• Rosemarijn Renckens, Joris J T H Roelofs, Sylvia Knapp, Alex F de Vos, Sandrine Florquin, and Tom van der Poll.
• Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. r.renckens@amc.uva.nl
• J. Infect. Dis. 2006 Jan 15;193(2):187-95.

BackgroundAcinetobacter baumannii is an emerging pathogen in nosocomial pneumonia. Trauma and postsurgical patients display a profound acute-phase protein response and are susceptible to pneumonia.MethodsTo study the way in which the acute-phase response induced by sterile tissue injury influences pulmonary host defense, mice were injected subcutaneously with turpentine or saline in both hind limbs either 2 or 5 days before intranasal inoculation with A. baumannii.ResultsTurpentine-injected mice demonstrated strong increases in levels of the acute-phase proteins serum amyloid A (SAA) and serum amyloid P. The inflammatory response to A. baumannii was significantly impaired in turpentine-injected mice, as shown by decreased local cytokine and chemokine levels, reduced neutrophil influx and lung myeloperoxidase activity, less pulmonary inflammation on histological examination, and lower total protein levels in their bronchoalveolar lavage fluid, which was associated with reduced bacterial clearance of A. baumannii. The late acute-phase protein response still caused lower pulmonary cytokine levels and neutrophil recruitment. Furthermore, previous injection of SAA, a major acute-phase protein, also reduced inflammatory responses to A. baumannii pneumonia.ConclusionsThese data suggest that the acute-phase response and SAA inhibit the local inflammatory response to A. baumannii pneumonia, which may facilitate bacterial outgrowth.

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