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      Acute Moraxella catarrhalis airway infection of chronically smoke-exposed mice increases mechanisms of emphysema development: A pilot study

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          In chronic obstructive pulmonary disease (COPD), acute exacerbations and emphysema development are characteristics for disease pathology. COPD is complicated by infectious exacerbations with acute worsening of respiratory symptoms with Moraxella catarrhalis as one of the most frequent pathogens. Although cigarette smoke (CS) is the primary risk factor, additional molecular mechanisms for emphysema development induced by bacterial infections are incompletely understood. We investigated the impact of M. catarrhalis on emphysema development in CS exposed mice and asked whether an additional infection would induce a solubilization of pro-apoptotic and pro-inflammatory endothelial monocyte-activating-protein-2 (EMAPII) to exert its activities in the pulmonary microvasculature and other parts of the lungs not exposed directly to CS.

          Mice were exposed to smoke (6 or 9 months) and/or infected with M. catarrhalis. Lungs, bronchoalveolar lavage fluid (BALF), and plasma were analyzed.

          CS exposure reduced ciliated area, caused rarefaction of the lungs, and induced apoptosis. EMAPII was increased independent of prior smoke exposure in BALF of infected mice. Importantly, acute M. catarrhalis infection increased release of matrixmetalloproteases-9 and -12, which are involved in emphysema development and comprise a mechanism of EMAPII release.

          Our data suggest that acute M. catarrhalis infection represents an independent risk factor for emphysema development in smoke-exposed mice.

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          Most cited references 30

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          Requirement for macrophage elastase for cigarette smoke-induced emphysema in mice.

          To determine which proteinases are responsible for the lung destruction characteristic of pulmonary emphysema, macrophage elastase-deficient (MME-/-) mice were subjected to cigarette smoke. In contrast to wild-type mice, MME-/- mice did not have increased numbers of macrophages in their lungs and did not develop emphysema in response to long-term exposure to cigarette smoke. Smoke-exposed MME-/- mice that received monthly intratracheal instillations of monocyte chemoattractant protein-1 showed accumulation of alveolar macrophages but did not develop air space enlargement. Thus, macrophage elastase is probably sufficient for the development of emphysema that results from chronic inhalation of cigarette smoke.
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            Pathogenesis of chronic obstructive pulmonary disease.

            The current epidemic of chronic obstructive pulmonary disease (COPD) has produced a worldwide health care burden, approaching that imposed by transmittable infectious diseases. COPD is a multidimensional disease, with varied intermediate and clinical phenotypes. This Review discusses the pathogenesis of COPD, with particular focus on emphysema, based on the concept that pulmonary injury involves stages of initiation (by exposure to cigarette smoke, pollutants, and infectious agents), progression, and consolidation. Tissue damage entails complex interactions among oxidative stress, inflammation, extracellular matrix proteolysis, and apoptotic and autophagic cell death. Lung damage by cigarette smoke ultimately leads to self-propagating processes, resulting in macromolecular and structural alterations - features similar to those seen in aging.
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              Requirement for Macrophage Elastase for Cigarette Smoke-Induced Emphysema in Mice


                Author and article information

                European Journal of Microbiology and Immunology
                Akadémiai Kiadó
                December 2018
                : 8
                : 4
                : 128-134
                [ 1 ]Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Infectious Diseases and Respiratory Medicine , Berlin, Germany
                [ 2 ]Septomics Research Center, Jena University Hospital , Jena, Germany
                [ 3 ]Department of Internal Medicine V – Pulmonology, Allergology, Respiratory Intensive Care Medicine, University of the Saarland , Homburg Saar, Germany
                [ 4 ]Department of Veterinary Pathology, Freie Universität , Berlin, Germany
                [ 5 ]Pathology and Laboratory Medicine, IU School of Medicine , Indianapolis, Indiana, USA
                [ 6 ]Indiana Center for Vascular Biology and Medicine and Department of Cellular and Integrative Physiology, Indiana University , Indianapolis, Indiana, USA
                [ 7 ]Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Division of Pulmonary Inflammation , Berlin, Germany
                Author notes

                Author for correspondence: Septomics Research Center, Jena University Hospital, Albert-Einstein Str. 10, 07745 Jena, Germany; Email: E-mail: hortense.slevogt@ ; Tel: +49 3641 9 396520.

                © 2018 The Author(s)

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes - if any - are indicated.

                Page count
                Pages: 7
                Original Research Paper


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