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American Journal of Respiratory Cell and Molecular Biology

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https://www.readbyqxmd.com/read/28328242/human-airway-epithelial-cells-direct-significant-rhinovirus-replication-in-monocytic-cells-by-enhancing-icam1-expression
#1
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
#2
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
#3
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
#4
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
#5
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
#6
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
#7
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
https://www.readbyqxmd.com/read/28272906/regulation-of-muc5b-expression-in-idiopathic-pulmonary-fibrosis
#8
Britney A Helling, Anthony N Gerber, Vineela Kadiyala, Sarah K Sasse, Brent S Pedersen, Lenore Sparks, Yasushi Nakano, Tsukasa Okamoto, Christopher M Evans, Ivana V Yang, David A Schwartz
The gain-of-function MUC5B promoter variant rs35705950 confers the largest risk, genetic or otherwise, for the development of idiopathic pulmonary fibrosis (IPF); however, the mechanisms underlying the regulation of MUC5B expression have yet to be elucidated. Here, we identify a critical regulatory domain that contains the MUC5B promoter variant and has a highly conserved FOXA2 binding motif. This region is differentially methylated in association with IPF, MUC5B expression, and rs35705950. Additionally, we show that this locus binds FOXA2 dynamically, and that binding of FOXA2 is necessary for enhanced expression of MUC5B...
March 8, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28257580/a-novel-antifibrotic-mechanism-of-nintedanib-and-pirfenidone-inhibition-of-collagen-fibril-assembly
#9
Larissa Knüppel, Yoshihiro Ishikawa, Michaela Aichler, Katharina Heinzelmann, Rudolf Hatz, Jürgen Behr, Axel Walch, Hans Peter Bächinger, Oliver Eickelberg, Claudia A Staab-Weijnitz
RATIONALE: Idiopathic pulmonary fibrosis (IPF) is characterized by excessive deposition of extracellular matrix, in particular collagens. Two IPF therapeutics, nintedanib and pirfenidone, decelerate lung function decline, but their underlying mechanisms of action are poorly understood. In this study we sought to analyze their effects on collagen synthesis and maturation at important regulatory levels. METHODS: Primary human fibroblasts from IPF patients and healthy donors were treated with nintedanib (0...
March 3, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28257236/human-rhinovirus-infection-of-epithelial-cells-modulates-airway-smooth-muscle-migration
#10
Sami Shariff, Christopher Shelfoon, Neil S Holden, Suzanne L Traves, Shahina Wiehler, Cora Kooi, David Proud, Richard Leigh
RATIONALE: Airway remodeling, a characteristic feature of asthma, begins in early life. Recurrent human rhinovirus (HRV) infections are a potential inciting stimulus for remodeling. One component of airway remodeling is an increase in airway smooth muscle cell mass with a greater proximity of the airway smooth muscle cells (ASMC) to the airway epithelium. We asked whether human bronchial epithelial cells infected with HRV produced mediators that are chemotactic for ASMC. METHODS: ASMC migration was investigated using the modified Boyden Chamber and the xCELLigence Real-Time Cell Analyzer...
March 3, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28257233/three-unique-interstitial-macrophages-in-the-murine-lung-at-steady-state
#11
Sophie L Gibbings, Stacey M Thomas, Shaikh M Atif, Alexandra L McCubbrey, A Nicole Desch, Thomas Danhorn, Sonia M Leach, Donna L Bratton, Peter M Henson, William J Janssen, Claudia V Jakubzick
RATIONALE: The current paradigm in macrophage biology is that some tissues mainly contain macrophages from embryonic origin such as microglia in the brain, while other tissues contain postnatal-derived macrophages, such as the gut. However, in the lung and in other organs such as the skin, there are both embryonic and postnatal-derived macrophages. OBJECTIVES: In this study, we demonstrate in the steady-state lung that the mononuclear phagocyte system is comprised of three newly identified interstitial macrophages (IMs), alveolar macrophages (AMs), dendritic cells (DCs) and few extravascular monocytes...
