Traumatic injury is the leading cause of death from ages 1-44 in the United States, responsible for over 2 million hospital admissions per year and approximately 200,000 deaths annually, with a similar impact globally. Bleeding is the leading cause of preventable death in these patients, where traumatic coagulopathy is diagnosed in ~25% of polytrauma patients and its presence increases mortality risk by 4-fold. It is widely recognized that the profound immunoinflammatory responses to major injury are a driver, if not the predominant cause, of coagulation perturbations that contribute to these early coagulopathies. Conversely, coagulopathy is a harbinger of delayed complications like organ failure, sepsis, and delayed death that are rooted in dysregulated immune function. While there is a clear link between coagulation and immune responses to generate such immunocoagulopathies, targeted therapies to improve outcomes have remained elusive.
This issue will focus on providing both expert reviews and original science in traumatic immunocoagulopathy and immunopathology. A primary goal will be to highlight areas of active research and potential therapeutic opportunities to improve survival after traumatic injury through improved understanding of the cellular and molecular intercommunication of the immune response to traumatic injury and the coagulation system.
Both Original Research and expert Review articles will be considered for publication. While non-exhaustive, the principal areas of interest to highlight the integral role of the immune system and coagulation in influencing one another after major traumatic injury include:
- The intercommunication between cellular immune responses to trauma (e.g. neutrophils, monocytes) and coagulation/fibrinolysis responses to trauma
- The intercommunication between molecular immune responses to trauma (e.g. complement, chemokines/cytokines) and coagulation/fibrinolysis responses to trauma
- The role of platelets in altering immune responses and generation of coagulopathy after injury
- The role of the endothelium in recruiting and integrating these pathologic communications between immune system responses and coagulation/fibrinolysis perturbations after injury
Traumatic injury is the leading cause of death from ages 1-44 in the United States, responsible for over 2 million hospital admissions per year and approximately 200,000 deaths annually, with a similar impact globally. Bleeding is the leading cause of preventable death in these patients, where traumatic coagulopathy is diagnosed in ~25% of polytrauma patients and its presence increases mortality risk by 4-fold. It is widely recognized that the profound immunoinflammatory responses to major injury are a driver, if not the predominant cause, of coagulation perturbations that contribute to these early coagulopathies. Conversely, coagulopathy is a harbinger of delayed complications like organ failure, sepsis, and delayed death that are rooted in dysregulated immune function. While there is a clear link between coagulation and immune responses to generate such immunocoagulopathies, targeted therapies to improve outcomes have remained elusive.
This issue will focus on providing both expert reviews and original science in traumatic immunocoagulopathy and immunopathology. A primary goal will be to highlight areas of active research and potential therapeutic opportunities to improve survival after traumatic injury through improved understanding of the cellular and molecular intercommunication of the immune response to traumatic injury and the coagulation system.
Both Original Research and expert Review articles will be considered for publication. While non-exhaustive, the principal areas of interest to highlight the integral role of the immune system and coagulation in influencing one another after major traumatic injury include:
- The intercommunication between cellular immune responses to trauma (e.g. neutrophils, monocytes) and coagulation/fibrinolysis responses to trauma
- The intercommunication between molecular immune responses to trauma (e.g. complement, chemokines/cytokines) and coagulation/fibrinolysis responses to trauma
- The role of platelets in altering immune responses and generation of coagulopathy after injury
- The role of the endothelium in recruiting and integrating these pathologic communications between immune system responses and coagulation/fibrinolysis perturbations after injury
