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American Journal of Respiratory Cell and Molecular Biology

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https://www.readbyqxmd.com/read/29141155/neutrophil-mediated-suppression-of-influenza-induced-pathology-requires-cd11b-cd18-mac-1
#1
Tamar Tak, Tomasz P Rygiel, Guruswamy Karnam, Okan W Bastian, Louis Boon, Marco Viveen, Frank E Coenjaerts, Linde Meyaard, Leo Koenderman, Janesh Pillay
Severe influenza virus infection can lead to life-threatening pathology through immune-mediated tissue damage. In various experimental models, this damage is dependent on T-cells. There is conflicting evidence regarding the role of neutrophils in influenza-mediated pathology. Neutrophils are often regarded as cells causing tissue damage, but in recent years it has become clear that a subset of human neutrophils is capable of suppressing T-cells, which is dependent on Mac-1 (CD11b/CD18). Therefore, we tested the hypothesis that immune suppression by neutrophils can reduce T-cell mediate pathology after influenza infection...
November 15, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29115860/lysyl-oxidase-like-1-protein-deficiency-protects-mice-from-adtgf-%C3%AE-1-induced-pulmonary-fibrosis
#2
Pierre-Simon Bellaye, Chiko Shimbori, Chandak Upagupta, Seidai Sato, Wei Shi, Jack Gauldie, Kjetil Ask, Martin Kolb
Idiopathic pulmonary fibrosis (IPF) is a progressive disease characterised by excessive deposition of extracellular matrix (ECM) in the lung parenchyma. The abnormal ECM deposition slowly overtakes normal lung tissue disturbing gas-exchange and leading to respiratory failure and death. ECM cross-linking and subsequent stiffening is thought to be a major contributor of disease progression and also promotes the activation of TGF-β1, one of the main pro-fibrotic growth factors. Lysyl oxidase-like1 (LOXL1) belongs to the crosslinking enzyme family and has been shown to be upregulated in active fibrotic regions of bleomycin-treated mice and IPF patients...
November 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29115856/lps-induced-acute-lung-injury-involves-the-nf-%C3%AE%C2%BAb-mediated-downregulation-of-sox18
#3
Christine M Gross, Manuela Kellner, Ting Wang, Qing Lu, Xutong Sun, Evgeny A Zemskov, Satish Noonepalle, Archana Kangath, Sanjiv Kumar, Manuel Gonzalez-Garay, Ankit A Desai, Saurabh Aggarwal, Boris Gorshkov, Christina Klinger, Alexander D Verin, John D Catravas, Jeffrey R Jacobson, Jason X-J Yuan, Ruslan Rafikov, Joe G N Garcia, Stephen M Black
One of the early events in the progression of lipopolysaccharide (LPS)-mediated acute lung injury (ALI) in mice is the disruption of the pulmonary endothelial barrier resulting in lung edema. However, the molecular mechanisms by which the endothelial barrier becomes compromised remain unresolved. The SRY-related High Mobility Group box (Sox) group-F family member, Sox18, is a barrier- protective protein through its ability to increase the expression of the tight junction protein, Claudin-5. Thus, the purpose of this study was to determine if down-regulation of the Sox18-Claudin-5 axis plays a role in the pulmonary endothelial barrier disruption associated with LPS exposure...
November 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29115853/extracellular-vesicles-new-players-in-lung-immunity
#4
Yu Fujita, Tsukasa Kadota, Jun Araya, Takahiro Ochiya, Kazuyoshi Kuwano
Extracellular vesicles (EVs), such as exosomes and microvesicles, play an important autocrine/paracrine role in intercellular communication. Details on the involvement of EVs in the pathogenesis of lung diseases have emerged over the past several years. Moreover, EVs package numerous DNA, proteins, mRNAs, and microRNAs (miRNAs) that can regulate immune responses in recipient cells. Almost all respiratory cells release EVs, and these EVs can have protective or detrimental functions depending on the type of donor cells, type of stimuli, and components...
