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American Journal of Respiratory Cell and Molecular Biology

Xiu-Zhi Wu, Qiong Zhou, Hua Lin, Kan Zhai, Xiao-Juan Wang, Wei-Bing Yang, Huan-Zhong Shi
RATIONALE: Toll like receptor (TLR) 2 is well known by sensing multiple ligands; however, its role in the development of malignant pleural effusion (MPE) remains unknown. We performed the present study to explore the impact of TLR2 signaling on the development of MPE, and to define the underline mechanisms by which TLR2 works. METHODS: Development of MPE was compared between TLR2-/- and wild type (WT) mice. The effect of TLR2 on differentiation of Th17, Th9, and Th2 cells in MPE was explored...
October 21, 2016: American Journal of Respiratory Cell and Molecular Biology
Christine M Freeman, Jeffrey L Curtis
Hallmarks of chronic obstructive pulmonary disease (COPD) include innate inflammation and remodeling of small airways that begin in early disease and the development of lung lymphoid follicles (LLF), indicative of adaptive immunity, in more spirometrically-severe stages. Common to these processes in all stages is orchestration by dendritic cells (DC). Recently improved understanding of the analogous lung DC subsets in humans and mice has allowed for better integration and interpretation of the experimental and clinical pathological literature...
October 21, 2016: American Journal of Respiratory Cell and Molecular Biology
Khalil Bdeir, Kandace Gollomp, Marta Stasiak, Junjie Mei, Izabela Papiewska-Pajak, Guohua Zhao, G Scott Worthen, Douglas B Cines, Mortimer Poncz, M Anna Kowalska
RATIONALE: Platelets and neutrophils contribute to the development of acute lung injury (ALI). However, the mechanism by which platelets make this contribution is incompletely understood. We asked whether the two most abundant platelet chemokines, CXCL7, which induces neutrophil chemotaxis and activation, and CXCL4, which does neither, mediate ALI through complementary pathogenic pathways. OBJECTIVES: To examine the role of platelet-derived chemokines in the pathogenesis of ALI using Cxcl7-/- and Cxcl4-/- knockout mice and mice that express human CXCL7 or CXCL4...
October 18, 2016: American Journal of Respiratory Cell and Molecular Biology
Crystal N Marconett, Beiyun Zhou, Mitsuhiro Sunohara, Tiffany M Pouldar, HongJun Wang, Yixin Liu, Megan E Rieger, Evelyn Tran, Per Flodby, Kimberly D Siegmund, Edward D Crandall, Ite A Laird-Offringa, Zea Borok
Diseases involving the distal lung alveolar epithelium include chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF) and lung adenocarcinoma. Accurate labeling of specific cell types is critical for determining the contribution of each to pathogenesis of these diseases. The distal lung alveolar epithelium is comprised of two cell types, alveolar epithelial type 1 (AT1) and type 2 (AT2) cells. While cell type-specific markers, most prominently surfactant protein C (SFTPC), have allowed detailed lineage tracing studies of AT2 cell differentiation and their roles in disease, studies of AT1 cells have been hampered by lack of genes with expression unique to AT1 cells...
October 17, 2016: American Journal of Respiratory Cell and Molecular Biology
Jun Ren, Xiuqing Ding, John J Greer
Inhalation of capsaicin based sprays can cause central respiratory depression and lethal apneas. There are contradictory reports regarding the sites of capsaicin action. Further, an understanding of the neurochemical mechanisms underlying capsaicin-induced apneas and the development of pharmacological interventions are lacking. The main objectives were to perform a systematic study of the mechanisms of action of capsaicin-induced apneas and to provide insights relevant to pharmacological intervention. In vitro and in vivo rat and TRPV1-null mouse models were used to measure respiratory parameters and seizure-like activity in the presence of capsaicin and compounds that modulate glutamatergic neurotransmission...
