6,017 results match your criteria American Journal of Respiratory Cell and Molecular Biology[Journal]


IL-13Rα2 Glycosylation Holds the Dance Card for Partnering with IL-13.

Am J Respir Cell Mol Biol 2020 May 27. Epub 2020 May 27.

University of Arizona, Medicine, Tucson, Arizona, United States;

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http://dx.doi.org/10.1165/rcmb.2020-0165EDDOI Listing

Exploring New Therapeutic Pathways in Pulmonary Hypertension: Metabolism, Proliferation, and Personalized Medicine.

Am J Respir Cell Mol Biol 2020 May 26. Epub 2020 May 26.

UCSF, 8785, Medicine , San Francisco, California, United States.

In this State-of-the-Field article, we explore the main themes from the 62nd Annual Aspen Lung Conference: hypoxia, cellular metabolism, inflammatory pathways, aberrant proliferation, and personalized medicine, and highlight challenges and opportunities in the coming decade of pulmonary vascular disease. Read More

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http://dx.doi.org/10.1165/rcmb.2020-0099TRDOI Listing

Assessing Human Airway Epithelial Progenitor Cells for Cystic Fibrosis Cell Therapy.

Am J Respir Cell Mol Biol 2020 May 21. Epub 2020 May 21.

University of North Carolina, Department of Cell Biology & Physiology, Chapel Hill, North Carolina, United States;

Cystic fibrosis (CF) is caused by loss-of-function mutations in the CF transmembrane regulator (CFTR) gene. Pharmacologic therapies directed at CFTR have been developed but are not effective for mutations that result in little or no mRNA or protein expression. Cell therapy is a potential mutation-agnostic approach to treatment. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0384OCDOI Listing

N-Glycosylation Regulates Chitinase 3-like-1 and IL-13 Ligand Binding to IL-13 Receptor α2.

Am J Respir Cell Mol Biol 2020 May 13. Epub 2020 May 13.

Brown University, 6752, Medicine and Biologic Science, Providence, Rhode Island, United States.

Chitinase 3-like-1 (Chi3l1) and IL-13 are both ligands of IL-13 receptor α2 (IL-13Rα2). The binding of the former activates MAPK, AKT and Wnt/β-catenin signaling and plays important roles in innate and adaptive immunity, cellular apoptosis, oxidative injury, allergic inflammation, tumor metastasis and wound healing, fibrosis and repair in the lung. In contrast, the latter binding is largely a decoy event that diminishes the effects of IL-13. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0446OCDOI Listing

Reply to 'Comments on "Air Space Distension Precedes Spontaneous Fibrotic Remodeling and Impaired Cholesterol Metabolism in the Absence of Surfactant Protein C"'.

Am J Respir Cell Mol Biol 2020 May 13. Epub 2020 May 13.

Hannover Medical School, 9177, Institute of Functional and Applied Anatomy, Hannover, Germany.

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http://dx.doi.org/10.1165/rcmb.2020-0158LEDOI Listing

Comments on "Air Space Distension Precedes Spontaneous Fibrotic Remodeling and Impaired Cholesterol Metabolism in the Absence of Surfactant Protein C".

Am J Respir Cell Mol Biol 2020 May 13. Epub 2020 May 13.

Siena University, Department of Molecular and Developmental Medicine , Siena, Italy.

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http://dx.doi.org/10.1165/rcmb.2020-0125LEDOI Listing

APOE in Asthmatic Inflammatory Response: Friend or Foe?

Am J Respir Cell Mol Biol 2020 May 8. Epub 2020 May 8.

Department of Biomedical Sciences, University of North Dakota, Grand Forks, North Dakota, United States;

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http://dx.doi.org/10.1165/rcmb.2020-0106EDDOI Listing

Novel Therapy of Bicarbonate, Glutathione and Ascorbic Acid Improves Cystic Fibrosis Mucus Transport.

Am J Respir Cell Mol Biol 2020 May 6. Epub 2020 May 6.