November 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29112457/fosl1-promotes-kras-induced-lung-cancer-through-amphiregulin-and-cell-survival-gene-regulation
#5
Indira M Elangovan, Michelle Vaz, Chandramohan R Tamatam, Haranatha R Potteti, Narsa M Reddy, Sekhar P Reddy
RATIONALE: FOSL1/AP-1 transcription factor regulates gene expression controlling various pathophysiological processes. It is a major effector of RAS-ERK1/2 signaling and activated in human lung epithelia by tumorigenic stimuli. Recent evidence shows an inverse correlation between FOSL1 expression and the survival of lung cancer patients with adenocarcinomas; however its role in lung tumorigenesis remains elusive. OBJECTIVES: To determine the role of FOSL1 in Kras-induced lung adenocarcinoma in vivo, and its downstream effector mechanisms...
November 7, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29111771/staphylococcus-aureus-alpha-toxin-induces-actin-filament-remodeling-in-human-airway-epithelial-model-cells
#6
Sabine Ziesemer, Ina Eiffler, Alfrun Schönberg, Christian Müller, Falko Hochgräfe, Achim G Beule, Jan-Peter Hildebrandt
Exposure of cultured human airway epithelial model cells (16HBE14o-, S9) to Staphylococcus aureus alpha-toxin (hemolysin A, Hla) induces changes in cell morphology and cell layer integrity which are due to the inability of the cells to maintain stable cell-cell or focal contacts and to properly organize their actin cytoskeleton. The aim of this study was to identify Hla-activated signaling pathways involved in regulating the phosphorylation level of the actin depolymerizing factor cofilin. We used recombinant wild-type Hla (rHla) as well as a variant of Hla (rHla-H35L) that is unable to form functional transmembrane pores to treat immortalized human airway epithelial cells (16HBE14o-, S9) as well as freshly isolated human nasal tissue...
November 7, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29111769/xpc-deficiency-alters-cigarette-smoke-dna-damage-cell-fate-and-accelerates-emphysema-development
#7
Catherine R Sears, Huaxin Zhou, Matthew J Justice, Amanda J Fisher, Jacob Saliba, Isaac Lamb, Jessica Wicker, Kelly S Schweitzer, Irina Petrache
Cigarette smoke (CS) exposure is a major risk factor for the development of emphysema, a common disease characterized by loss of cells comprising the lung parenchyma. The mechanisms of cell injury leading to emphysema are not completely understood but are thought to involve persistent cytotoxic or mutagenic DNA damage induced by CS. Using complementary cell culture and mouse models of CS exposure, we investigated the role of the DNA repair protein xeroderma pigmentosum group C (XPC) on CS-induced DNA damage repair and emphysema...
November 7, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29100477/activation-of-anoctamin-1-limits-pulmonary-endothelial-cell-proliferation-via-p38-mapk-dependent-apoptosis
#8
Ayed M Allawzi, Alexander Vang, Richard T Clements, Bong Sook Jhun, Nouaying R Kue, Thomas J Mancini, Amy K Landi, Dmitry Terentyev, Jin O-Uchi, Suzy A Comhair, Serpil C Erzurum, Gaurav Choudhary
Hyperproliferative endothelial cells (ECs) play an important role in the pathogenesis of PAH. Anoctamin-1 (Ano1), a calcium activated chloride channel, can regulate cell proliferation and cell cycle in multiple cell types. However, the expression and function of Ano1 in the pulmonary endothelium is unknown. We examined whether Ano1 was expressed in pulmonary ECs and if altering Ano1 activity would affect EC survival. Expression and localization of Ano1 in rat lung microvascular ECs (RLMVECs) was assessed using immunoblot, immunofluorescence, and subcellular fractionation...
November 3, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29096066/epigenetics-of-mucus-hypersecretion-in-chronic-respiratory-diseases
#9
Tara V Saco, Mason T Breitzig, Richard F Lockey, Narasaiah Kolliputi
Asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF) are three chronic pulmonary diseases that affect an estimated 420 million individuals across the globe. A key factor contributing to each of these conditions is mucus hypersecretion. While management of these diseases is vastly studied, researchers have only begun to scratch the surface of the mechanisms contributing to mucus hypersecretion. Epigenetic regulation of mucus hypersecretion, other than micro RNA (miRNA) post-translational modification, is even more scarcely researched...
