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American Journal of Physiology. Lung Cellular and Molecular Physiology

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https://www.readbyqxmd.com/read/29025713/neutrophil-elastase-increases-airway-ceramide-levels-via-upregulation-of-serine-palmitoyltransferase
#1
Sophia Karandashova, Apparao B Kummarapurugu, Shuo Zheng, Charles Chalfant, Judith A Voynow
Altered sphingolipid metabolism is associated with increased inflammation; however, the impact of inflammatory mediators, including neutrophil elastase (NE), on airway sphingolipid homeostasis remains unknown. Using a well-characterized mouse model of NE oropharyngeal aspiration, we investigated a potential link between NE-induced airway inflammation and increased synthesis of various classes of sphingolipids, including ceramide species. Sphingolipids in bronchoalveolar lavage fluids (BAL) were identified and quantified using reverse phase high-performance liquid chromatography/electrospray ionization tandem mass spectrometry analysis...
October 12, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29025712/ion-channels-of-the-lung-and-their-role-in-disease-pathogenesis
#2
Rafal Bartoszewski, Sadis Matalon, James F Collawn
Maintenance of normal epithelial ion and water transport in the lungs includes providing a thin layer of surface liquid that coats the conducting airways. This airway surface liquid is critical for normal lung function in a number of ways, but perhaps most importantly, is required for normal mucociliary clearance and bacterial removal. Preservation of the appropriate level of hydration, pH and viscosity for the airway surface liquid requires the proper regulation and function of a battery of different types of ion channels and transporters...
October 12, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29025711/toll-like-receptor-2-and-4-have-opposing-roles-in-the-pathogenesis-of-cigarette-smoke-induced-chronic-obstructive-pulmonary-disease
#3
Tatt Jhong Haw, Malcolm R Starkey, Stelios Pavlidis, Michael Fricker, Anya L Arthurs, Prema Mono Nair, Gang Liu, Irwan Hanish, Richard Y Kim, Paul S Foster, Jay C Horvat, Ian M Adcock, Philip M Hansbro
Chronic Obstructive Pulmonary Disease (COPD) is the third leading cause of morbidity and death and imposes major socioeconomic burdens globally. It is a progressive and disabling condition that severely impairs breathing and lung function. There is a lack of effective treatments for COPD, which is a direct consequence of the poor understanding of the underlying mechanisms involved in driving the pathogenesis of the disease. Toll-like receptor (TLR)2 and TLR4 are implicated in chronic respiratory diseases, including COPD, asthma and pulmonary fibrosis...
October 12, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28982738/intranasal-administration-of-recombinant-progranulin-inhibits-bronchial-smooth-muscle-hyperresponsiveness-in-mouse-allergic-asthma
#4
Yoshihiko Chiba, Shunta Danno, Rena Suto, Wataru Suto, Yamato Yamane, Motohiko Hanazaki, Hiroshi Katayama, Hiroyasu Sakai
Progranulin (PGRN) is a growth factor with multiple biological functions, and has been suggested as an endogenous inhibitor of TNFα-mediated signaling. TNFα is believed as one of the important mediators of the pathogenesis of asthma, including airway hyperresponsiveness (AHR). In the present study, effects of recombinant PGRN on the TNFα-mediated signaling and the antigen-induced hyper-contractility were examined in bronchial smooth muscles (BSMs) both in vitro and in vivo. Cultured human BSM cells (hBSMCs) and male BALB/c mice were used...
October 5, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28982737/evaluation-of-a-splunc1-derived-peptide-for-the-treatment-of-cystic-fibrosis-lung-disease
#5
Shawn T Terryah, Robert C Fellner, Saira Ahmad, Patrick John Moore, Boris Reidel, Juliana I Sesma, Christine S Kim, Alaina L Garland, David W Scott, Juan R Sabater, Jerome Carpenter, Scott H Randell, Mehmet Kesimer, William M Abraham, William J Arendshorst, Robert Tarran
In cystic fibrosis (CF) lungs, epithelial Na+ channel (ENaC) hyperactivity causes a reduction in airway surface liquid (ASL) volume, leading to decreased mucocilliary clearance and lung damage. Inhibition of ENaC is an attractive therapeutic option. However, ENaC antagonists have failed clinically due to off-target renal effects. The S18 peptide is a naturally occurring short palate lung and nasal epithelial clone 1 (SPLUNC1)-derived ENaC antagonist that restores ASL height for up to 24 h in CF human bronchial epithelial cultures...