University of Alabama at Birmingham, Medicine, Cystic Fibrosis Center, Birmingham, Alabama, United States;

Defective airway mucus clearance is a defining characteristic of CF lung disease, and improvements to current mucolytic strategies are needed. Novel approaches targeting a range of contributing mechanisms are in various stages of preclinical and clinical development. ARINA-1 is a new, nebulized product comprised of ascorbic acid, glutathione, and bicarbonate. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0287OCDOI Listing

Impaired Autophagic Activity Contributes to the Pathogenesis of Bronchopulmonary Dysplasia: Evidence from Murine and Baboon Models.

Am J Respir Cell Mol Biol 2020 May 6. Epub 2020 May 6.

Brigham and Women's Hospital, 1861, Boston, Massachusetts, United States.

Rationale: The incidence of bronchopulmonary dysplasia (BPD) has been increasing due to improved survival of extremely low birth weight infants. The pathogenesis of BPD is incompletely understood and there is a shortage of effective treatments. Autophagy may play a protective role in BPD. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0445OCDOI Listing

Fibroblast Growth Factors Inhibitors in Lung Fibrosis: Friends or Foes?

Authors:
Robert Guzy

Am J Respir Cell Mol Biol 2020 May 5. Epub 2020 May 5.

University of Chicago, 2462, Chicago, Illinois, United States;

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http://dx.doi.org/10.1165/rcmb.2020-0156EDDOI Listing

May Highlights/Papers by Junior Investigators/NIH News.

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Am J Respir Cell Mol Biol 2020 May;62(5)

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http://dx.doi.org/10.1165/rcmb.625vDOI Listing

Surfactant Injury in the Early Phase of Severe Meconium Aspiration Syndrome.

Am J Respir Cell Mol Biol 2020 Apr 29. Epub 2020 Apr 29.

South Paris University Hospitals, "A.Beclere" Medical Center, Physiopathology and Therapeutic Innovation Unit-INSERM U999, Clamart (Paris), France.

Rationale: No in vivo data are available about the effect of meconium on human surfactant in the early stages of severe meconium aspiration syndrome (MAS).

Objectives: To characterize the changes in surfactant composition, function and structure during the early phase of meconium injury.

Methods: We designed a translational, prospective, cohort study on nonbronchoscopic bronchoalveolar lavages of neonates with severe MAS (n=14) or no lung disease (n=18). Read More

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http://dx.doi.org/10.1165/rcmb.2019-0413OCDOI Listing

Targeting BMPR2 Trafficking with Chaperones - An Important Step Towards Precision Medicine in Pulmonary Arterial Hypertension.

Am J Respir Cell Mol Biol 2020 Apr 27. Epub 2020 Apr 27.

Stanford University, 6429, Pulmonary and Critcal Care, Stanford, California, United States;

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http://dx.doi.org/10.1165/rcmb.2020-0130EDDOI Listing

Apolipoprotein E Signals via TLR4 to Induce CXCL5 Secretion by Asthmatic Airway Epithelial Cells.

Am J Respir Cell Mol Biol 2020 Apr 27. Epub 2020 Apr 27.

NHLBI, National Institutes of Health, Pulmonary Branch, Bethesda, Maryland, United States;

The primary function of apolipoprotein E (APOE) is to mediate the transport of cholesterol- and lipid-containing lipoprotein particles into cells by receptor-mediated endocytosis. APOE also has pro- and anti-inflammatory effects, which are both context- and concentration-dependent. For example, Apoe-/- mice have enhanced airway remodeling and hyperreactivity in experimental asthma, whereas increased APOE levels in lung epithelial lining fluid induce IL-1β secretion from human asthmatic alveolar macrophages. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0209OCDOI Listing

Exposure to Cigarette Smoke Enhances the Stemness of Alveolar Type 2 Cells.

Am J Respir Cell Mol Biol 2020 Apr 27. Epub 2020 Apr 27.

Keio University School of Medicine Graduate School of Medicine, 38084, Division of Pulmonary Medicine, Department of Medicine, Tokyo, Japan.