November 2, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29087726/fibrocytes-in-asthma-and-copd-variations-on-the-same-theme
#10
Isabelle Dupin, Cécile Contin-Bordes, Patrick Berger
Fibrocytes are circulating cells that have fibroblast properties. They are produced by the bone marrow stroma, and they move from the blood to injured organs using multiple chemokine pathways. They exhibit marked functional and phenotypic plasticity in response to the local tissue microenvironment to ensure a pro-inflammatory or a more resolving phenotype. They can adopt immune cell properties and modulate conventional immune cell functions. Although their exact function is not always clear, they have emerged as key effector cells in several fibrotic diseases like keloid, scleroderma, and idiopathic pulmonary fibrosis...
October 31, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29077507/multi-ethnic-meta-analysis-identifies-rai1-as-a-possible-obstructive-sleep-apnea-related-quantitative-trait-locus-in-men
#11
Han Chen, Brian E Cade, Kevin J Gleason, Andrew C Bjonnes, Adrienne M Stilp, Tamar Sofer, Matthew P Conomos, Sonia Ancoli-Israel, Raanan Arens, Ali Azarbarzin, Graeme I Bell, Jennifer E Below, Sung Chun, Daniel S Evans, Ralf Ewert, Alexis C Frazier-Wood, Sina A Gharib, José Haba-Rubio, Erika W Hagen, Raphael Heinzer, David R Hillman, W Craig Johnson, Zoltan Kutalik, Jacqueline M Lane, Emma K Larkin, Seung Ku Lee, Jingjing Liang, Jose S Loredo, Sutapa Mukherjee, Lyle J Palmer, George J Papanicolaou, Thomas Penzel, Paul E Peppard, Wendy S Post, Alberto R Ramos, Ken Rice, Jerome I Rotter, Scott A Sands, Neomi A Shah, Chol Shin, Katie L Stone, Beate Stubbe, Jae-Hoon Sul, Mehdi Tafti, Kent D Taylor, Alexander Teumer, Timothy A Thornton, Gregory J Tranah, Chaolong Wang, Heming Wang, Simon C Warby, D Andrew Wellman, Phyllis C Zee, Craig L Hanis, Cathy C Laurie, Daniel J Gottlieb, Sanjay R Patel, Xiaofeng Zhu, Shamil R Sunyaev, Richa Saxena, Xihong Lin, Susan Redline
Obstructive sleep apnea (OSA) is a common heritable disorder displaying marked sexual dimorphism in disease prevalence and progression. Previous genetic association studies have identified a few genetic loci associated with OSA and related quantitative traits, but they have only focused on single ethnic groups and a large proportion of the heritability remains unexplained. The apnea hypopnea index (AHI) is a commonly used quantitative measure characterizing OSA severity. Since OSA differs by sex, and the pathophysiology of obstructive events differ in rapid eye movement (REM) and non-REM (NREM) sleep, we hypothesized that additional genetic association signals would be identified by analyzing the NREM/REM-specific AHI and by conducting sex-specific analyses in multi-ethnic samples...
October 27, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29077485/the-splicing-factor-hnrnpa1-regulates-alternate-splicing-of-the-mylk-gene
#12
Joseph B Mascarenhas, Alex Y Tchourbanov, Sergei M Danilov, Tong Zhou, Ting Wang, Joe G N Garcia
Profound lung vascular permeability is a cardinal feature of Acute Respiratory Distress Syndrome (ARDS) and Ventilator-Induced Lung injury (VILI), two syndromes known to centrally involve the non-muscle isoform of myosin light chain kinase (nmMLCK) in vascular barrier dysregulation. Two main splice variants, nmMLCK1 and nmMLCK2, are well represented in human lung endothelial cells and encoded by MYLK and differ only in the presence of exon 11 in nmMLCK1 which contains critical phosphorylation sites (Y464 and Y471) that influence nmMLCK enzymatic activity, cellular translocation, and localization in response to vascular agonists...
