• S Hippenstiel, M Witzenrath, B Opitz, H Schütte, S Rosseau, and N Suttorp.
• Medizinische Klinik mit Schwerpunkt Infektiologie und Pneumologie, Charité - Universitätsmedizin Berlin, Augustenburger Platz 1, 13353 Berlin. stefan.hippenstiel@charite.de
• Internist (Berl). 2007 May 1; 48 (5): 459467459-60, 462-4, 466-7.

AbstractPneumonia can lead to the critical impairment of gas exchange in the lung. Due to the great variability of pneumonia causing pathogens, a large variety of diverse virulence factors act on the lung. Besides stimulation of unspecific defense mechanisms, activation of receptor-dependent cell-mediated innate immune defense mechanisms are critical for the pulmonary immune defense. Pathogen-associated molecules are detected via transmembraneous and cytosolic receptors of the host. This interaction stimulates the expression of immunomodulatory molecules via signal cascades. Of particular importance, in addition to direct pathogen-caused lung damage, is the overwhelming activation of the inflammatory response which can result in lung barrier failure and impairment of pulmonary gas exchange. In addition to the design of new antibiotics, innovative therapeutic strategies should therefore concentrate on the enhancement of antimicrobial mechanisms by concurrent limitation of inflammation.

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