Chronic exposure to cigarette smoke (CS) causes chronic inflammation, oxidative stress, and apoptosis of epithelial cells, which results in destruction of the lung matrix. However, the mechanism by which the lung fails to repair the CS-induced damage, thereby succumbing to emphysema, remains unclear. Alveolar type (AT)2 cells comprise the stem cells of the alveolar compartments and are responsible for repairing and maintaining lung tissues. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0188OCDOI Listing

Blockade of Pan-fibroblast Growth Factor Receptors Mediates Bidirectional Effects in Lung Fibrosis.

Am J Respir Cell Mol Biol 2020 Apr 27. Epub 2020 Apr 27.

Graduate School of Biomedical Sciences, Tokushima University, Department of Respiratory Medicine and Rheumatology, Tokushima, Japan;

[Rationale] Fibroblast growth factors (FGF) are major factors associated with the pathogenesis of pulmonary fibrosis. Nintedanib, a tyrosine kinase inhibitor targeting several growth factor receptors including the FGF receptor (FGFR), has been approved for the treatment of idiopathic pulmonary fibrosis (IPF). On the other hand, recent reports suggest that FGF are required for epithelial recovery. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0090OCDOI Listing

CD70 Activation Decreases Pulmonary Fibroblast Production of Extracellular Matrix Proteins.

Am J Respir Cell Mol Biol 2020 Apr 22. Epub 2020 Apr 22.

University of Alabama at Birmingham, 9968, Medicine, Birmingham, Alabama, United States;

Idiopathic pulmonary fibrosis (IPF) is a lethal, medically refractory syndrome characterized by intrapulmonary accumulations of extracellular matrix (ECM) proteins produced by fibroblasts. Activation, clonal expansions, and differentiation of lymphocytes are also frequently present in IPF. Activated T-cells are known to exert several effects that promote ECM production, but opposing homeostatic actions, wherein T-cells can inhibit fibrosis, are less well understood. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0450OCDOI Listing

A Call for Rational Intensive Care in the Era of COVID-19.

Am J Respir Cell Mol Biol 2020 Apr 21. Epub 2020 Apr 21.

Northwestern University Feinberg School of Medicine, 12244, Chicago, Illinois, United States.

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http://dx.doi.org/10.1165/rcmb.2020-0151LEDOI Listing

MultiOMICs of WTC-Particulate Induced Persistent Airway Hyperreactivity: Role of Receptor for Advanced Glycation End Products.

Am J Respir Cell Mol Biol 2020 Apr 21. Epub 2020 Apr 21.

New York University School of Medicine, 12296, Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine , New York, New York, United States.

Pulmonary disease after World Trade Center particulate matter(WTC-PM) exposure is associated with dyslipidemia and the receptor for advanced glycation end products (RAGE); however, the mechanisms are not well understood. We utilized a murine model and a multiOMIC assessment to understand the role of RAGE in the pulmonary long-term effects of a single high intensity exposure to WTC-PM. After 1-month(1-M), WTC-PM exposed wild-type(WT) mice had airway hyperreactivity(AHR) while RAGE-deficient(Ager-/-) were protected. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0064OCDOI Listing

The Airway Epithelial Response to Air Pollution: It's Not Just Inflammation.

Am J Respir Cell Mol Biol 2020 Apr 20. Epub 2020 Apr 20.

University of Chicago, 2462, Chicago, Illinois, United States.

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http://dx.doi.org/10.1165/rcmb.2020-0116EDDOI Listing

S1P Contributes to Endotoxin-enhanced B Cell Functions Involved in Hypersensitivity Pneumonitis.

Am J Respir Cell Mol Biol 2020 Apr 14. Epub 2020 Apr 14.

Quebec Heart and Lung Institute, 55973, Quebec, Quebec, Canada.

Background: In a proportion of patients with hypersensitivity pneumonitis, biological and environmental factors sustaining inflammation are ill-defined, resulting in no effective treatment option. Bioaerosols found in occupational settings are complex and often include Toll-like receptor ligands, such as endotoxins. How Toll-like receptor ligands contribute to the persistence of hypersensitivity pneumonitis, however, remains poorly understood. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0339OCDOI Listing

Genome-wide Analysis Reveals Mucociliary Remodeling of the Nasal Airway Epithelium Induced by Urban PM2.5.

