Severe trauma to the chest with pulmonary contusion still causes approximately a quarter of all civil trauma-related deaths [
1]. Especially for lung injury inflicted by blasts (e.g. in the crime/military setting), the underlying pathophysiology and development of the inflammatory response is still poorly understood [
2]. Various biological mediators seem to play a central role in the pathophysiology of blunt chest trauma, including cytokines, complement (e.g. C5a) and coagulation factors [
3]. Persistent elevation of pro-inflammatory cytokines in the lungs with subsequent suppression (or increasing paralysis) of the immune system is associated with an enhanced risk for acute lung injury (ALI) progression and is known to increase mortality. We have previously demonstrated, that lung contusion is the major contributor to posttraumatic inflammation even in combined injury and in the presence of hemorrhagic shock, suggesting that the degree of pulmonary inflammation is an important determinant for the clinical course post-trauma [
4]. Many cytokines and other pro-inflammatory mediators, such as complement activation products, involved in the development and progression of ALI are known to be regulated via the transcriptional regulatory factor nuclear factor (NF)-κB. Yet, ALI is a highly complex poly-etiological syndrome, which cannot only be triggered by various local damage (such as lung contusion, blunt chest trauma, pneumonia or ventilatory damage to the lung [
2]), but it may also be triggered by limited remote injury (such as long bone fractures, head trauma) and also by different systemic insults such as large volume blood transfusions, burn injuries, shock, polytrauma [
5], systemic inflammatory response syndrome (SIRS) and sepsis. However, the underlying changes in protein expression profiles are rather speculative. Therefore, in the present study, we used a 9240 element rat cDNA microarray to analyze pulmonary gene-expression patterns in a well-characterized rat model of blunt chest trauma [
6]. Various pro-inflammatory mediators are currently routinely measured in plasma in the face of a very dynamic and rapidly changing environment in trauma to assess the “trauma load” and serve as predictive markers for the patient´s course and outcome [
7]. In contrast, data from and extrapolations to individual organs are hardly achievable in the clinical setting. Based on our blunt chest trauma model, microarray analysis of pulmonary gene expression may provide important insights into the pulmonary pathophysiology after blunt chest trauma, which might ultimately help to mitigate or, perhaps, prevent the progression to ALI/ARDS. Furthermore, the present findings identify potential new candidates and facilitate prediction of the clinical outcome supporting the development of new therapeutic strategies.