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      Asthma and COPD - The C/EBP Connection

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          Abstract

          Asthma and chronic obstructive pulmonary disease (COPD) are the two most prominent chronic inflammatory lung diseases with increasing prevalence. Both diseases are associated with mild or severe remodeling of the airways. In this review, we postulate that the pathologies of asthma and COPD may result from inadequate responses and/or a deregulated balance of a group of cell differentiation regulating factors, the CCAAT/Enhancer Binding Proteins (C/EBPs). In addition, we will argue that the exposure to environmental factors, such as house dust mite and cigarette smoke, changes the response of C/EBPs and are different in diseased cells. These novel insights may lead to a better understanding of the etiology of the diseases and may provide new aspects for therapies.

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          eIF4 initiation factors: effectors of mRNA recruitment to ribosomes and regulators of translation.

          A Gingras, B Raught, N. Sonenberg (1999)
          Eukaryotic translation initiation factor 4F (eIF4F) is a protein complex that mediates recruitment of ribosomes to mRNA. This event is the rate-limiting step for translation under most circumstances and a primary target for translational control. Functions of the constituent proteins of eIF4F include recognition of the mRNA 5' cap structure (eIF4E), delivery of an RNA helicase to the 5' region (eIF4A), bridging of the mRNA and the ribosome (eIF4G), and circularization of the mRNA via interaction with poly(A)-binding protein (eIF4G). eIF4 activity is regulated by transcription, phosphorylation, inhibitory proteins, and proteolytic cleavage. Extracellular stimuli evoke changes in phosphorylation that influence eIF4F activity, especially through the phosphoinositide 3-kinase (PI3K) and Ras signaling pathways. Viral infection and cellular stresses also affect eIF4F function. The recent determination of the structure of eIF4E at atomic resolution has provided insight about how translation is initiated and regulated. Evidence suggests that eIF4F is also implicated in malignancy and apoptosis.
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            The global burden of disease, 1990-2020.

            A. Lopez, C C Murray (1998)
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              Respiratory syncytial virus in early life and risk of wheeze and allergy by age 13 years.

              R T Stein, D. Sherrill, W J Morgan … (1999)
              The relation between lower respiratory tract illnesses in early life caused by the respiratory syncytial virus (RSV) and the subsequent development of wheezing and atopy in childhood is not well understood. We studied this relation in children who had lower respiratory tract illnesses that occurred before 3 years of age. Children were enrolled at birth and cases of lower respiratory tract illness were ascertained by a physician. Viral tests were done for specimens collected at the time of the illness. Children were classified into five groups according to type and cause of lower respiratory tract illness. Children were then followed prospectively up to age 13, and we measured frequency of wheezing, pulmonary function, and atopic status (allergy skin-prick tests, serum IgE concentrations). RSV lower respiratory tract illnesses were associated with an increased risk of infrequent wheeze (odds ratio 3.2 [95% CI 2.0-5.0], p < 0.001), and an increased risk of frequent wheeze (4.3 [2.2-8.7], p < or = 0.001) by age 6. Risk decreased markedly with age and was not significant by age 13. There was no association between RSV lower respiratory tract illnesses and subsequent atopic status. RSV lower respiratory tract illnesses were associated with significantly lower measurements of forced expiratory volume (2.11 [2.05-2.15], p < or = 0.001) when compared with those of children with no lower respiratory tract illnesses, but there was no difference in forced expiratory volume after inhalation of salbutamol. RSV lower respiratory tract illnesses in early childhood are an independent risk factor for the subsequent development of wheezing up to age 11 years but not at age 13. This association is not caused by an increased risk of allergic sensitisation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Open Respir Med J
                Journal ID (iso-abbrev): Open Respir Med J
                Journal ID (publisher-id): TORMJ
                Title: The Open Respiratory Medicine Journal
                Publisher: Bentham Open
                ISSN (Electronic): 1874-3064
                Publication date (Electronic): 20 April 2012
                Publication date Collection: 2012
                Volume: 6
                Pages: 1-13
                Affiliations
                Pulmonary Cell Research, Departments of Biomedicine and Pneumology, University Hospital Basel, Switzerland
                Author notes
                [* ]Address correspondence to this author at the Pulmonary Cell Research, University of Basel, Department of Biomedicine, Hebelstrasse 20, CH - 4031 Basel, Switzerland; Tel: +61 41 265 3254; Fax: +61 41 265 2350; E-mail: pieter.borger@ 123456unibas.ch
                Article
                Publisher ID: TORMJ-6-1
                DOI: 10.2174/1874306401206010001
                PMC ID: 3377872
                PubMed ID: 22715349
                SO-VID: c44f2ea9-b94b-447c-8aa2-73a8ff10cab9
                Copyright © © Miglino et al.; Licensee Bentham Open.
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 6 April 2012
                Date revision received : 6 April 2012
                Date accepted : 11 April 2012
                Categories
                Subject: Article

                ScienceOpen disciplines: Respiratory medicine
                Keywords: airway wall remodelling,airway inflammation,asthma,copd,ccaat-enhancer binding proteins.
                Data availability:
                ScienceOpen disciplines: Respiratory medicine
                Keywords: airway wall remodelling, airway inflammation, asthma, copd, ccaat-enhancer binding proteins.

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