October 6, 2016: American Journal of Respiratory Cell and Molecular Biology
Mingyuan Han, Jun Young Hong, Suraj Jaipalli, Charu Rajput, Jing Lei, Joanna L Hinde, Qiang Chen, Natalie M Hershenson, J Kelley Bentley, Marc B Hershenson
Early-life wheezing-associated infections with rhinovirus (RV) have been associated with asthma development in children. We have shown that RV infection of six day-old mice induces mucous metaplasia and airways hyperresponsiveness which is dependent on IL-13, IL-25 and type 2 innate lymphoid cells (ILC2s). Infection of immature mice fails to induce lung IFN-γ expression, in contrast to mature 8 week-old mice with a robust IFN-γ response, consistent with the notion that deficient IFN-γ production in immature mice permits RV-induced type 2 immune responses...
September 28, 2016: American Journal of Respiratory Cell and Molecular Biology
Joseph A Sennello, Alexander V Misharin, Annette S Flozak, Sergejs Berdnikovs, Paul Cheresh, John Varga, David W Kamp, G R Scott Budinger, Cara J Gottardi, Anna P Lam
Previous studies established that attenuating Wnt/β-catenin signaling limits lung fibrosis in the bleomycin mouse model of this disease, but the contribution of this pathway to distinct lung cell phenotypes relevant to tissue repair and fibrosis remains incompletely understood. Using microarray analysis, we found that bleomycin-injured lungs from mice that lack the Wnt co-receptor Lrp5 and exhibit reduced fibrosis, showed enrichment for pathways related to extracellular matrix processing, immunity, and lymphocyte proliferation, suggesting the contribution of an immune-matrix remodeling axis relevant to fibrosis...
September 26, 2016: American Journal of Respiratory Cell and Molecular Biology
Ken-Ichiro Tanaka, Fumiya Tamura, Toshifumi Sugizaki, Masahiro Kawahara, Keiji Kuba, Yumiko Imai, Tohru Mizushima
RATIONALE: For acute respiratory distress syndrome (ARDS), mechanical ventilation (MV) is a life-saving intervention without alternative, however, MV can cause ventilator-induced lung injury (VILI). Reactive oxygen species (ROS) play important roles in the pathogenesis of both ARDS and VILI. Lecithinized superoxide dismutase (PC-SOD) has overcome limitations of SOD such as low tissue affinity and low stability in plasma. OBJECTIVES: In this study, we have examined the effect of PC-SOD on tissue injury, edema and inflammation in the lung and other organs of mice subjected to cecal ligation and puncture (CLP), lipopolysaccharide (LPS) administration or MV...
September 26, 2016: American Journal of Respiratory Cell and Molecular Biology
Bas C Mourik, Pieter J M Leenen, Gerjo J de Knegt, Ruth Huizinga, Bram C J van der Eerden, Jinshan Wang, Charles R Krois, Joseph L Napoli, Irma A J M Bakker-Woudenberg, Jurriaan E M de Steenwinkel
RATIONALE: Immune-modulating drugs that target myeloid-derived suppressor cells or stimulate Natural Killer T-cells have been shown to reduce mycobacterial loads in tuberculosis. OBJECTIVES: We aimed to determine if a combination of these drugs as adjunct immunotherapy to conventional antibiotic treatment could also increase therapeutic efficacy against tuberculosis.. METHODS: In our model of pulmonary tuberculosis in mice, we applied treatment with isoniazid, rifampicin and pyrazinamide for 13 weeks alone or combined with immunotherapy consisting of all-trans-retinoic acid, 1,25(OH)2-vitamin D3 and α-galactosylceramide...
September 21, 2016: American Journal of Respiratory Cell and Molecular Biology
Sara Brilha, Tarangini Sathyamoorthy, Laura H Stuttaford, Naomi F Walker, Robert J Wilkinson, Shivani Singh, Rachel C Moores, Paul T Elkington, Jon S Friedland
Tuberculosis (TB) causes disease worldwide and multi-drug resistance is an increasing problem. Matrix metalloproteinases (MMPs), particularly the collagenase MMP-1, cause lung extracellular matrix destruction which drives disease transmission and morbidity. The role in such tissue damage of the stromelysin MMP-10, a key activator of the collagenase MMP-1, was investigated in direct Mycobacterium tuberculosis (Mtb) infected macrophages and in conditioned medium from Mtb infected monocytes (CoMtb)-stimulated cells...
