Publikationsdatenbank

Acute Moraxella catarrhalis airway infection of chronically smoke-exposed mice increases mechanisms of emphysema development:
a pilot study (2018)

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

Fischer, Katja

Doehn, Jan-Moritz

Herr, Christian

Lachner, Carolin

Heinrich, Annina

Kershaw, Olivia (WE 12)

Voss, Meike

Jacobson, Max H

Gruber, A.D. (WE 12)

Clauss, Matthias

Witzenrath, Martin

Bals, Robert

Gutbier, Birgitt

Slevogt, Hortense

Quelle

European journal of microbiology & immunology

Bandzählung: 8

Heftzählung: 4

Seiten: 128 – 134

ISSN: 2062-509x

Sprache

Englisch

Verweise

DOI: 10.1556/1886.2018.00019

Pubmed: 30719329

Kontakt

Institut für Tierpathologie

Robert-von-Ostertag-Str. 15
14163 Berlin
+49 30 838 62450
pathologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

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 microvas-culature 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.