Am J Respir Cell Mol Biol 2020 Apr 10. Epub 2020 Apr 10.

National Jewish Health, 2930, Center for Genes, Environment and Health, Denver, Colorado, United States.

Air pollution particulate matter <2.5 microns (PM2.5) is associated with poor respiratory outcomes. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0454OCDOI Listing

Hiding in Plain Sight: The Basement Membrane in Pulmonary Vascular Remodeling.

Am J Respir Cell Mol Biol 2020 Apr 10. Epub 2020 Apr 10.

Stanford University, 6429, Medicine, Stanford, California, United States;

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http://dx.doi.org/10.1165/rcmb.2020-0100EDDOI Listing

High CO Levels Impair Lung Wound Healing.

Am J Respir Cell Mol Biol 2020 Apr 10. Epub 2020 Apr 10.

Northwestern University Feinberg School of Medicine, 12244, Pulmonary and Critical Care Medicine, Chicago, Illinois, United States.

Delayed lung repair leads to alveolo-pleural fistulae which are a major cause of morbidity following lung resections. We have reported that intrapleural hypercapnia is associated with delayed lung repair after lung resection. Here, we provide new evidence that hypercapnia delays wound closure of both large airway and alveolar epithelial cell monolayers due to inhibition of epithelial cell migration. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0354OCDOI Listing
April 2020
3.985 Impact Factor

4PBA Restores Signalling of a Cysteine-substituted Mutant BMPR2 Receptor Found in Patients with PAH.

Am J Respir Cell Mol Biol 2020 Apr 7. Epub 2020 Apr 7.

University of Cambridge, Cambridge, United Kingdom of Great Britain and Northern Ireland;

Mutations in the gene encoding the bone morphogenetic protein type 2 receptor, BMPR2, are the major cause of heritable pulmonary arterial hypertension (HPAH). Point mutations in the BMPR2 ligand binding domain involving cysteine residues (such as C118W) are causative of PAH and predicted to cause protein misfolding. Using heterologous overexpression systems, we showed previously that these mutations lead to retention of BMPR2 in the endoplasmic reticulum, but are partially rescued by chemical chaperones. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0321OCDOI Listing

Alpha-tocopherol Attenuates the Severity of -induced Pneumonia.

Am J Respir Cell Mol Biol 2020 Apr 3. Epub 2020 Apr 3.

University of Alabama at Birmingham, Department of Anesthesiology and Perioperative Medicine, Birmingham, Alabama, United States;

Pseudomonas aeruginosa is a lethal pathogen that causes high mortality and morbidity in immunocompromised and critically ill patients. The Type III secretion system (T3SS) of P. aeruginosa mediates many of the adverse effects of infection with this pathogen including increased lung permeability in a toll-like receptor 4/Rho A/plasminogen activator inhibitor (PAI)-1-dependent manner. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0185OCDOI Listing

April Highlights/Papers by Junior Investigators/NIH News.

Authors:

Am J Respir Cell Mol Biol 2020 Apr;62(4):iv

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http://dx.doi.org/10.1165/rcmb.624ivDOI Listing

Join or Leave the Club: Jagged1 and Notch2 Dictate the Fate of Airway Epithelial Cells.

Am J Respir Cell Mol Biol 2020 Mar 31. Epub 2020 Mar 31.

University of Groningen, University Medical Center Groningen, Pathology and Medical Biology, Groningen, Netherlands.

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http://dx.doi.org/10.1165/rcmb.2020-0104EDDOI Listing

Revisiting mTOR and Epithelial-mesenchymal Transition.

Am J Respir Cell Mol Biol 2020 Mar 31. Epub 2020 Mar 31.

Northwestern University, Pulmonary and Critical Care Medicine, Chicago, Illinois, United States;

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http://dx.doi.org/10.1165/rcmb.2020-0109EDDOI Listing

A Fresh Take on the "TCA" Cycle: TETs, Citrate, and Asthma.

Authors:
Steven Huang

Am J Respir Cell Mol Biol 2020 Mar 30. Epub 2020 Mar 30.

