Activated platelets enhance microparticle formation and platelet-leukocyte interaction in severe trauma and sepsis. Enhanced platelet-leukocyte interaction is dependent on P-selectin expression and may be involved in the systemic inflammatory response after severe inflammatory insult.

Severe trauma stimulated acute-phase priming in PMNL and inhibited apoptosis. Infections after trauma induced second-hit priming in PMNL, but the unchanged serum levels of thrombomodulin suggest that priming per se may not cause systemic vascular endothelial damage.

Sepsis-induced disseminated intravascular coagulation (DIC) is a major cause of death in patients admitted to intensive care units. Endothelial injury with microparticle production is reported in the pathogenesis of sepsis. Endothelial microparticles (EMPs) present several cell-specific surface antigens with different bioactivities, for example, tissue factor (TF), thrombomodulin (TM), and endothelial protein C receptor (EPCR). We investigated associations between these three different surface antigen–positive EMPs and sepsis-induced DIC. This cross-sectional study composed of 24 patients with sepsis and 23 healthy controls was conducted from November 2012 to September 2013. Blood samples were collected from patients within 24 h of diagnosis of severe sepsis and from healthy controls. Numbers of TF-positive EMPs (TF+ EMPs), TM-positive EMPs (TM+ EMPs), and EPCR-positive EMPs (EPCR+ EMPs) were measured by flow cytometry immediately thereafter. Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores were assessed in the severe sepsis patients at enrollment. We assessed DIC with the International Society of Thrombosis and Haemostasis (ISTH) overt DIC diagnostic criteria algorithm. Numbers of antigen-positive EMPs were increased significantly in both severe sepsis patients and controls and with the increase in ISTH DIC score. Numbers of TF+ EMPs and EPCR+ EMPs correlated significantly with Sequential Organ Failure Assessment score, and numbers of EPCR+ EMPs correlated significantly with Acute Physiology and Chronic Health Evaluation II score. Numbers of the three antigen-positive EMPs were increased significantly in severe sepsis patients versus those in healthy controls and with the increase of ISTH DIC score, suggesting that the specific bioactivity of each antigen-positive EMP may play a role in the progression of sepsis-induced DIC.

Activated vascular endothelial cells with increased procoagulant activity enhance production of microparticles with increased binding to leukocytes in patients with severe SIRS. Endothelial microparticles may be involved in the pathogenesis of endothelial injury after severe insult.

Innate immunity plays an important role in host defense after severe insult. gammadelta T lymphocytes are recognized as the first line of defense against microbial invasion. In this study, we evaluated gammadelta T lymphocytes in the peripheral blood of patients with severe systemic inflammatory response syndrome (SIRS), and examined on role of these cells. Thirty-seven patients with severe SIRS (SIRS criteria and serum C-reactive protein > or = 10 mg/dL) and 27 healthy volunteers were studied. Severe SIRS was caused by trauma in 14 patients (Injury Severity Score of 30.1 +/- 10.8) and by sepsis in 23 patients. The counts of gammadelta and alphabeta T lymphocytes were determined by flow cytometry of cells stained with monoclonal antibodies to gammadelta and alphabeta T lymphocyte receptors. The activation of these cells was evaluated by flow cytometry of cells stained with monoclonal antibodies to CD69 and HLA-DR. Serial counts and activation of gammadelta and alphabeta T lymphocytes were also determined in eight trauma patients (Injury Severity Score of 31.0 +/- 13.5) during a 2-week observation period. The count of gammadelta T lymphocytes in the peripheral blood of SIRS patients (30.1 +/- 6.0/microL) was significantly lower (P < 0.05) than that of the healthy volunteers (104.3 +/- 10.9/microL). The expression of CD69, an index of early activation of T lymphocytes, was significantly greater on gammadelta T lymphocytes from SIRS patients (patients 23.9% +/- 3.4%, healthy controls 4.8% +/- 0.6%, P < 0.05). In trauma patients, the expression of CD69 on gammadelta T lymphocytes increased rapidly within 48 h after injuries. In conclusion, gammadelta T lymphocytes are activated and decreased in the peripheral blood of severe SIRS patients. In trauma patients, the activation of gammadelta T lymphocytes occurs in the fairly acute phase after injuries. These results suggest a significant role for gammadelta T lymphocytes as early responders after severe insult.