October 27, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29053339/ecm-crosslinking-enhances-fibroblast-growth-and-protects-against-matrix-proteolysis-in-lung-fibrosis
#13
Christopher J Philp, Ivonne Siebeke, Debbie Clements, Suzanne Miller, Anthony Habgood, Alison E John, Vidya Navaratnam, Richard B Hubbard, Gisli Jenkins, Simon R Johnson
Idiopathic pulmonary fibrosis (IPF) is characterised by accumulation of extra cellular matrix (ECM) proteins and fibroblast proliferation. ECM cross-linking enzymes have been implicated in fibrotic diseases and we hypothesised that the ECM in IPF is abnormally cross-linked which enhances fibroblast growth and resistance to normal ECM turnover. We used a combination of in vitro ECM preparations and in vivo assays to examine the expression of cross-linking enzymes and the effect of their inhibitors on fibroblast growth and ECM turnover...
October 20, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29053336/interplay-between-ezh2-and-g9a-regulates-cxcl10-gene-repression-in-idiopathic-pulmonary-fibrosis
#14
William R Coward, Oliver J Brand, Alice Pasini, Gisli Jenkins, Alan J Knox, Linhua Pang
Selective repression of the antifibrotic gene CXCL10 contributes to tissue remodelling in idiopathic pulmonary fibrosis (IPF). We have previously reported that histone deacetylation and histone H3 lysine 9 (H3K9) methylation are involved in CXCL10 repression. This study explored the role of H3K27 methylation and the interplay between the two histone lysine methyltransferases, Enhancer of Zest Homolog 2 (EZH2) and G9a, in CXCL10 repression in IPF. By applying chromatin immunoprecipitation (ChIP), Re-ChIP and proximity ligation assays, we demonstrated that, like G9a-mediated H3K9 methylation, EZH2-mediated H3K27me3 was significantly enriched at the CXCL10 promoter in fibroblasts from IPF lungs (F-IPF) compared with fibroblasts from non-fibrotic lungs (F-NL) and that EZH2 and G9a physically interacted with each other...
October 20, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29019707/glutaminolysis-promotes-collagen-translation-and-stability-via-%C3%AE-ketoglutarate-mediated-mtor-activation-and-proline-hydroxylation
#15
Jing Ge, Huachun Cui, Na Xie, Sami Banerjee, Sijia Guo, Shubham Dubey, Stephen Barnes, Gang Liu
Glutaminolysis is the metabolic process of glutamine, of which aberration has been implicated in several pathogeneses. While we and others recently found a diversity of metabolic dysregulations in organ fibrosis, it is unknown if glutaminolysis regulates the pro-fibrotic activities of myofibroblasts, the primary effector in this pathology. In this study, we found that lung myofibroblasts demonstrated significantly augmented glutaminolysis that was mediated by elevated Glutaminase 1 (Gls1). Inhibition of glutaminolysis by specific Gls1 inhibitors CB-839 and BPTES as well as Gls1 siRNA blunted the expression of collagens, but not that of Fibronectin, Elastin or myofibroblastic marker smooth muscle actin α (SMA-α)...
October 11, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/29019702/inhibition-of-phgdh-attenuates-bleomycin-induced-pulmonary-fibrosis
#16
Robert B Hamanaka, Recep Nigdelioglu, Angelo Y Meliton, Yufeng Tian, Leah J Witt, Erin O'Leary, Kaitlyn A Sun, Parker S Woods, David Wu, Brandon Ansbro, Shawn Ard, Jason M Rohde, Nickolai O Dulin, Robert D Guzy, Gökhan M Mutlu
Organ fibrosis, including idiopathic pulmonary fibrosis (IPF), is associated with significant morbidity and mortality. Since currently available therapies have limited effect, there is need to better understand the mechanisms by which organ fibrosis occurs. We have recently reported that TGF-β, a key cytokine which promotes fibrogenesis, induces the expression of the enzymes of the de novo serine and glycine synthesis pathway in human lung fibroblasts and that phosphoglycerate dehydrogenase (PHGDH, the first and rate limiting enzyme of the pathway) is required to promote collagen protein synthesis downstream of TGF-β...
