hypertrophy. We integrated transcriptome data from KLF15 overexpression with genome-wide analysis of RNA Polymerase II (RNAPII) and glucocorticoid receptor (GR) occupancy (i.e. ChIP-seq) to identify PLCD1 as both a KLF15-regulated gene and a novel repressor of ASM hypertrophy...
April 4, 2017: American Journal of Respiratory Cell and Molecular Biology
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