Publikationsdatenbank

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

Bandzählung: 40

Heftzählung: 6

Seiten: 1458 – 1467

ISSN: 0903-1936

Sprache

Englisch

Verweise

DOI: 10.1183/09031936.00186911

Pubmed: 22441740

Kontakt

Institut für Tierpathologie

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

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.