University of Michigan, Pulmonary and Critical Care Medicine, Ann Arbor, Michigan, United States;

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http://dx.doi.org/10.1165/rcmb.2020-0101EDDOI Listing

Asthma - An Untoward Consequence of Endurance Sports?

Am J Respir Cell Mol Biol 2020 Mar 30. Epub 2020 Mar 30.

Institut universitaire de cardiologie et de pneumologie de Québec, 55973, Québec, Quebec, Canada.

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http://dx.doi.org/10.1165/rcmb.2020-0092EDDOI Listing

Comparison of Human and Experimental Pulmonary Veno-Occlusive Disease.

Am J Respir Cell Mol Biol 2020 Mar 25. Epub 2020 Mar 25.

Centre Chirurgical Marie Lannelongue, INSERM U999, Le Plessis Robinson, France;

Pulmonary veno-occlusive disease (PVOD) occurs in humans either as heritable form (hPVOD) due to biallelic inactivating mutations of EIF2AK4 (encoding GCN2), or as a sporadic form at older age (sPVOD). The chemotherapeutic agent Mitomycin C is a potent inducer of PVOD in humans and in rats (MMC-PVOD). Here we compared human hPVOD and sPVOD, and MMC-PVOD pathophysiology at the histological, cellular and molecular levels to unravel common altered pathomechanisms. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0015OCDOI Listing

Active mTOR in Lung Epithelium Promotes Epithelial-Mesenchymal Transition and Enhances Lung Fibrosis.

Am J Respir Cell Mol Biol 2020 Mar 25. Epub 2020 Mar 25.

The University of Tokyo, 13143, Department of Respiratory Medicine, Tokyo, Japan.

Rationale: The mTOR pathway is one of the key signal cascades in the pathogenesis of idiopathic pulmonary fibrosis. Previous studies have mainly focused on this pathway in the fibroblasts and/or myofibroblasts, but not in the epithelial cells.

Objectives: To investigate the role of the mTOR pathway in lung epithelial cells in lung fibrosis. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0255OCDOI Listing

Phenotypic Diversity Caused by Differential Expression of -Cre Transgenic Alleles.

Am J Respir Cell Mol Biol 2020 Mar 24. Epub 2020 Mar 24.

University of Pittsburgh Department of Medicine, 199716, Pulmonary, Allergy, and Critical Care Medicine, Pittsburgh, Pennsylvania, United States;

Type II alveolar epithelial cells (AEC2s) play an essential role in the function and maintenance of the pulmonary epithelium. Several transgenic mice have been developed to study the function of these cells in vivo by using the human surfactant protein C (SFTPC) promoter to drive expression of Cre recombinase. The precise activity of each of these transgenic alleles has not been studied and previous reports suggest that their activity can depend on breeding strategies. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0416MADOI Listing

Single Cell Flow Cytometry Profiling of Bronchoalveolar Lavage in Children.

Am J Respir Cell Mol Biol 2020 Mar 24. Epub 2020 Mar 24.

Murdoch Children's Research Institute, Parkville, Victoria, Australia.

Childhood pulmonary diseases not only cause childhood morbidity and mortality, but can also cause long term pulmonary impairment. The clinical management of many childhood pulmonary diseases is hampered by a limited understanding of the underlying pathophysiological mechanisms. Flow cytometry, which can be used to phenotype individual cell populations or isolate cells for downstream analysis, represents a crucial technology which can help to elucidate the pathophysiology of these conditions. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0453MADOI Listing
March 2020
3.985 Impact Factor

Cysteinyl Leukotriene synthesis via Phospholipase A2 Group IV Mediates Exercise-induced Bronchoconstriction and Airway Remodeling.

Am J Respir Cell Mol Biol 2020 Mar 17. Epub 2020 Mar 17.

Niigata University Graduate School of Medical and Dental Sciences, Department of Respiratory Medicine and Infectious Diseases, Niigata, Japan.

Rationale: It is well known that the prevalence of asthma is higher in athletes, such as Olympic athletes than in the general population.

Objective: In this study, we analyzed the mechanism of exercise-induced bronchoconstriction by using animal models of athlete asthma.

