Visualization of complicated fractures by 3D-printed models for teaching and surgery: hands-on transitional fractures of the ankle.

AIMS: Understanding the orientation of fracture lines and mechanisms is the essential key to sufficient surgical therapy, but there is still a lack of visualization and teaching methods in traumatology and fracture theory. 3D-printed models offer easy approach to those fractures. This paper explains the use of the teaching possibility with 3-dimensional models of transitional fractures of the ankle. METHODS AND RESULTS: For generating 3D printable models, already obtained CT data were used and segmented into its different tissues, especially parts concerning the fracture. After the segmentation process, the models were produced with FFF (fused filament fabrication) printing technology. The fracture models then were used for hands-on teaching courses in AO course (Arbeitsgemeinschaft für Osteosynthesefragen) of pediatric traumatology in 2020 in Frankfurt. In the course fracture anatomy with typical fracture lines, approaches, and screw placement could be shown, discussed and practiced. CONCLUSION: The study shows the use of 3D-printed teaching models and helps to understand complicated fractures, in this case, transitional fractures of the ankle. The teaching method can be adapted to numerous other use cases.

The effect of age and sex on outcomes following isolated moderate to severe traumatic brain injury.

PURPOSE: The impact of female sex on traumatic brain injury (TBI) outcomes remains controversial. The combined impact of age and sex on TBI outcomes must be clarified. We hypothesized that females have better outcomes than males in the premenopausal age group. METHODS: Data from the 2007-2016 National Trauma Data Bank of the Committee on Trauma-American College of Surgeons were used. Of a total of 686,549 patients with moderate to severe TBI (AIS ≥ 3), 251,491 were female. Comparison analyses of clinical characteristics and outcomes between females and males were conducted at different age groups: < 45 years, 45-55, and > 55 years. Logistic regressions were performed to assess the impact of age and female sex on mortality and complications. RESULTS: Mortality rate between females and males aged < 45 and 45-55 years was similar, but significantly reduced in the > 55 years group. After multivariate logistic regression analysis controlling for multiple confounding factors, we found that females aged > 55 years had markedly decreased risk of mortality (AOR: 0.857, 95% CI 0.835-0.879, p < 0.001) and complications. CONCLUSION: Female patients in the postmenopausal stage have better outcomes following TBI than males, but pre- and perimenopausal females do not, suggesting that female sexual hormones may not provide a significant protective effect on clinical outcomes following isolated moderate to severe TBI.

Anti-inflammatory Effects of Alcohol Are Associated with JNK-STAT3 Downregulation in an In Vitro Inflammation Model in HepG2 Cells.

BACKGROUND: In several preclinical and in vitro models of acute inflammation, alcohol (ethanol, EtOH) has been described as an immunomodulatory agent. Similarly, in different pathologies, clinical observations have confirmed either pro- or anti-inflammatory effects of EtOH. The liver plays an important role in immunity and alcohol metabolism; therefore, we analysed dose- and time-dependent effects of EtOH on the inflammatory response of human liver cells in an in vitro model of acute inflammation. METHODS: HepG2 cells were stimulated with IL-1ß and subsequently exposed to EtOH in a low or high dose (85 mM, LoD or 170 mM, HiD) for 1 h (acute exposure) or 72 h (prolonged exposure). IL-6 and TNF-α release was determined by ELISA. Cell viability, adhesion of isolated neutrophils to HepG2 monolayers, their ICAM-1 expression, and the activation of stress-induced protein kinase/c-Jun N-terminal kinase (SAPK/JNK) or signal transducer and activator of transcription 3 (STAT3) were analysed. RESULTS: In this experimental design, EtOH did not markedly change the cell viability. Acute and prolonged exposure to EtOH significantly reduced dose-independent IL-1ß-induced IL-6 and TNF-α release, as well as adhesion capacity to pretreated HepG2 cells. Acute exposure to EtOH significantly decreased the percentage of ICAM-1-expressing cells. IL-1ß stimulation notably increased the activation of SAPK/JNK. However, low-dose EtOH exposure reduced this activation considerably, in contradiction to high-dose EtOH exposure. Acute exposure to LoD EtOH significantly diminished the IL-1ß-induced STAT3 activation, whereas an acute exposure of cells to either HiD EtOH or in a prolonged setting showed no effects on STAT3 activation. CONCLUSION: EtOH exerts anti-inflammatory potential in this in vitro model of hepatic inflammation. These effects are associated with the reduced activation of JNK/STAT3 by EtOH, particularly in the condition of acute exposure to low-dose EtOH.