October 5, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28982736/an-epoxide-hydrolase-secreted-by-pseudomonas-aeruginosa-decreases-mucociliary-transport-and-hinders-bacterial-clearance-from-the-lung
#6
Kelli L Hvorecny, Emily Dolben, Sophie Moreau-Marquis, Thomas H Hampton, Tamer B Shabaneh, Becca A Flitter, Christopher D Bahl, Jennifer M Bomberger, Bruce D Levy, Bruce A Stanton, Deborah A Hogan, Dean R Madden
The opportunistic pathogen Pseudomonas aeruginosa colonizes the lungs of susceptible individuals by deploying virulence factors targeting host defenses. The secreted CFTR inhibitory factor (Cif) dysregulates the endocytic recycling of CFTR and thus reduces CFTR abundance in host epithelial membranes. We have postulated that the decrease in ion secretion mediated by Cif would slow mucociliary transport and decrease bacterial clearance from the lungs. To test this hypothesis, we explored the effects of Cif in cultured epithelia and in the lungs of mice...
October 5, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28982735/acidosis-exacerbates-in-vivo-il-1-dependent-inflammatory-responses-and-neutrophil-recruitment-during-pulmonary-pseudomonas-aeruginosa-infection
#7
Iviana M Torres, Yash R Patankar, Brent L Berwin
Acidic microenvironments commonly occur at sites of inflammation and bacterial infections. In the context of a Pseudomonas aeruginosa infection, we previously demonstrated that acidosis enhances the cellular proinflammatory IL-1β response in vitro. However, how pH alterations affect in vivo IL-1β responses and subsequent IL-1 driven inflammation during infection with P. aeruginosa is unclear. We report herein that acidosis enhances in vivo IL-1β production and downstream IL-1R-dependent responses during infection with P...
October 5, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28982734/the-use-of-proper-statistical-techniques-for-research-studies-with-small-samples
#8
Charity Johanna Morgan
In this editorial we discuss the appropriateness of various statistical methods for use with small sample sizes. We review the assumptions and limitations of these methods and provide our recommendations for figures and statistical tests.
October 5, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28982733/atp-catabolism-by-tissue-non-specific-alkaline-phosphatase-contributes-to-development-of-ards-in-influenza-infected-mice
#9
Parker S Woods, Lauren May Doolittle, Judy M Hickman-Davis, Ian Christopher Davis
Influenza A viruses are highly contagious respiratory pathogens that are responsible for significant morbidity and mortality worldwide on an annual basis. We have shown previously that influenza infection of mice leads to increased ATP and adenosine accumulation in the airway lumen. Moreover, we demonstrated that A1-adenosine receptor activation contributes significantly to influenza-induced acute respiratory distress syndrome (ARDS). However, we found that development of ARDS in influenza-infected mice does not require catabolism of ATP to adenosine by ecto-5'-nucleotidase (CD73)...
October 5, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28971978/activation-of-the-sweet-taste-receptor-t1r3-by-the-artificial-sweetener-sucralose-regulates-the-pulmonary-endothelium
#10
Elizabeth O Harrington, Alexander Vang, Julie Braza, Aparna Shil, Havovi Chichger
A hallmark of acute respiratory distress syndrome (ARDS) is pulmonary vascular permeability. In these settings, loss of barrier integrity is mediated by cell-contact disassembly and actin-remodelling. Studies into molecular mechanisms responsible for improving microvascular barrier function are therefore vital in the development of therapeutic targets for reducing vascular permeability in ARDS. The sweet taste receptor, T1R3 is a GPCR, activated following exposure to sweet molecules, to trigger a gustducin-dependent signal cascade...
September 28, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28971977/human-lung-branching-morphogenesis-is-orchestrated-by-the-spatio-temporal-distribution-of-acta2-sox2-and-sox9
#11
Soula Danopoulos, Irving Alonso, Matthew Thornton, Brendan Grubbs, Saverio Bellusci, David Warburton, Denise Al Alam
Lung morphogenesis relies on a number of important processes including proximal-distal patterning, cell proliferation, migration and differentiation, as well as epithelial-mesenchymal interactions. In mouse lung development, SOX2+ cells are localized in the proximal epithelium whereas SOX9+ cells are present in the distal epithelium. We show that in human lung, expression of these transcription factors differs, in that during the pseudoglandular stage distal epithelial progenitors at the tips co-express SOX2 and SOX9...
