Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome (ARDS), can result from both direct and indirect pulmonary damage caused by trauma and shock. In the course of ALI/ARDS, mediators released from resident cells, such as alveolar macrophages, may act as chemoattractants for invading cells and stimulate local cells to build up a proinflammatory micromilieu. Depending on the trauma setting, the role of alveolar macrophages is differentially defined. This review focuses on alveolar macrophage function after blunt chest trauma, ischemia/reperfusion, hemorrhagic shock, and thermal burns.
*Departments of Trauma Surgery, Hand, Plastic and Reconstructive Surgery, and †Anesthesiology and Intensive Care, Center for Biomedical Research, University of Ulm, Ulm, Germany
Received 27 Jan 2014; first review completed 12 Feb 2014; accepted in final form 4 Mar 2014
Address reprint requests to Ulrike Niesler, PhD, Trauma Lab, Department of Trauma Surgery, Hand, Plastic and Reconstructive Surgery, Center for Biomedical Research, Ulm University. Helmholtzstr. 8/2, 89081 Ulm, Germany. E-mail: email@example.com.
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This work was supported by grants from the Deutsche Forschungsgemeinschaft (DFG KFO 200, KN 475/5-2; DFG KFO 200, HU 823/3-2).
None of the authors have any financial interests or affiliations with commercial organizations whose products or services are related to the subject matter of this article (no existing conflicts of interest).