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    Streptococcus Pneumoniae-induced Regulation of Cyclooxygenase-2 in Human Lung Tissue (2012)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Szymanski, Kolja V
    Toennies, Mario
    Becher, Anne
    Fatykhova, Diana
    N'Guessan, Philippe D
    Gutbier, Birgitt
    Klauschen, Frederick
    Neuschaefer-Rube, Frank
    Schneider, Paul
    Rueckert, Jens
    Neudecker, Jens
    Bauer, Torsten T
    Dalhoff, Klaus
    Drömann, Daniel
    Gruber, Achim D
    Kershaw, Olivia
    Temmesfeld-Wollbrueck, Bettina
    Suttorp, Norbert
    Hippenstiel, Stefan
    Hocke, Andreas C
    Quelle
    The European respiratory journal; 40(6) — S. 1458–1467
    ISSN: 0903-1936
    Sprache
    Englisch
    Verweise
    DOI: 10.1183/09031936.00186911
    Pubmed: 22441740
    Kontakt
    Institut für Tierpathologie

    Robert-von-Ostertag-Str. 15
    Gebäude 12
    14163 Berlin
    +49 30 838 62450

    Abstract / Zusammenfassung

    The majority of cases of community-acquired pneumonia are caused by Streptococcus pneumoniae and most studies on pneumococcal host interaction are based on cell culture or animal experiments. Thus, little is known about infections in human lung tissue. Cyclooxygenase-2 and its metabolites play an important regulatory role in lung inflammation. Therefore, we established a pneumococcal infection model on human lung tissue demonstrating mitogen-activated protein kinase (MAPK)-dependent induction of cyclooxygenase-2 and its related metabolites. In addition to alveolar macrophages and the vascular endothelium, cyclooxygenase-2 was upregulated in alveolar type II but not type I epithelial cells, which was confirmed in lungs of patients suffering from acute pneumonia. Moreover, we demonstrated the expression profile of all four E prostanoid receptors at the mRNA level and showed functionality of the E prostanoid(4) receptor by cyclic adenosine monophosphate production. Additionally, in comparison to previous studies, cyclooxygenase-2/prostaglandin E(2) related pro- and anti-inflammatory mediator regulation was partly confirmed in human lung tissue after pneumococcal infection. Overall, cell type-specific and MAPK-dependent cyclooxygenase-2 expression and prostaglandin E(2) formation in human lung tissue may play an important role in the early phase of pneumococcal infections.