September 28, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28971976/recent-advances-in-our-understanding-of-the-mechanisms-of-late-lung-development-and-bronchopulmonary-dysplasia
#12
David Emanuel Surate Solaligue, José Alberto Rodríguez-Castillo, Katrin Ahlbrecht, Rory E Morty
The objective of lung development is to generate an organ of gas exchange that provides both a thin gas diffusion barrier and a large gas diffusion surface area, which concomitantly generates a steep gas-diffusion concentration gradient. As such, the lung is perfectly structured to undertake the function of gas exchange: a large number of small alveoli provide extensive surface area within the limited volume of the lung, and a delicate alveolo-capillary barrier brings circulating blood into close proximity to the inspired air...
September 28, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28971975/tbx4-is-involved-in-the-super-enhancer-driven-transcriptional-programs-underlying-features-specific-to-lung-fibroblasts
#13
Masafumi Horie, Naoya Miyashita, Yu Mikami, Satoshi Noguchi, Yasuhiro Yamauchi, Maho Suzukawa, Takeshi Fukami, Ken Ohta, Yoshihide Asano, Shinichi Sato, Yoko Yamaguchi, Mitsuhiro Ohshima, Hiroshi Suzuki, Akira Saito, Takahide Nagase
Lung fibroblasts participate in the pathogenesis of respiratory diseases, including lung cancer and pulmonary fibrosis. Although fibroblasts are ubiquitous constituents of various organs, their cellular diversity among different organs has been poorly characterized. Here, we aimed to investigate the distinct gene signature of lung fibroblasts that represents its pulmonary origin, and the underlying gene regulatory networks. Promoter-level differential expression analysis by cap analysis of gene expression (CAGE) sequencing revealed distinct gene expression patterns of fibroblasts derived from different anatomical sites and identified 88 coding genes with higher expression in lung fibroblasts relative to other fibroblasts...
September 28, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28971974/hypoxia-induced-changes-in-plasma-micrornas-correlate-with-pulmonary-artery-pressure-at-high-altitude
#14
Birgit Blissenbach, Christos T Nakas, Martin Krönke, Thomas Geiser, Tobias M Merz, Jacqueline Pichler Hefti
In vitro and animal studies revealed miRs to be involved in modulation of hypoxia-induced pulmonary hypertension (HPH). However, knowledge on circulating miRs in humans in the context of HPH is very limited. Since symptoms of HPH are non-specific and non-invasive diagnostic parameters do not exist, a disease-specific and hypoxemia-independent biomarker indicating HPH would be of clinical value. To examine whether plasma miR levels correlate with hypoxia-induced increase in pulmonary artery pressures, plasma miRs were assessed in a model of hypoxia-related pulmonary hypertension in humans exposed to extreme altitude...
September 28, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28935640/attenuation-of-pulmonary-ace2-activity-impairs-inactivation-of-des-arg9-bradykinin-bkb1r-axis-and-facilitates-lps-induced-neutrophil-infiltration
#15
Chhinder P Sodhi, Christine Wohlford-Lenane, Yukihiro Yamaguchi, Thomas Prindle, William B Fulton, Sanxia Wang, Paul B McCray, Mark C Chappell, David J Hackam, Hongpeng Jia
Angiotensin converting enzyme 2 (ACE2) is a terminal carboxypeptidase with important functions in the renin angiotensin system and plays a critical role in inflammatory lung diseases. ACE2 cleaves single terminal residues from several bioactive peptides such as angiotensin II. However, few of its substrates in the respiratory tract have been identified and the mechanism underlying the role of ACE2 in inflammatory lung disease has not been fully characterized. In an effort to identify biological targets of ACE2 in the lung, we tested its effects on des-arg9 bradykinin (DABK) in airway epithelial cells based upon a hypothesis that DABK is a biological substrate of ACE2 in the lung and ACE2 plays an important role in the pathogenesis of acute lung inflammation partly through modulating DABK/BKB1R axis signaling...