Enhanced pro-inflammatory response and higher mortality rates in geriatric trauma patients.

BACKGROUND: Age has been associated with increased morbidity and mortality after traumatic injury. Disregarding trauma-related factors, this may be caused by the diminished ability to cope with stressors due to limited reserve, the so-called frailty. Inflammation is assumed to promote frailty, and thus, pro-inflammatory markers may constitute as being predictive factors in geriatric trauma patients (TP). Here, we analyzed the influence of age on systemic inflammatory markers and outcome parameters in TP. PATIENTS AND METHODS: 204 TP with injury severity score (ISS) ≥ 16 were included and grouped to younger vs. geriatric, defining an age of 65 as cut-off. ISS, vital signs, physiological parameters, stay at the intensive-care unit (ICU) or in-hospital, and outcome parameters were analyzed. Systemic fibrinogen, interleukin (IL)-6, and IL-10 levels were determined upon admission. A p value < 0.05 was considered statistically significant. RESULTS: 43 geriatric and 161 younger TP were included. ISS (24.19 ± 9.59 vs. 26.93 ± 9.68) was comparable between both groups. Abbreviated Injury Scale (AIS) ≥ 3 of head trauma was more prevalent in geriatric TP (74.42 vs. 64.59%). In both groups, there were significantly more male than female patients; however, this disparity was significantly more distinct in younger TP. Geriatric group showed significantly lower shock indices, higher fibrinogen, and lower IL-10 levels (all p < 0.05). A significant spearman´s rank correlation with age was found for fibrinogen (positive correlation, r = 0.364, p < 0.05), and for IL-10 (negative correlation, r = - 0.168, p < 0.05). In-hospital mortality was significantly increased in geriatric TP. CONCLUSIONS: An enhanced inflammatory response is associated with higher mortality rates in geriatric trauma patients.

Alcohol Binge Reduces Systemic Leukocyte Activation and Pulmonary PMN Infiltration After Blunt Chest Trauma and Hemorrhagic Shock.

Blunt chest (thoracic) trauma (TxT) and hemorrhagic shock (HS)-induced local and systemic inflammation with increased neutrophil activity often result in an impaired organ function. Next to increasing the trauma risk, binge drinking causes anti-inflammatory effects due to immunomodulatory properties of alcohol (ethanol, EtOH). The impact of clinically relevant acute binge drinking scenario on local and systemic inflammatory changes, notably regarding the activity and longevity of leukocytes, has been analyzed in a combinatory trauma model of TxT + H/R. Twenty-four female Lewis rats (190-240 g) received alcohol (5 g/kg, 30%) or saline gavage. Two hours after alcohol gavage, TxT with subsequent HS (60 min) and resuscitation (TxT + H/R) were induced. Sham-operated animals underwent surgical procedures. Bronchoalveolar lavage fluid (BAL), lung tissue, and blood were harvested 2 h after resuscitation. Pulmonary infiltration with PMN, IL-6 gene expression, systemic PMN activation, neutrophil and monocyte apoptosis (caspase-3/7), and pyroptosis/inflammasome activation (caspase-1) were evaluated. Lung damage was evaluated by hematoxylin-eosin (H/E) staining and determination of the total protein content in BAL (ANOVA, p < 0.05 was significant). TxT + H/R-induced increases in IL-6, PMN infiltration and BAL-protein concentration were significantly reduced by EtOH; however, histological morphology changes after trauma remained unaltered by EtOH. TxT + H/R-induced systemic leukocyte activation (increased CD11b and CD31, reduced CD62L expression) as well as inflammasome activation in monocytes were significantly diminished by EtOH. Apoptosis was prolonged only in PMN after TxT + H/R and was further prolonged by EtOH, an effect that was observed in sham animals as a trend as well. Acute EtOH exposure inhibits the activation of circulating leukocytes after trauma compared to controls. These EtOH-driven systemic changes may be associated with reduced infiltration with PMN after trauma as well as reduced local tissue inflammation.