March 3, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28248572/transcriptomic-analysis-of-lung-tissue-from-cigarette-smoke-induced-emphysema-murine-models-and-human-copd-show-shared-and-distinct-pathways
#12
Jeong H Yun, Jarrett Morrow, Caroline A Owen, Weiliang Qiu, Kimberly Glass, Taotao Lao, Zhiqiang Jiang, Mark Perrella, Edwin K Silverman, Xiaobo Zhou, Craig P Hersh
Although cigarette smoke (CS) is the primary risk factor for chronic obstructive pulmonary disease (COPD), the underlying molecular mechanisms for the significant variability in developing COPD in response to CS are incompletely understood. We performed lung gene expression profiling of two different wild-type murine strains (C57BL/6, NZW/LacJ) and two genetic models with mutations in COPD genome-wide association study (GWAS) genes (HHIP, FAM13A) after six months of chronic CS exposure and compared the results to human COPD lung tissues...
March 1, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28248570/the-diacetyl-exposed-human-airway-epithelial-secretome-new-insights-into-flavoring-induced-airways-disease
#13
David M Brass, William M Gwinn, Ashlee M Valente, Francine L Kelly, Christie D Brinkley, Andrew E Nagler, M Arthur Moseley, Daniel L Morgan, Scott M Palmer, Matthew W Foster
Bronchiolitis obliterans (BO) is an increasingly important lung disease characterized by fibroproliferative airway lesions and decrements in lung function. Occupational exposure to the artificial food flavoring ingredient diacetyl, commonly used to impart a buttery flavor to microwave popcorn, has been associated with BO development. In the occupational setting, diacetyl vapor is first encountered by the airway epithelium. To better understand the effects of diacetyl vapor on the airway epithelium we used an unbiased proteomic approach to characterize both the apical and basolateral secretomes of air liquid interface cultures of primary human airway epithelial cells from four unique donors after exposure to an occupationally relevant ~1100 ppm of diacetyl vapor or PBS as a control on alternating days...
March 1, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28248553/synergistic-role-of-endothelial-erg-and-fli1-in-mediating-pulmonary-vascular-homeostasis
#14
Agnieszka P Looney, Rong Han, Lukasz Stawski, Grace Marden, Masahiro Iwamoto, Maria Trojanowska
Endothelial cell (EC) activation underlies many vascular diseases, including pulmonary arterial hypertension (PAH). Several members of the E-twenty six (ETS) family of transcription factors are important regulators of the gene network governing endothelial homeostasis, and their aberrant expression is associated with pathological angiogenesis. The goal of this study was to determine whether deficiencies of the ETS family member FLI1 and its closest homolog ERG are associated with PAH. We found that endothelial ERG was significantly reduced in the lung samples from patients with PAH, as well as in chronically hypoxic mice...
March 1, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28245149/airborne-particulate-matter-induces-non-allergic-eosinophilic-sinonasal-inflammation-in-mice
#15
Murugappan Ramanathan, Nyall R London, Anuj Tharakan, Nitya Surya, Thomas E Sussan, Xiaoquan Rao, Sandra Y Lin, Elina Toskala, Sanjay Rajagopalan, Shyam Biswal
RATIONALE: Exposure to airborne particulate matter has been linked to aggravation of respiratory symptoms, increased risk of cardiovascular disease, and all-cause mortality. While the health effects of particulate matter on the lower pulmonary airway have been extensively studied, little is known regarding the impact of chronic particulate matter exposure on the upper sinonasal airway. OBJECTIVES: To test the impact of chronic airborne particulate matter exposure on the upper respiratory system in vivo...
February 28, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28245135/connexin43-controls-the-myofibroblastic-differentiation-of-bronchial-fibroblasts-from-asthmatic-patients
#16
Milena Paw, Izabela Borek, Dawid Wnuk, Damian Ryszawy, Katarzyna Piwowarczyk, Katarzyna Kmiotek, Katarzyna A Wójcik-Pszczoła, Małgorzata Pierzchalska, Zbigniew Madeja, Marek Sanak, Przemysław Błyszczuk, Marta Michalik, Jarosław Czyż
Pathologic accumulation of myofibroblasts in asthmatic bronchi is regulated by extrinsic stimuli and by the intrinsic susceptibility of bronchial fibroblasts to transforming growth factor-β (TGF-β). The specific function of gap junctions and connexins in this process remained unknown. Here, we investigated the role of connexin (Cx)43 in TGF-β-induced myofibroblastic differentiation of fibroblasts derived from bronchoscopic biopsies of asthmatic patients and non-asthmatic donors. Asthmatic fibroblasts expressed considerably higher levels of Cx43 and were more susceptible to TGF-β1-induced myofibroblastic differentiation than their non-asthmatic counterparts...