September 21, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28935639/isolation-and-characterization-of-endothelial-to-mesenchymal-transition-cells-in-pulmonary-arterial-hypertension
#16
Toshio Suzuki, Erica J Carrier, Megha H Talati, Anandharajan Rathinasabapathy, Xinping Chen, Rintaro Nishimura, Yuji Tada, Koichiro Tatsumi, James D West
Endothelial-to-mesenchymal transition (EndMT) is a process in which endothelial cells lose polarity and cell-to-cell contacts, and undergo a dramatic remodeling of the cytoskeleton. It has been implicated in initiation and progression of pulmonary arterial hypertension (PAH). However, the characteristics of cells which have undergone EndMT-cells in vivo have not been reported and so remain unclear. To study this, sugen5416 and hypoxia (SuHx)-induced PAH was established in Cdh5-Cre / Gt(ROSA)26Sor(tm4(ACTB-tdTomato,-EGFP)Luo)/J double-transgenic mice, in which GFP was stably expressed in pan-endothelial cells...
September 21, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28935638/phagocytosis-of-microparticles-by-alveolar-macrophages-during-acute-lung-injury-requires-mertk
#17
Michael P Mohning, Stacey M Thomas, Lea Barthel, Kara J Mould, Alexandra L McCubbrey, S Courtney Frasch, Donna Bratton, Peter M Henson, William J Janssen
Microparticles are a newly recognized class of mediators in the pathophysiology of lung inflammation and injury, but little is known about the factors that regulate their accumulation and clearance. The primary objective of our study was to determine whether alveolar macrophages engulf microparticles and to elucidate the mechanisms by which this occurs. Alveolar microparticles were quantified in bronchoalveolar fluid of mice with lung injury induced by LPS and hydrochloric acid. Microparticle numbers were greatest at the peak of inflammation and declined as inflammation resolved...
September 21, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28912382/versican-is-produced-by-trif-and-type-i-interferon-dependent-signaling-in-macrophages-and-contributes-to-fine-control-of-innate-immunity-in-lungs
#18
Mary Y Chang, Inkyung Kang, Michael Gale, Anne M Manicone, Michael G Kinsella, Kathleen R Braun, Tara Wigmosta, William C Parks, William A Altemeier, Thomas N Wight, Charles W Frevert
Growing evidence suggests that versican is important in the innate immune response to lung infection. Our goal was to understand the regulation of macrophage-derived versican and the role it plays in innate immunity. We first defined the signaling events that regulate versican expression using bone marrow derived macrophages (BMDM) from mice lacking specific Toll-like receptors (TLR), TLR adaptor molecules or the type I interferon receptor (IFNAR1). We show that LPS and polyinosinic-polycytidylic acid [Poly(I:C)] trigger a signaling cascade involving TLR3 or 4, the Trif adaptor, Type I interferons and IFNAR1, leading to increased expression of versican by macrophages and implicating versican as an interferon-stimulated gene...
September 14, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28912381/invariant-natural-killer-t-cells-promote-immunogenic-maturation-of-lung-dendritic-cells-in-mouse-models-of-asthma
#19
Qing He, Linlin Liu, Qiaoyu Yang, Ailing Wang, Shuo Chen, Ruiyun Li, Yi Huang, Guqin Zhang, Xuhong Ding, Hongying Yu, Suping Hu, Hanxiang Nie
Our previous study showed that invariant natural killer T (iNKT) cells might act as an adjuvant to promote Th2 inflammatory responses in an OVA-induced mouse model of allergic asthma, but the mechanism remains unknown. To clarify the underlying mechanism through which iNKT cells promote Th2 inflammatory responses, we investigated the modulatory influence of iNKT cells on phenotypic and functional maturation of lung dendritic cells (LDCs) using iNKT cell-knockout mice, specific iNKT cell activation, co-culture experiments, and adoptive transfer of iNKT cells in mouse models of asthma...
September 14, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/28912380/exposure-of-neonatal-mice-to-bromine-impairs-their-alveolar-development-and-lung-function
#20
Tamas Jilling, Changchun Ren, Aaron Jefthy Yee, Saurabh Aggarwal, Brian Halloran, Namasivayam Ambalavanan, Sadis Matalon
The halogen bromine (Br2) is used extensively in industry and stored and transported in large quantities. Its accidental or malicious release into the atmosphere has resulted in significant casualties. The pathophysiology of Br2-induced lung injury has been studied in adult animals, but the consequences of Br2 exposure to the developing lung are completely unknown. We exposed neonatal mouse littermates on postnatal day 3 (P3) to either Br2 at 400 ppm for 30 minutes (400/30), to Br2 at 600 ppm for 30 minutes (600/30), or to room air, then returned them to their dams and observed until P14...
September 14, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
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