Reduced NLRP3 Gene Expression Limits the IL-1ß Cleavage via Inflammasome in Monocytes from Severely Injured Trauma Patients.

OBJECTIVE: Traumatic injury or severe surgery leads to a profound immune response with a diminished functionality of monocytes and subsequently their IL-1ß release. IL-1ß plays an important role in host immunity and protection against infections. Its biological activation via IL-1ß-precursor processing requires the transcription of inflammasome components and their activation. Deregulated activity of NOD-like receptor inflammasomes (NLR) like NLRP3 that leads to the maturation of IL-1ß has been described in various diseases. While the role of other inflammasomes has been studied in monocytes, nothing is known about NLRP3 inflammasome after a traumatic injury. Here, the role of the NLRP3 inflammasome in impaired monocyte functionality after a traumatic injury was analyzed. MEASUREMENTS AND MAIN RESULTS: Ex vivo-in vitro stimulation of isolated CD14+ monocytes with lipopolysaccharide (LPS) showed a significantly higher IL-1ß secretion in healthy volunteers (HV) compared to trauma patients (TP) after admission. Reduced IL-1ß secretion was paralleled by significantly lowered gene expression of NLRP3 in monocytes from TP compared to those of HV. Transfection of monocytes with NLRP3-encoding plasmid recovered the functionality of monocytes from TP regarding the IL-1ß secretion. CONCLUSIONS: This study demonstrates that CD14+ monocytes from TP are significantly diminished in their function and that the presence of NLRP3 components is necessary in recovering the ability of monocytes to produce active IL-1ß. This recovery of the NLRP3 inflammasome in monocytes may imply a new target for treatment and therapy of immune suppression after severe injury.

Suppression of the interleukin-1ß-induced inflammatory response of human Chang liver cells by acute and subacute exposure to alcohol: an in vitro study.

AIM: To evaluate protective immunosuppressive dose and time-dependent effects of ethanol in an in vitro model of acute inflammation in human Chang liver cells. METHOD: The study was performed in 2016 and 2017 in the research laboratory of the Department of Trauma, Hand and Reconstructive Surgery, the University Hospital of the Goethe-University Frankfurt. Chang liver cells were stimulated with either interleukin (IL)-1ß or IL-6 and subsequently treated with low-dose ethanol (85 mmol/L) or high-dose ethanol (170 mmol/L) for one hour (acute exposure) or 72 hours (subacute exposure). IL-6 and IL-1ß release were determined by enzyme-linked immunosorbent assay. Neutrophil adhesion to Chang liver monolayers, production of reactive oxygen species, and apoptosis or necrosis were analyzed. RESULTS: Contrary to high-dose ethanol, acute low-dose ethanol exposure significantly reduced IL-1ß-induced IL-6 and IL-6-induced IL-1ß release (P<0.05). Subacute ethanol exposure did not change proinflammatory cytokine release. Acute low-dose ethanol exposure significantly decreased inflammation-induced formation of reactive oxygen species (P<0.05) and significantly improved cell survival (P<0.05). Neither acute nor subacute high-dose ethanol exposure significantly changed inflammation-induced changes in reactive oxygen species or survival. Acute and subacute ethanol exposure, independently of the dose, significantly decreased neutrophil adhesion to inflamed Chang liver cells (P<0.05). CONCLUSION: Acute treatment of inflamed Chang liver cells with ethanol showed its immunosuppressive potential. However, the observed effects were limited to low-dose setting, indicating the relevance of ethanol dose in the modulation of inflammatory cell response.

