Human acute inflammatory recovery is defined by co-regulatory dynamics of white blood cell and platelet populations

Inflammation is the physiologic reaction to cellular and tissue damage caused by trauma, ischemia, infection, and other pathologic conditions. Elevation of white blood cell count (WBC) and altered levels of other acute phase reactants are cardinal signs of inflammation, but the dynamics of these changes and their resolution are not well established. Here we studied inflammatory recovery from trauma, ischemia, and infection by tracking longitudinal dynamics of clinical laboratory measurements in hospitalized patients. We identified a universal recovery trajectory defined by exponential WBC decay and delayed linear growth of platelet count (PLT). Co-regulation of WBC-PLT dynamics is a fundamental mechanism of acute inflammatory recovery and provides a generic approach for identifying high-risk patients: 32x relative risk (RR) of adverse outcomes for cardiac surgery, 9x RR of death from COVID-19, 9x RR of death from sepsis, and 5x RR of death from myocardial infarction. Inflammation is a protective response of the body. Here, authors show that healthy inflammation induces remarkably consistent changes in white cell and platelet populations, regardless of the underlying cause, including heart attack, infection and trauma.

Automated summary

The study examines the recovery process of inflammation caused by trauma, ischemia, and infection by tracking the longitudinal dynamics of clinical laboratory measurements in hospitalized patients. The findings reveal a universal recovery trajectory characterized by exponential white blood cell decay and delayed linear growth of platelet count. The co-regulation of white blood cells and platelet dynamics provides a generic approach for identifying high-risk patients and predicting adverse outcomes.