Methods: Mice were made to exercise on a treadmill for a total duration of 1 week, 3 weeks, or 5 weeks. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0325OCDOI Listing

The Transient Receptor Potential Channel Vanilloid 1 (TRPV1) is Critical in Innate Airway Epithelial Responses to Protease Allergens.

Am J Respir Cell Mol Biol 2020 Mar 17. Epub 2020 Mar 17.

University of Vermont, Pathology, Burlington, Vermont, United States;

The airway epithelium plays a critical role in innate responses to airborne allergens by secreting IL-1 family cytokines such as interleukin (IL)-1α and IL-33, as alarmins that subsequently orchestrate appropriate immune responses. Previous studies revealed that epithelial IL-33 secretion by allergens such as A. alternaria (ALT) or house dust mite (HDM) involves Ca2+-dependent signaling, via initial activation of ATP-stimulated type 2 purinoceptors (P2YR2) and subsequent activation of the NADPH oxidase DUOX1. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0170OCDOI Listing

Antisense Oligonucleotides Targeting Jagged 1 Reduce House Dust Mite-Induced Goblet Cell Metaplasia in the Adult Murine Lung.

Am J Respir Cell Mol Biol 2020 Mar 16. Epub 2020 Mar 16.

Ionis Pharmaceuticals Inc, 448132, Carlsbad, California, United States;

Goblet cell metaplasia, excessive mucus production, and inadequate mucus clearance accompany and exacerbate multiple chronic respiratory disorders, such as asthma and COPD. Notch signaling plays a central role in controlling the fate of multiple cell types in the lung, including goblet cells. Here, we explored the therapeutic potential of modulating the Notch pathway in the adult murine lung using chemically-modified antisense oligonucleotides (ASOs). Read More

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http://dx.doi.org/10.1165/rcmb.2019-0257OCDOI Listing

Loss of C/EBPα in Chronic Cigarette Smoke Exposure: A SAD Day for COPD.

Am J Respir Cell Mol Biol 2020 Mar 16. Epub 2020 Mar 16.

University of Washington, Medicine, Seattle, Washington, United States;

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http://dx.doi.org/10.1165/rcmb.2020-0069EDDOI Listing

Macrophage Signaling Pathways in Pulmonary Nontuberculous Mycobacteria Infections.

Am J Respir Cell Mol Biol 2020 Mar 11. Epub 2020 Mar 11.

Emory University School of Medicine, 12239, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Atlanta, Georgia, United States.

The incidence and prevalence of nontuberculous mycobacterial lung disease (NTM-LD) is rising worldwide and accounts for most clinical cases of NTM. NTM infections occur in both immunocompetent and immunocompromised hosts. Macrophages are the primary host cells that initiate an immune response to NTM. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0241TRDOI Listing

Basement Membrane Remodelling Controls Endothelial Function in IPAH.

Am J Respir Cell Mol Biol 2020 Mar 11. Epub 2020 Mar 11.

Ludwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.

The extracellular matrix (ECM) increasingly emerges as an active driver in several diseases, including idiopathic pulmonary arterial hypertension (IPAH). The basement membrane (BM) is a specialized class of ECM proteins. In pulmonary arteries, the BM is in close contact and direct proximity to vascular cells including endothelial cells. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0303OCDOI Listing

Vitamin D: Feel it in More Than Just Your Bones!

Am J Respir Cell Mol Biol 2020 Mar 11. Epub 2020 Mar 11.

Stanford University, Pediatrics, Stanford, California, United States;

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http://dx.doi.org/10.1165/rcmb.2020-0072EDDOI Listing

Role of Isocitrate Dehydrogenase 2 on DNA Hydroxymethylation in Human Airway Smooth Muscle Cells.

Am J Respir Cell Mol Biol 2020 Mar 9. Epub 2020 Mar 9.