Danger signals in trauma.

This review summarizes a short list of currently discussed trauma-induced danger-associated molecular patterns (DAMP). Due to the bivalent character and often pleiotropic effects of a DAMP, it is difficult to describe its "friend or foe" role in post-traumatic inflammation and regeneration, both systemically as well locally in tissues. DAMP can be used as biomarkers to indicate or monitor disease or injury severity, but also may serve as clinically applicable parameters for better indication and timing of surgery. Due to the inflammatory processes at the local tissue level or the systemic level, the precise role of DAMP is not always clear to define. While in vitro and experimental studies allow for the detection of these biomarkers at the different levels of an organism-cellular, tissue, circulation-this is not always easily transferable to the human setting. Increased knowledge exploring the dual role of DAMP after trauma, and concentrating on their nuclear functions, transcriptional targets, release mechanisms, cellular sources, multiple functions, their interactions and potential therapeutic targeting is warranted.

Ethyl pyruvate ameliorates hepatic injury following blunt chest trauma and hemorrhagic shock by reducing local inflammation, NF-kappaB activation and HMGB1 release.

BACKGROUND: The treatment of patients with multiple trauma including blunt chest/thoracic trauma (TxT) and hemorrhagic shock (H) is still challenging. Numerous studies show detrimental consequences of TxT and HS resulting in strong inflammatory changes, organ injury and mortality. Additionally, the reperfusion (R) phase plays a key role in triggering inflammation and worsening outcome. Ethyl pyruvate (EP), a stable lipophilic ester, has anti-inflammatory properties. Here, the influence of EP on the inflammatory reaction and liver injury in a double hit model of TxT and H/R in rats was explored. METHODS: Female Lewis rats were subjected to TxT followed by hemorrhage/H (60 min, 35±3 mm Hg) and resuscitation/R (TxT+H/R). Reperfusion was performed by either Ringer`s lactated solution (RL) alone or RL supplemented with EP (50 mg/kg). Sham animals underwent all surgical procedures without TxT+H/R. After 2h, blood and liver tissue were collected for analyses, and survival was assessed after 24h. RESULTS: Resuscitation with EP significantly improved haemoglobin levels and base excess recovery compared with controls after TxT+H/R, respectively (p<0.05). TxT+H/R-induced significant increase in alanine aminotransferase levels and liver injury were attenuated by EP compared with controls (p<0.05). Local inflammation as shown by increased gene expression of IL-6 and ICAM-1, enhanced ICAM-1 and HMGB1 protein expression and infiltration of the liver with neutrophils were also significantly attenuated by EP compared with controls after TxT+H/R (p<0.05). EP significantly reduced TxT+H/R-induced p65 activation in liver tissue. Survival rates improved by EP from 50% to 70% after TxT+H/R. CONCLUSIONS: These data support the concept that the pronounced local pro-inflammatory response in the liver after blunt chest trauma and hemorrhagic shock is associated with NF-κB. In particular, the beneficial anti-inflammatory effects of ethyl pyruvate seem to be regulated by the HMGB1/NF-κB axis in the liver, thereby, restraining inflammatory responses and liver injury after double hit trauma in the rat.

Ethyl pyruvate reduces acute lung damage following trauma and hemorrhagic shock via inhibition of NF-κB and HMGB1.