September 21, 2016: American Journal of Respiratory Cell and Molecular Biology
Sailaja Ghanta, Konstantin Tsoyi, Xiaoli Liu, Kiichi Nakahira, Bonna Ith, Anna A Coronata, Laura E Fredenburgh, Joshua A Englert, Claude A Piantadosi, Augustine M K Choi, Mark A Perrella
Oxidative stress resulting from inflammatory responses that occur during acute lung injury and sepsis can initiate changes in mitochondrial function. Autophagy regulates cellular processes in the setting of acute lung injury, sepsis, and oxidative stress by modulating the immune response and facilitating turnover of damaged cellular components. We have shown that mesenchymal stromal cells (MSCs) improve survival in murine models of sepsis by also regulating the immune response. However, the effect of autophagy on MSC and MSC mitochondrial function during oxidative stress is unknown...
September 16, 2016: American Journal of Respiratory Cell and Molecular Biology
Huachun Cui, Jing Ge, Na Xie, Sami Banerjee, Yong Zhou, Veena B Antony, Victor J Thannickal, Gang Liu
Cellular senescence has been implicated in diverse pathologies. However, there has been conflicting evidence on the role of this process in tissue fibrosis. While dysregulation of miRNAs is a key mechanism in the pathogenesis of lung fibrosis, it is unclear whether they function by regulating cellular senescence in the disease. In this study, we found that miR-34a demonstrated greater expression in lungs of patients with IPF and mice with experimental pulmonary fibrosis, with its primary localization in lung fibroblasts...
September 16, 2016: American Journal of Respiratory Cell and Molecular Biology
Theodore J Kottom, Deanne M Hebrink, Paige E Jenson, Jorge H Ramirez-Prado, Andrew H Limper
N-acetylglucosamine (GlcNAc), serves as an essential structural sugar on the cell surface of organisms. For example, GlcNAc is a major component of bacterial peptidoglycan, it is an important building block of fungal cell walls, including a major constituent of chitin and mannoproteins, and it also required for extracellular matrix generation by animal cells. Herein, we provide evidence for a uridine diphospho-N-acetylglucosamine (UDP-GlcNAc) pathway in Pneumocystis species. Using in silico search of the P...
September 15, 2016: American Journal of Respiratory Cell and Molecular Biology
Moumita Ghosh, Shama Ahmad, Carl W White, Susan D Reynolds
Cell therapy has the potential to cure disease through replacement of malfunctioning cells. While the tissue stem cell (TSC) is thought to be the optimal therapeutic cell, transplantation of TSC/progenitor cell mixtures has saved lives. We previously purified the mouse tracheobronchial epithelial TSC and reported that in vitro amplification generated numerous TSC. However, these cultures also contained TSC-derived progenitor cells and TSC re-purification by flow cytometry compromised TSC self-renewal. These limitations caused us to determine if a TSC/progenitor cell mixture would repopulate the injured airway epithelium...
September 15, 2016: American Journal of Respiratory Cell and Molecular Biology
Sujin Kim, Min-Ji Kim, Chang-Hoon Kim, Ju Wan Kang, Ha Kyung Shin, Dong-Young Kim, Tae-Bin Won, Doo Hee Han, Chae Seo Rhee, Joo-Heon Yoon, Hyun Jik Kim
RATIONALE AND OBJECTIVES: Here we studied the interferon (IFN)-regulated innate immune response against influenza A virus (IAV) infection in the mouse lung and the therapeutic effect of IFN-λ2/3 in acute IAV lung infection. . METHODS: For viral infections, IAV (WS/33, H1N1, PR8 H1N1, H5N1) were inoculated into WT mice by intranasal delivery and IAV mRNA level and viral titer were measured. To compare the antiviral effect of IFNs in vivo lung, neutralizing antibodies and recombinant IFNs were used...
