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Titel: Acute Moraxella catarrhalis Airway Infection of Chronically Smoke-Exposed Mice Increases Mechanisms of Emphysema Development : A Pilot Study
VerfasserIn: Fischer, Katja
Doehn, Jan-Moritz
Herr, Christian
Lachner, Carolin
Heinrich, Annina
Kershaw, Olivia
Voss, Meike
Jacobson, Max H.
Gruber, Achim D.
Clauss, Matthias
Witzenrath, Martin
Bals, Robert
Gutbier, Birgitt
Slevogt, Hortense
Sprache: Englisch
Titel: European Journal of Microbiology & Immunology
Bandnummer: 8
Heft: 4
Seiten: 128–134
Verlag/Plattform: Akadémiai Kiadó
Erscheinungsjahr: 2018
Freie Schlagwörter: chronic smoke exposure
COPD
M. catarrhalis
emphysema
EMAPII
DDC-Sachgruppe: 610 Medizin, Gesundheit
Dokumenttyp: Journalartikel / Zeitschriftenartikel
Abstract: 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 proinflammatory 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.
DOI der Erstveröffentlichung: 10.1556/1886.2018.00019
URL der Erstveröffentlichung: https://akjournals.com/view/journals/1886/8/4/article-p128.xml
Link zu diesem Datensatz: urn:nbn:de:bsz:291--ds-366867
hdl:20.500.11880/33329
http://dx.doi.org/10.22028/D291-36686
ISSN: 2062-509X
Datum des Eintrags: 7-Jul-2022
Bezeichnung des in Beziehung stehenden Objekts: Supplementary Material
In Beziehung stehendes Objekt: https://akjournals.com/supplemental/journals/1886/8/4/article-p128.xml/1886.2018.00019_esm.pdf
Fakultät: M - Medizinische Fakultät
Fachrichtung: M - Innere Medizin
Professur: M - Prof. Dr. Robert Bals
Sammlung:SciDok - Der Wissenschaftsserver der Universität des Saarlandes



Diese Ressource wurde unter folgender Copyright-Bestimmung veröffentlicht: Lizenz von Creative Commons Creative Commons