Philipp Störmann1, Birgit Auner1, Lukas Schimunek1, Rafael Serve1, Klemens Horst2, Tim-P Simon3, Roman Pfeifer4, Kernt Köhler5, Frank Hildebrand6, Sebastian Wutzler1, Hans-Christoph Pape4, Ingo Marzi1, Borna Relja7. 1. Department of Trauma, Hand and Reconstructive Surgery, Goethe University Frankfurt, 60590 Frankfurt, Germany. 2. Department of Orthopaedic Trauma, RWTH Aachen University, Germany; Harald Tscherne Research Laboratory, RWTH Aachen University, Germany. 3. Department of Intensive Care and Intermediate Care, RWTH Aachen University, Germany. 4. Department of Orthopaedic Trauma Surgery, University Hospital Zurich, University of Zurich, Switzerland. 5. Institute of Veterinary Pathology, Justus Liebig University Giessen, Giessen, Germany. 6. Department of Orthopaedic Trauma, RWTH Aachen University, Germany. 7. Department of Trauma, Hand and Reconstructive Surgery, Goethe University Frankfurt, 60590 Frankfurt, Germany. Electronic address: bornarelja@kgu.de.
Abstract
BACKGROUND: Recognizing patients at risk for pulmonary complications (PC) is of high clinical relevance. Migration of polymorphonuclear leukocytes (PMN) to inflammatory sites plays an important role in PC, and is tightly regulated by specific chemokines including interleukin (IL)-8 and other mediators such as leukotriene (LT)B4. Previously, we have reported that LTB4 indicated early patients at risk for PC after trauma. Here, the relevance of LTB4 to indicating lung integrity in a newly established long-term porcine severe trauma model (polytrauma, PT) was explored. METHODS: Twelve pigs (3 months old, 30 ± 5kg) underwent PT including standardized femur fracture, lung contusion, liver laceration, hemorrhagic shock, subsequent resuscitation and surgical fracture fixation. Six animals served as controls (sham). After 72h lung damage and inflammatory changes were assessed. LTB4 was determined in plasma before the experiment, immediately after trauma, and after 2, 4, 24 or 72h. Bronchoalveolar lavage (BAL)-fluid was collected prior and after the experiment. RESULTS: Lung injury, local gene expression of IL-8, IL-1β, IL-10, IL-18 and PMN-infiltration into lungs increased significantly in PT compared with sham. Systemic LTB4 increased markedly in both groups 4h after trauma. Compared with declined plasma LTB4 levels in sham, LTB4 increased further in PT after 72h. Similar increase was observed in BAL-fluid after PT. CONCLUSIONS: In a severe trauma model, sustained changes in terms of lung injury and inflammation are determined at day 3 post-trauma. Specifically, increased LTB4 in this porcine long-term model indicated a rapid inflammatory alteration both locally and systemically. The results support the concept of LTB4 as a biomarker for PC after severe trauma and lung contusion.
BACKGROUND: Recognizing patients at risk for pulmonary complications (PC) is of high clinical relevance. Migration of polymorphonuclear leukocytes (PMN) to inflammatory sites plays an important role in PC, and is tightly regulated by specific chemokines including interleukin (IL)-8 and other mediators such as leukotriene (LT)B4. Previously, we have reported that LTB4 indicated early patients at risk for PC after trauma. Here, the relevance of LTB4 to indicating lung integrity in a newly established long-term porcine severe trauma model (polytrauma, PT) was explored. METHODS: Twelve pigs (3 months old, 30 ± 5kg) underwent PT including standardized femur fracture, lung contusion, liver laceration, hemorrhagic shock, subsequent resuscitation and surgical fracture fixation. Six animals served as controls (sham). After 72h lung damage and inflammatory changes were assessed. LTB4 was determined in plasma before the experiment, immediately after trauma, and after 2, 4, 24 or 72h. Bronchoalveolar lavage (BAL)-fluid was collected prior and after the experiment. RESULTS:Lung injury, local gene expression of IL-8, IL-1β, IL-10, IL-18 and PMN-infiltration into lungs increased significantly in PT compared with sham. Systemic LTB4 increased markedly in both groups 4h after trauma. Compared with declined plasma LTB4 levels in sham, LTB4 increased further in PT after 72h. Similar increase was observed in BAL-fluid after PT. CONCLUSIONS: In a severe trauma model, sustained changes in terms of lung injury and inflammation are determined at day 3 post-trauma. Specifically, increased LTB4 in this porcine long-term model indicated a rapid inflammatory alteration both locally and systemically. The results support the concept of LTB4 as a biomarker for PC after severe trauma and lung contusion.