October 11, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28984468/tgf-%C3%AE-1-evokes-human-airway-smooth-muscle-cell-shortening-and-hyperresponsiveness-via-smad3
#17
Christie A Ojiaku, Gaoyuan Cao, Wanqu Zhu, Edwin J Yoo, Maya Shumyatcher, Blanca E Himes, Steven S An, Reynold A Panettieri
Transforming growth factor beta 1 (TGF-β1), a cytokine whose levels are elevated in the airways of patients with asthma, perpetuates airway inflammation and modulates airway structural cell remodeling. However, the role of TGF-β1 in excessive airway narrowing in asthma, or airway hyperresponsiveness (AHR), remains unclear. In this study, we set out to investigate the direct effects of TGF-β1 on human airway smooth muscle (HASM) cell shortening and hyperresponsiveness. The dynamics of AHR and single-cell excitation-contraction (E-C) coupling were measured in human precision-cut lung slices (hPCLS) and in isolated HASM cells using supravital microscopy and magnetic twisting cytometry (MTC), respectively...
October 6, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28960101/relb-deficient-dendritic-cells-promote-the-development-of-spontaneous-allergic-airway-inflammation
#18
Prema M Nair, Malcolm R Starkey, Tatt Jhong Haw, Roland Ruscher, Gang Liu, Muralidhara R Maradana, Ranjeny Thomas, Brendan J O'Sullivan, Philip M Hansbro
RATIONALE: RelB is a member of the NF-κB family that is essential for dendritic cell (DC) function and maturation. However, the contribution of RelB to the development of allergic airway inflammation (AAI) is unknown. Here, we identify a pivotal role for RelB in the development of spontaneous AAI, independent of exogenous allergen exposure. METHODS: We assessed AAI in two strains of RelB-deficient ((-/-)) mice, one with a targeted deletion and another mutant expressing an major histocompatibility complex (MHC) transgene...
September 29, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28960086/maternal-e-cigarette-exposure-in-mice-alters-dna-methylation-and-lung-cytokine-expression-in-offspring
#19
Hui Chen, Gerard Li, Yik Lung Chan, David G Chapman, Suporn Sukjamnong, Tara Nguyen, Tiara Annissa, Kristine C McGrath, Pawan Sharma, Brian G Oliver
INTRODUCTION: E-cigarette usage is increasing, especially among the young, with both the general population and physicians perceiving them as a safe alternative to tobacco smoking. Worryingly, e-cigarettes are commonly used by pregnant women. As nicotine is known to adversely affect children in-utero, we hypothesised that nicotine delivered via e-cigarettes would negatively affect lung development. To test this we developed a mouse model of maternal e-vapour (nicotine and nicotine-free) exposure, and investigated the impact on the growth and lung inflammation in both offspring and mothers...
September 29, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28957638/augmented-responses-to-ozone-in-obese-mice-require-il-17a-and-gastrin-releasing-peptide
#20
Joel A Mathews, Nandini Krishnamoorthy, David I Kasahara, John Hutchinson, Youngji Cho, Jeffrey D Brand, Alison S Williams, Allison P Wurmbrand, Luiza Ribeiro, Frank Cuttitta, Mary E Sunday, Bruce D Levy, Stephanie A Shore
Ozone and obesity both increase IL-17A in the lungs. In mice, obesity augments the airway hyperresponsiveness and neutrophil recruitment induced by acute ozone exposure. Therefore, we examined the role of IL-17A in obesity-related increases in the response to ozone observed in obese mice. Lean wildtype and obese db/db mice were pretreated with IL-17A blocking or isotype antibodies, exposed to air or ozone (2 ppm for 3 h), and evaluated 24 h later. Microarray analysis of lung tissue gene expression was used to examine the mechanistic basis for effects of anti-IL-17A...
September 28, 2017: American Journal of Respiratory Cell and Molecular Biology
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