Johns Hopkins University Bloomberg School of Public Health, 25802, Baltimore, Maryland, United States;

Global DNA hydroxymethylation mediated by the ten-eleven translocation (TET) enzyme was induced in allergen-induced airway hyper-responsiveness (AHR) in mouse lung tissues and specifically in isolated airway smooth muscle (ASM) cells. TET is an α-ketoglutarate (α-KG)-dependent enzyme, and the production of α-KG is catalyzed by isocitrate dehydrogenase (IDH). However, the role of IDHs in the regulation of DNA hydroxymethylation in ASM cells is unknown. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0323OCDOI Listing

Direct eNAMPT Involvement in Pulmonary Hypertension and Vascular Remodeling: Transcriptional Regulation by SOX and HIF2α.

Am J Respir Cell Mol Biol 2020 Mar 6. Epub 2020 Mar 6.

University of Arizona College of Medicine, 12216, Department of Medicine, Tucson, Arizona, United States;

Rationale: We previously demonstrated involvement of nicotinamide phosphoribosyl-transferase in pulmonary arterial hypertension (PAH) and now examine NAMPT regulation and extracellular NAMPT's role in PAH vascular remodeling.

Methods: transcription and protein expression in human lung endothelial cell (EC) was assessed in response to PAH-relevant stimuli (PDGF, VEGF, TGFβ1 and hypoxia). Endothelial to mesenchymal transition (EndMT) was detected by SANI1 and PECAM1 immunofluorescence. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0164OCDOI Listing

Maternal Vitamin D Deficiency Causes Sustained Impairment of Lung Structure and Function and Increases Susceptibility to Hyperoxia-Induced Lung Injury in Infant Rats.

Am J Respir Cell Mol Biol 2020 Mar 5. Epub 2020 Mar 5.

University of Colorado School of Medicine, Professor, Department of Pediatrics, Denver, Colorado, United States.

Background: Vitamin D deficiency (VDD) during pregnancy is associated with increased respiratory morbidities and risk for chronic lung disease after preterm birth. However, the direct effects of maternal VDD on perinatal lung structure and function and whether maternal VDD increases the susceptibility of lung injury due to hyperoxia are uncertain.

Objective: To determine whether maternal VDD is sufficient to impair lung structure and function and whether VDD increases the impact of hyperoxia (HX) on the developing rat lung. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0295OCDOI Listing

Extracellular Vesicles: A New Frontier for Research in Acute Respiratory Distress Syndrome.

Am J Respir Cell Mol Biol 2020 Feb 28. Epub 2020 Feb 28.

Cardiovascular Research Institute (CVRI), University of San Francisco, Medicine and Anesthesia, San Francisco, California, United States;

Recent research on extracellular vesicles (EVs) has provided new insights into pathogenesis and potential therapeutic options for acute respiratory distress syndrome (ARDS). EVs are membrane-bound anuclear structures which carry important inter-cellular communication mechanisms, allowing targeted transfer of diverse biologic cargo including protein, mRNA and microRNA among several different cell types. In this review, we discuss the important role EVs play in both inducing and attenuating inflammatory lung injury in ARDS as well as in sepsis, the most important clinical cause of ARDS. Read More

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http://dx.doi.org/10.1165/rcmb.2019-0447TRDOI Listing
February 2020

Pneumocystis Pneumonia: Checkpoint Inhibition to the Rescue?

Am J Respir Cell Mol Biol 2020 Feb 28. Epub 2020 Feb 28.

Universities of Giessen and Marburg Lung Center (UGMLC), member of the German Center for Lung Research (DZL), Justus-Liebig-University, Department of Internal Medicine II, Giessen, Germany;

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http://dx.doi.org/10.1165/rcmb.2020-0051EDDOI Listing
February 2020

The Roles of ORMDL3 in Rhinovirus Infections.

Am J Respir Cell Mol Biol 2020 Feb 28. Epub 2020 Feb 28.

Imperial college, National Heart and Lung, London, United Kingdom of Great Britain and Northern Ireland;

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http://dx.doi.org/10.1165/rcmb.2020-0052EDDOI Listing
February 2020

March Highlights/Papers by Junior Investigators/NIH News.

Authors:

Am J Respir Cell Mol Biol 2020 Mar;62(3):iii

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http://dx.doi.org/10.1165/rcmb.623iiiDOI Listing