Patients in the ICU are already predisposed to nosocomial infections, which are both costly and potentially life threatening, and it appears that the immune paralysis of sepsis may put these patients at greater risk for secondary infections, though this has not been proven conclusively. One measure of this sepsis-induced immune suppression is monocyte deactivation. The investigators hypothesize that, as a cornerstone of the monocytic innate immune response to infection, the inflammasome is critical to monocyte function during sepsis.
Sepsis is a systemic inflammatory response to a severe infection. Despite the high incidence and societal costs of sepsis, the mechanism by which it kills remains unclear. The pathophysiology of sepsis is not completely understood, but many investigators now believe that sepsis induces a prolonged state of immune suppression. This study will attempt to quantify the degree of immune suppression during the first 5 days of sepsis by measuring the immune function of peripheral blood monocytes and the inflammasome constituent proteins in peripheral blood monocytes and alveolar macrophages.
Study Type
OBSERVATIONAL
Enrollment
50
The Ohio State University
Columbus, Ohio, United States
Immune suppression during the recovery from critical illness is greater in severe sepsis patients compared to non-septic patients.
Blood and BAL fluid will be collected at Day 1
Time frame: Day 1
Immune suppression during the recovery from critical illness is greater in severe sepsis patients compared to non-septic patients.
Blood and BAL fluid will be collected at Day 3
Time frame: Day 3
Immune suppression during the recovery from critical illness is greater in severe sepsis patients compared to non-septic patients.
Blood and BAL fluid will be collected at Day 5
Time frame: Day 5
This platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.