September 15, 2016: American Journal of Respiratory Cell and Molecular Biology
Bum-Yong Kang, Kathy Park, Jennifer M Kleinhenz, Tamara C Murphy, Roy L Sutliff, David Archer, C Michael Hart
Pulmonary hypertension (PH), a serious complication of sickle cell disease (SCD), causes significant morbidity and mortality. While recent study determined that hemin release during hemolysis triggers endothelial dysfunction in SCD, the pathogenesis of SCD-PH remains incompletely defined. This study examines peroxisome proliferator-activated receptor gamma (PPARγ) regulation in SCD-PH and endothelial dysfunction. PH and right ventricular hypertrophy (RVH) were studied in Townes humanized sickle cell (SS) and littermate control (AA) mice...
September 9, 2016: American Journal of Respiratory Cell and Molecular Biology
Jessica L Werner, Sylvia G Escolero, Jeff T Hewlett, Tim N Mak, Brian P Williams, Yoshinobu Eishi, Gabriel Núñez
Sarcoidosis is characterized by non-caseating granulomas with an unknown etiology that present primarily in the lung. Propionibacterium acnes, an immunogenic commensal skin bacterium involved in acne vulgaris, has been implicated as a possible causative agent of sarcoidosis. Here we demonstrate that a viable strain of P. acnes isolated from a sarcoidosis patient and instilled intratracheally into wild-type mice can generate pulmonary granulomas similar to those observed in sarcoidosis patients. The formation of these granulomas is dependent on administration of viable P...
September 8, 2016: American Journal of Respiratory Cell and Molecular Biology
Belinda J Thomas, Keiko Kan-O, Kate Loveland, Jack A Elias, Philip G Bardin
Transforming growth factor beta (TGFB) regulates cell proliferation, differentiation, apoptosis and matrix homeostasis and is intimately involved in fibrosis. TGFB expression is increased in fibrotic lung diseases such as idiopathic pulmonary fibrosis (IPF) but also in chronic inflammatory conditions such as chronic obstructive pulmonary disease (COPD) and asthma. In addition to profibrotic activities, the molecule also exhibits profound immune-suppressive actions involving both innate and adaptive responses, but this aspect of TGFB biology is often overlooked...
September 7, 2016: American Journal of Respiratory Cell and Molecular Biology
John A Gebe, Koshika Yadava, Shannon M Ruppert, Payton Marshall, Paul Hill, Ben A Falk, Johanna M Sweere, Hongwei Han, Gernot Kaber, Carlos Medina, Katalin Mikecz, Steven F Ziegler, Swathi Balaji, Sundeep G Keswani, Vinicio A de Jesus Perez, Manish J Butte, Kari Nadeau, William A Altemeier, Neil Fanger, Paul L Bollyky
BACKGROUND: The extracellular matrix in asthmatic lungs contains abundant low-molecular-weight hyaluronan (LMW-HA) and this is known to promote antigen presentation and allergic responses. Conversely, high-molecular-weight hyaluronan, typical of un-inflamed tissues, is known to suppress inflammation. OBJECTIVE: We asked whether HMW-HA can be adapted to adapted to promote tolerance to airway allergens. METHODS: HMW-HA was thiolated to prevent its catabolism and tethered it to allergens via thiol linkages...
September 6, 2016: American Journal of Respiratory Cell and Molecular Biology
Shuo Zheng, Apparao B Kummarapurugu, Daniel K Afosah, Nehru Viji Sankaranarayanan, Rio S Boothello, Umesh R Desai, Thomas Kennedy, Judith A Voynow
High mobility group box 1 (HMGB1) is an alarmin released from macrophages following infection or inflammation, and a biomarker of lung disease progression in cystic fibrosis. We reported that 2-O, 3-O desulfated heparin (ODSH) inhibits release of HMGB1 from murine macrophages triggered by neutrophil elastase (NE) both in vivo and in vitro. HMGB1 shuttles between the nucleus and the cytoplasm. When acetylated at lysine residues in the nuclear localization signal domains, HMGB1 is sequestered in the cytoplasm and is fated for secretion...
September 1, 2016: American Journal of Respiratory Cell and Molecular Biology
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