OBJECTIVE: After blunt thoracic trauma (TxT) and hemorrhagic shock with resuscitation (H/R) intense local inflammatory response and cell loss frequently impair the pulmonary function. Ethyl pyruvate (EP) has been reported to improve the pathophysiologic derangements in models of acute inflammation. Here, we studied the effects of EP on inflammation and lung damage after TxT+H/R. METHODS: Twenty four female Lewis rats (180-240g) were randomly divided into 3 groups: two groups underwent TxT followed by hemorrhagic shock (35±3mmHg) for 60min and resuscitation with either Ringers-Lactat (RL) alone or RL supplemented with EP (EP, 50mg/kg). Sham operated animals underwent surgical procedures. Two hours later bronchoalveolar lavage fluid (BAL), lung tissue and blood were collected for analyses. RESULTS: EP significantly improved pO2 levels compared to RL after TxT+H/R. TxT+H/R induced elevated levels of lactate dehydrogenase, total protein concentration in BAL and lung damage as evidenced by lung histology; these effects were significantly reduced by EP. Local inflammatory markers, lung TNF-alpha protein levels and infiltration with polymorphonuclear leukocytes (PMNL) significantly decreased in EP vs. RL group after TxT+H/R. Indicators of apoptosis as reduced BCL-2 and increased FAS gene expression after TxT+H/R were significantly increased or decreased, respectively, by EP after TxT+H/R. EP reduced TxT+H/R-induced p65 phosphorylation, which was concomitant with reduced HMGB1 levels in lung sections. CONCLUSIONS: Taken together, TxT+H/R induced strong inflammatory response and apoptotic changes as well as lung injury which were markedly diminished by EP. Our results suggest that this might be mediated via NF-κB and/or HMGB1 dependent mechanism.

Ethanol Decreases Inflammatory Response in Human Lung Epithelial Cells by Inhibiting the Canonical NF-kB-Pathway.

BACKGROUND/AIMS: Alcohol (ethanol, EtOH) as significant contributor to traumatic injury is linked to suppressed inflammatory response, thereby influencing clinical outcomes. Alcohol-induced immune-suppression during acute inflammation (trauma) was linked to nuclear factor-kappaB (NF-ĸB). Here, we analyzed alcohol`s effects and mechanisms underlying its influence on NF-ĸB-signaling during acute inflammation in human lung epithelial cells. METHODS: A549-cells were stimulated with interleukin (IL)-1ß, or sera from trauma patients (TP) or healthy volunteers, with positive/negative blood alcohol concentrations (BAC), and subsequently exposed to EtOH (170 Mm, 1h). IL-6-release and neutrophil adhesion to A549 were analyzed. Specific siRNA-NIK mediated downregulation of non-canonical, and IKK-NBD-inhibition of canonical NF-ĸB signaling were performed. Nuclear levels of activated p50 and p52 NF-ĸB-subunits were detected using TransAm ELISA. RESULTS: Both stimuli significantly induced IL-6-release (39.79±4.70 vs. 0.58±0.8 pg/ml) and neutrophil adhesion (132.30±8.80 vs. 100% control, p<0.05) to A549-cells. EtOH significantly decreased IL-6-release (22.90±5.40, p<0.05) and neutrophil adherence vs. controls (105.40±14.5%, p<0.05). IL-1ß-induced significant activation of canonical/p50 and non-canonical/p52 pathways. EtOH significantly reduced p50 (34.90±23.70 vs. 197.70±36.43, p<0.05) not p52 activation. Inhibition of canonical pathway was further increased by EtOH (less p50-activation), while p52 remained unaltered. Inhibition of non-canonical pathway was unchanged by EtOH. CONCLUSION: Here, alcohol`s anti-inflammatory effects are mediated via decreasing nuclear levels of activated p50-subunit and canonical NF-ĸB signaling pathway.

Acute Alcohol Binge Deteriorates Metabolic and Respiratory Compensation Capability After Blunt Chest Trauma Followed by Hemorrhagic Shock-A New Research Model.

