Respiratory tract diseases articles within Nature Communications

Featured

• Article | 11 September 2014

  Circadian rhythm reprogramming during lung inflammation

  Whether circadian rhythms occur in settings where clock gene expression is suppressed, such as systemic inflammation, is unclear. Here, the authors examine gene expression and metabolites in the lungs of endotoxemic mice and show that inflammation causes changes in circadian rhythms at the cellular and molecular level.

  • Jeffrey A. Haspel
  • , Sukrutha Chettimada
  •  & Augustine M.K. Choi

• Article | 02 September 2014

  Pseudomonas aeruginosa adaptation in the nasopharyngeal reservoir leads to migration and persistence in the lungs

  Pseudomonas aeruginosa causes chronic infections in patients with lung damage. Here, Fothergill et al. develop an intranasal inhalation model of P. aeruginosainfection and describe genetic and phenotypic changes that the bacteria undergo during adaptation and spread through the respiratory tract.

  • Joanne L. Fothergill
  • , Daniel R. Neill
  •  & Aras Kadioglu

• Article | 22 July 2014

  MCIDAS mutations result in a mucociliary clearance disorder with reduced generation of multiple motile cilia

  Reduced generation of multiple motile cilia (RGMC) is a rare mucociliary clearance disorder, characterized by chronic airway disease. Here, the authors identify mutations in the Multicilin gene, MCIDAS, and suggest that these mutations cause RGMC through disruption of multiciliated cell differentiation.

  • Mieke Boon
  • , Julia Wallmeier
  •  & Heymut Omran

• Article | 18 July 2014

  Treatment of acute lung injury by targeting MG53-mediated cell membrane repair

  MG53 acts as a membrane repair protein in striatal muscle. Here the authors report that MG53 is also expressed in the lung, where it exerts a similar repair function in the context of pulmonary epithelial damage, and show that administration of recombinant MG53 ameliorates lung injury in mice.

  • Yanlin Jia
  • , Ken Chen
  •  & Jianjie Ma

• Article | 06 May 2014

  Angiotensin-converting enzyme 2 protects from lethal avian influenza A H5N1 infections

  H5N1 avian influenza viruses can be highly pathogenic. Here, the authors show that H5N1 infection leads to increased serum levels of angiotensin II in patients and mice, and that administration of angiotensin-converting enzyme 2 ameliorates lung injury in infected mice.

  • Zhen Zou
  • , Yiwu Yan
  •  & Chengyu Jiang

• Article | 05 November 2013

  Mepenzolate bromide displays beneficial effects in a mouse model of chronic obstructive pulmonary disease

  Chronic obstructive pulmonary disease (COPD) is a serious respiratory disease that is resistant to many forms of treatment. Tanake et al.screen compounds from a library of medicines and find that mepenzolate bromide reduces inflammatory responses and improves respiration in a mouse model of COPD.

  • Ken-Ichiro Tanaka
  • , Tomoaki Ishihara
  •  & Tohru Mizushima

• Article | 11 October 2013

  Deranged fatty acid composition causes pulmonary fibrosis in Elovl6-deficient mice

  The enzyme Elovl6 catalyses a rate-limiting step in the elongation of fatty acids. Here Sunaga et al. show that Elovl6 knockout mice are more susceptible to pulmonary fibrosis, suggesting that the dysregulation of lipid components impairs alveolar epithelial cell function and pulmonary homeostasis.

  • Hiroaki Sunaga
  • , Hiroki Matsui
  •  & Masahiko Kurabayashi

• Article
  21 May 2013 | Open Access

  Prothymosin α overexpression contributes to the development of pulmonary emphysema

  Pulmonary emphysema obstruct airflow in the lung and often develop in smokers. Here Su et al. show that prothymosin α contributes to emphysema development through alterations in the acetylation of histones and the transcription factor NF-κB, and that exposure to cigarette smoke increases prothymosin α expression.

  • Bing-Hua Su
  • , Yau-Lin Tseng
  •  & Chao-Liang Wu

• Article | 23 April 2013

  Control of lung vascular permeability and endotoxin-induced pulmonary oedema by changes in extracellular matrix mechanics

  Vascular permeability is increased by inflammation and in disorders such as acute respiratory distress syndrome. Mammoto et al. show that lung vascular permeability is controlled by the stiffness of the extracellular matrix and identify lysyl oxidase as a regulator of vascular leakage in pulmonary oedema in mice.

  • Akiko Mammoto
  • , Tadanori Mammoto
  •  & Donald E. Ingber

• Article
  10 April 2012 | Open Access

  CYLD negatively regulates transforming growth factor-β-signalling via deubiquitinating Akt

  Lung injury initiates a series of wound-healing responses, which if unregulated, can lead to fibrosis. Liet al. show that the deubquitinase CYLD has a key role in the prevention of fibrosis by inhibiting transforming growth factor β-signalling through the direct deubiquitination of the protein kinase Akt.

  • Jae Hyang Lim
  • , Hirofumi Jono
  •  & Jian-Dong Li

• Article
  31 January 2012 | Open Access

  Activation of TRPC6 channels is essential for lung ischaemia–reperfusion induced oedema in mice

  The signalling cascade involved in lung ischaemia–reperfusion-induced oedema is poorly understood. Using knockout mice, Weissmannet al. propose a model in which reactive oxygen species production by endothelial NOX2 leads to phospholipase C-γ activation, DAG kinase inhibition and subsequent TRPC6 activation.

  • Norbert Weissmann
  • , Akylbek Sydykov
  •  & Alexander Dietrich

• Article
  19 April 2011 | Open Access

  Respiratory distress and perinatal lethality in Nedd4-2-deficient mice

  In vitrostudies have suggested that the ubiquitin ligase, Nedd4-2, regulates several proteins, including the epithelial sodium channel. Here by examining Nedd4-2-deficient mice, the authors demonstrate that Nedd4-2 is essential for epithelial sodium channel regulation, fetal and postnatal lung function and animal survival.

  • Natasha A. Boase
  • , Grigori Y. Rychkov
  •  & Sharad Kumar