February 28, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28231019/pro-inflammatory-cytokines-impair-vitamin-d-induced-host-defense-in-cultured-airway-epithelial-cells
#17
Jasmijn A Schrumpf, Gimano D Amatngalim, Joris B Veldkamp, Renate M Verhoosel, Dennis K Ninaber, Soledad R Ordonez, Anne M van der Does, Henk P Haagsman, Pieter S Hiemstra
Vitamin D is a regulator of host defense against infections and induces expression of the antimicrobial peptide hCAP18/LL-37. Vitamin D deficiency is associated with chronic inflammatory lung diseases and respiratory infections. However, it is incompletely understood if and how (chronic) airway inflammation affects vitamin D metabolism and action. We hypothesized that long-term exposure of primary bronchial epithelial cells (PBEC) to pro-inflammatory cytokines alters their vitamin D metabolism, antibacterial activity and expression of hCAP18/LL-37...
February 23, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28225294/role-of-rock-isoforms-in-regulation-of-stiffness-induced-myofibroblast-differentiation-in-lung-fibrosis
#18
Su S Htwe, Byung H Cha, Kan Yue, Ali Khademhosseini, Alan J Knox, Amir M Ghaemmaghami
Fibrosis is a major cause of progressive organ dysfunction in several chronic pulmonary diseases. Rho associated coiled-coil forming kinase (ROCK) has shown to be involved in myofibroblast differentiation driven by altered matrix stiffness in fibrotic state. There are two known ROCK isoforms in human, ROCK1 (ROKβ) and ROCK2 (ROKα), but specific role of each isoform in myofibroblast differentiation in lung fibrosis remains unknown. To study this, we developed a Gelatin methacryloyl (GelMA) hydrogel based culture system with different stiffness levels relevant to healthy and fibrotic lungs...
February 22, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28208028/early-life-wildfire-smoke-exposure-is-associated-with-immune-dysregulation-and-lung-function-decrements-in-adolescence
#19
Carolyn Black, Joan E Gerriets, Justin H Fontaine, Richart W Harper, Nicholas J Kenyon, Fern Tablin, Edward S Schelegle, Lisa A Miller
RATIONALE: The long-term health effects of wildfire smoke exposure in pediatric populations are not known. OBJECTIVE: To determine if early life exposure to wildfire smoke can affect parameters of immunity and airways physiology that are detectable with maturity. METHODS: We studied a mixed gender cohort of rhesus macaque monkeys that were exposed as infants to ambient wood smoke from a series of Northern California wildfires in the summer of 2008...
February 16, 2017: American Journal of Respiratory Cell and Molecular Biology
https://www.readbyqxmd.com/read/28199134/genetic-control-of-fatty-acid-%C3%AE-oxidation-in-chronic-obstructive-pulmonary-disease
#20
Zhiqiang Jiang, Nelson H Knudsen, Gang Wang, Weiliang Qiu, Zun Zar Chi Naing, Yan Bai, Xingbin Ai, Chih-Hao Lee, Xiaobo Zhou
Bioenergetics homeostasis is important for cells to sustain normal functions and defend against injury. Genetics controls on bioenergetics homeostasis, especially lipid metabolism remain poorly understood in chronic obstructive pulmonary diseases (COPD), the third leading cause of death in the world. Additionally, biological function of most susceptible genes identified from genome-wide association studies (GWAS) in COPD remains unclear. Here, we aim to address 1) how fatty acid oxidation, specifically β-oxidation (FAO), a key lipid metabolism pathway that provides energy to cells, contributes to cigarette smoke (CS)-induced COPD; and 2) whether and how FAM13A (family with sequence similarity 13 member A), a well-replicated COPD GWAS gene, modulates FAO pathway...
February 15, 2017: American Journal of Respiratory Cell and Molecular Biology
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