BACKGROUND: The clinical relevance of blunt (thoracic) chest trauma (TxT) and hemorrhagic shock is indisputable due to the high prevalence of this injury type, as well as its close association with mortality and/or preventable deaths. Furthermore, there is an ongoing discussion about the influence of alcohol in trauma patients. Thus, we established a model of TxT followed by hemorrhagic shock with resuscitation (H/R) in alcohol-intoxicated rats. METHODS: Depending on group allocation, 12 (subacute) or 2 (acute) hours before experimentation, the animals received a single oral dose of alcohol (ethanol [EtOH]) or saline (NaCl) followed by TxT, hemorrhagic shock (35 ± 3 mm Hg), and resuscitation (TxT + H/R). Arterial blood gas analyses and continuous monitoring of blood pressure were performed during the experimentation period. Survival during the experimentation procedure was determined. RESULTS: Subacute and acute EtOH group exhibited lower baseline mean arterial blood pressure values compared with the corresponding NaCl group, respectively. Both EtOH groups showed lower maximal bleed-out volume, which was necessary to induce hemorrhagic shock compared to NaCl groups, and the recovery during the resuscitation period was attenuated. During the experimentation in all groups, a trend to acidic pH was observed. Acute EtOH group showed lowest pH values compared to all other groups. Higher pCO2 values were observed in both EtOH groups. All groups developed negative base excess and decreasing HCO3- values until the end of hemorrhagic shock and showed increasing base excess and HCO3- values during resuscitation. Significantly higher mortality rate was found in the acute EtOH group. CONCLUSIONS: This study indicates that alcohol limits the metabolic and respiratory compensation capability, thereby promoting mortality.

Phagocytizing activity of PMN from severe trauma patients in different post-traumatic phases during the 10-days post-injury course.

OBJECTIVE: Phagocytizing leukocytes (granulocytes and monocytes) play a fundamental role in immunological defense against pathogens and clearance of cellular debris after tissue injury due to trauma. According to the "two-hit hypothesis", phagocytes become primed due to/after trauma. Subsequently, a secondary stimulus may lead to their exaggerated response. This immune dysfunction can result in serious infectious complications, also depending on trauma injury pattern. Here, we investigated the phagocytizing capacity of leukocytes, and its correlation to trauma injury pattern. MATERIAL/METHODS: Peripheral whole blood was taken daily from 29 severely injured trauma patients (TP, Injury Severity Score, ISS≥28) for ten days (1-10) following admission to the emergency department (ED). Sixteen healthy volunteers served as controls (HV). Samples were incubated with opsonized Staphylococcus aureus labelled with pHrodo fluorescent reagent and the percentage of phagocytizing activity was assessed by flow cytometry. Abbreviated Injury Scales (AIS)≥3 of head, chest and extremities were used for injury pattern analysis. RESULTS: Overall distribution of active phagocytes (out of 100% phagocytizing leukocytes) in TP included granulocytes with 28.6±1.5% and monocytes with 59.3±1.9% at ED, and was comparable to HV (31.5±1.6% granulocytes and 60.1±1.6% monocytes). The percentage of phagocytizing granulocytes increased significantly after D2 (39.1±1.2%), while the percentage of phagocytizing monocytes (52.0±1.2%, p<0.05) decreased after D2. These changes persisted during the whole time course. Phagocytizing activity of granulocytes (27.9±2.8%) and monocytes (55.2±3.3%) was significantly decreased at ED compared to HV (42.4±4.1% and 78.1±3.1%, respectively). After D2 up to D10, phagocytizing activity was significantly enhanced in granulocytes. Phagocytizing activity of monocytes remained decreased on D1 and has risen continuously during the ten days time course to values comparable to HV. No significant differences in phagocytosis could be associated to certain injury pattern. CONCLUSIONS: Our data demonstrate that the increasing percentage of phagocytizing granulocytes may indicate their enhanced mobilization out of bone marrow persisting until post-injury day 10. Furthermore, an initially decreased phagocytizing activity of granulocytes is strongly increased in the 10-days post-injury course. The altered activity of phagocytes due to injury could not be linked to any trauma injury pattern, and emerged rather as a general characteristic of phagocytes after severe trauma.

Alcohol Intoxication Reduces Systemic Interleukin-6 Levels and Leukocyte Counts After Severe TBI Compared With Not Intoxicated TBI Patients.

