Mechanism for severe pneumonia identified
(Vienna, 1 Feb. 2011) A current research project at MedUni Vienna is deciphering the cause of severe pneumonia, which is triggered by multiresistant bacteria. This will also lead to new therapeutic approaches to prevent the usually fatal consequences.
Bacterial strains which are resistant to antibiotics are particularly hard to treat and, to the same extent, are often correspondingly life-threatening. The bacterial toxin PVL (Panton Valentine leucocidin) plays an important role here within the increasingly widespread and particularly aggressive CA-MRSA strains (community-acquired methicillin-resistant Staphylococcus aureus). The toxin attacks special white blood cells (neutrophilic granulocytes) in particular and leads to rapid cell death here.
Mag. Ana Zivkovic, a PhD student at MedUni Vienna from the research group of Ao. Univ. Prof. Dr. Sylvia Knapp, discovered that PVL is also able to activate alveolar macrophages, however. These cells on the surface of the alveoli normally break down dead material and foreign particles in the lung, but with activation by PVL a distinct inflammation of the lung is triggered.
This work, conducted on a mouse model, therefore shows for the first time that PVL does not only have an effect on granulocytes but also plays a very important role in the inflammatory response of the lung. Thanks to this discovery a new approach is now possible in the search for corresponding treatment options.
The importance of these results is underlined not least by the publication in the current issue of the “Journal of Immunology”. The project was the result of cooperation with the Center for Molecular Medicine (Ce-M-M), the Clinical Institutes of Laboratory Medicine and Pathology at the Medical University of Vienna as well as the Department of Pharmacology and Toxicology at the University of Vienna.
TLR2 and CD14 mediate innate immunity and lung inflammation to Staphylococcal Panton Valentine leucocidin in vivo.
Zivkovic A, Sharif O, Stich K, Doninger B, Biaggio M, Colinge J, Bilban M, Mesteri I, Hazemi P, Lemmens-Gruber R, Knapp S.
Journal of Immunology, doi: 10.4049/jimmunol.1001665