Traumatic injury produces excessive proinflammatory mediators and subsequent activating or recruiting immune cells into the target organs and results in systemic inflammatory response. Furthermore, traumatic injury is usually combined with massive blood loss and causes hemorrhagic shock that induces the development of organ dysfunction. Inflammatory response is usually associated with various traumatic insults. The injured organ increased the expression of local chemokine and cytokine levels, which include cytokine-induced neutrophil chemoattractant-1, intercellular adhesion molecule-1, and interleukin-6. The chemokines, adhesion molecules, and their receptors are the main regulators of leukocyte and T cell trafficking under homeostatic and inflammatory conditions. Traumatic injury is a significant clinical problem in the fields of trauma, inflammation, surgery, anesthesiology, critical care medicine, and so forth. However, the complex pathways and mechanisms of inflammatory responses on traumatic injury have not been clearly elucidated.

Therefore, we invite researchers and clinicians to submit original articles as well as review articles associated with inflammatory responses to traumatic injury. We are particularly interested in articles describing new insights and new findings on the effectiveness or mechanisms of inflammatory responses to injury. The work could be from animal studies, human studies, and clinical trials and may include anti-inflammatory prevention and treatment of traumatic injury.

Potential topics include, but are not limited to:

• Clinical and animal researches in inflammation
• Animal models of traumatic injury
• Effect and mechanism of inflammatory mediators of traumatic injury
• Immune responses and inflammatory processes after traumatic injury
• Current research and development with inflammatory aspects on traumatic injury
• New aspects of therapeutic strategies of anti-inflammatory prevention and treatment of traumatic injury