BACKGROUND: The effect of alcohol consumption on inflammatory state and outcome in brain-injured patients remains controversial. We analyzed the influence of positive blood alcohol concentration (BAC) on inflammatory changes, inhospital complications, and mortality in traumatic brain injury (TBI) patients. PATIENTS AND METHODS: Patients with an Injury Severity Score (ISS) at least 16 and Abbreviated Injury Scale of head (AIS-head) at least 3 were included upon arrival in the emergency room and grouped according to positive BAC (>0.5‰, BAC) vs. less than 0.5‰ alcohol (no BAC). Injury severity, vital signs, complications, mortality, and systemic interleukin (IL)-6 levels were prospectively determined, and BAC was quantified. According to ISS, AIS-head, age, and sex, we performed matched-pair analysis. RESULTS: A total of 101 TBI patients were included. Of them 74 patients were dedicated to no BAC group and 27 to BAC group. ISS was significantly higher in the no BAC group. Positive BAC group required significantly less packed red blood cells and fresh frozen plasma (P < 0.05). Shorter ICU stays were found in BAC-positive patients. Inhospital complications, including single/multiple organ failure, systemic inflammatory response syndrome, sepsis, pneumonia, and acute respiratory distress syndrome, showed no significant differences. Systemic IL-6 levels and leukocyte counts (IL-6: 65.0 ±â€Š8.0 vs. 151.8 ±â€Š22.3; leukocytes: 10.2 ±â€Š0.9 vs. 13.2 ±â€Š0.8, both P < 0.05) were significantly lower in BAC-positive patients. Matched-pair analysis was performed with 27 pairs. No significant differences in transfusions were monitored after matching. However, lowered systemic IL-6 levels and leukocyte counts in the BAC group were also detected after matching, indicating that this effect is ISS-independent. CONCLUSIONS: This study shows that positive BAC in TBI patients is associated with lower systemic IL-6 levels and leukocyte numbers, indicating that positive BAC may have immunosuppressive effects in this cohort of patients compared with TBI patients who were not alcohol intoxicated.

Influence of gender on systemic IL-6 levels, complication rates and outcome after major trauma.

BACKGROUND: While female gender was associated with lower rates of systemic inflammatory response syndrome (SIRS), sepsis and single and/or multiple organ failure (MOF), contradictory data suggest no correlation between gender and complication rates and/or outcome in trauma patients (TP). Here, we analyzed the gender influence on systemic interleukin (IL)-6 levels and outcome in TP. PATIENTS/METHODS: 343 TP with injury severity scores (ISS) ≥16 were included upon admittance to the emergency department (ED) and grouped to male (n=257) vs. female (n=86). Injury severity, vital signs, physiological parameters, length of intensive care unit (ICU) and in-hospital stay, outcome parameters including SIRS, sepsis, respiratory complications, single- and/or MOF and in-hospital mortality were analyzed. Systemic IL-6 levels during the first 10 post-injury days were determined daily. RESULTS: Age (45.0±1.0 vs. 48.2±2.1) and ISS (27.1±0.8 vs. 24.7±1.2) were comparable between both groups. Abbreviated Injury Scale (AIS) ≥3 of chest and abdominal body regions were significantly higher in male TP (chest:51.02% vs. 36.05%, abdomen:19.84% vs. 10.47%, p<0.05). IL-6 was significantly increased in male TP on post-injury days 1 and 2 (d1:363.9±72.58 vs. 163.7±25.98; d2:194.3±31.38 vs. 114.3±17.81pg/ml, p<0.05). Multivariate analysis excluded an association of increased chest or abdominal injury occurrence with IL-6 levels. Female vs. male TP had significantly lower SIRS and sepsis occurrence (SIRS:40.70% vs. 53.31%, sepsis:6.98% vs. 19.46%, p<0.05). There were no gender-based differences regarding ICU or in-hospital stay, single and/or MOF and respiratory complications. CONCLUSIONS: Taken together, higher systemic IL-6 levels after trauma are associated with enhanced susceptibility for SIRS and sepsis in male patients.