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American Journal of Respiratory Cell and Molecular Biology

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https://www.readbyqxmd.com/read/28445073/plasminogen-activator-inhibitor-1-is-critical-in-alcohol-enhanced-acute-lung-injury-in-mice
#1
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
#2
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
#3
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
#4
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
#5
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
#6
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
#7
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
#8
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
#9
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
#10
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
#11
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
https://www.readbyqxmd.com/read/28363030/integrated-stress-response-mediates-epithelial-injury-in-mechanical-ventilation
#12
Tamas Dolinay, Blanca E Himes, Maya Shumyatcher, Gladys Gray Lawrence, Susan S Margulies
RATIONALE: Ventilator-induced lung injury (VILI) is a severe complication of mechanical ventilation that can lead to acute respiratory distress syndrome (ARDS). VILI is characterized by damage to the epithelial barrier with subsequent pulmonary edema and profound hypoxia. Available lung protective ventilator strategies offer only modest benefit in preventing VILI because they cannot impede alveolar overdistension and concomitant epithelial barrier dysfunction in the inflamed lung regions...
March 31, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28362108/alpha1-antitrypsin-deficient-macrophages-have-increased-matriptase-mediated-proteolytic-activity
#13
Karina Krotova, George W Marek, Rejean L Wang, George Aslanidi, Brad E Hoffman, Nazli Khodayari, Farshid N Rouhani, Mark L Brantly
Alpha1-antitrypsin (AAT) deficiency-associated emphysema is largely attributed to insufficient inhibition of neutrophil elastase released from neutrophils. Correcting AAT levels by augmentation therapy only slows disease progression; the absence of full recovery indicates a more complex process of lung destruction. Because alveolar macrophages (Mɸ) express AAT, we propose that the expression and intracellular accumulation of mutated Z-AAT (the most common mutation is called Z) compromise Mɸ function and contribute to emphysema development...
March 31, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28328242/human-airway-epithelial-cells-direct-significant-rhinovirus-replication-in-monocytic-cells-by-enhancing-icam1-expression
#14
Xu Zhou, Lingxiang Zhu, Rosa Lizarraga, Yin Chen
Human rhinovirus (RV) is the major cause of common cold, and it also plays a significant role in asthma and asthma exacerbation. Airway epithelium is the primary site of RV infection and production. In contrast, monocytic cells (e.g. monocytes and macrophages) are believed to be non-permissive for RV replication. Instead, RV has been shown to modulate inflammatory gene expressions in these cells via a replication-independent mechanism. In the present study, RV16 (a major-group RV) replication was found to be significantly enhanced in monocytes when co-cultivated with airway epithelial cells...
March 22, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28326803/when-is-an-alveolar-type-2-cell-an-alveolar-type-2-cell-a-conundrum-for-lung-stem-cell-biology-and-regenerative-medicine
#15
Michael F Beers, Yuben Moodley
Generating mature, differentiated, adult lung cells from pluripotent cells such as induced pluripotent cells (iPS) and embryonic stem cells (ES) offers the hope of both generating disease specific in vitro models and creating definitive and personalized therapies for a host of debilitating lung parenchymal and airway diseases. With the goal of advancing lung regenerative medicine, several groups have developed and reported on protocols utilizing either defined media, co-culture with mesenchymal components, or sequential treatments mimicking lung development, to obtain distal lung epithelial cells from stem cell precursors...
March 22, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28324666/gene-expression-analysis-to-assess-the-relevance-of-rodent-models-to-human-lung-injury
#16
Timothy E Sweeney, Shane Lofgren, Purvesh Khatri, Angela J Rogers
Rationale The relevance of animal models to human diseases is an area of intense scientific debate. The degree to which mouse models of lung injury recapitulate human lung injury has never been assessed. Integrating data from both human and animal expression studies allows for increased statistical power and identification of conserved differential gene expression across organisms and conditions. Objectives Comprehensive integration of gene expression data in experimental ALI in rodents compared to humans. Methods We performed two separate gene expression multi-cohort analyses to determine differential gene expression in experimental animal and human lung injury...
March 21, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28314106/runt-related-transcription-factor-1-regulates-lps-induced-acute-lung-injury-via-nf-%C3%AE%C2%BAb-signaling
#17
Xiaoju Tang, Ling Sun, Xiaodong Jin, Yifan Chen, Hui Zhu, Yasha Liang, Qingbo Wu, Xing Han, Jianing Liang, Xiaojing Liu, Zongan Liang, Gang Wang, Fengming Luo
RATIONALE: RUNX1, a transcription factor expressed in multiple organs, plays important roles in embryonic development and hematopoiesis. While RUNX1 is highly expressed in pulmonary tissues, its role in lung function and homeostasis are unknown. OBJECTIVES: To assess the role of RUNX1 in the lung development and inflammation after lipopolysaccharide challenge. METHODS: Expression of RUNX1 was assessed in human respiratory epithelial cells...
March 17, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28296468/foxp3-regulatory-t-cell-expression-of-keratinocyte-growth-factor-enhances-lung-epithelial-proliferation
#18
Catherine F Dial, Miriya K Tune, Claire M Doerschuk, Jason R Mock
Repair of the lung epithelium after injury is a critical component for resolution; however, the processes necessary to drive epithelial resolution are not clearly defined. Published data demonstrate that Foxp3+ regulatory T cells (Tregs) enhance alveolar epithelial proliferation after injury, and Tregs in vitro directly promote type II alveolar epithelial cell (AT2) proliferation in part by a contact-independent mechanism. Therefore, we sought to determine the contribution of Treg-specific expression of a growth factor, keratinocyte growth factor (Kgf), known to be important in lung repair...
March 15, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28287822/efficiency-and-specificity-of-gene-deletion-in-lung-epithelial-doxycycline-inducible-cre-mice
#19
Meenal Sinha, Clifford A Lowell
Transgenic mouse strains, SP-C-rtTA, CCSP-rtTA and TetO-Cre, have been invaluable in spatiotemporally regulating gene deletion in pulmonary epithelium. In this study, we measured the efficiency and specificity of gene deletion achievable in these mice using the Rosa26-eYFP reporter. Triple transgenic mice (tTg or rtTA/TetO-Cre/Rosa-eYFP) were bred and treated with various doxycycline (dox) regimes to induce gene deletion, which was then quantified in various cell populations by flow cytometry. In these crosses, we found that the TetO-Cre transgene must be transmitted through the female parent to avoid germline gene deletion...
March 13, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28277743/obesity-induced-endoplasmic-reticulum-stress-causes-lung-endothelial-dysfunction-and-promotes-acute-lung-injury
#20
Dilip Shah, Freddy Romero, Zhi Guo, Jianxin Sun, Jonathan Li, Caleb B Kallen, Ulhas P Naik, Ross Summer
Obesity is a significant risk factor for the acute respiratory distress syndrome (ARDS). The mechanisms underlying this association are unknown. We recently showed that diet-induced obese (DIO) mice exhibit pulmonary vascular endothelial dysfunction which is associated with enhanced susceptibility to lipopolysaccharide (LPS)-induced lung injury. Here, we demonstrate that lung endothelial dysfunction in DIO mice coincides with increased endoplasmic reticulum (ER) stress. Specifically, we observed enhanced expression of the major sensors of misfolded proteins including PERK, IREα and ATF6, in whole lung and in lung endothelial cells isolated from DIO mice...
March 9, 2017: American Journal of Respiratory Cell and Molecular Biology
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