Immunohistochemical expression of E-selectin in sepsis-induced lung injury

The vascular endothelium controls leukocyte extravasation into tissue by the induction and modulation of endothelial cell adhesion molecules, such as E-selectin (CD62E). E-selectin is not expressed by non-stimulated endothelium, but is activated by cytokines and initiates neutrophil recruitment in sepsis-induced lung injury. The aim of the present study was to assess the value of the immunohistochemical expression of endothelial E-selectin for the post-mortem differentiation between death due to sepsis and death due to other causes. The immunohistochemical expression of E-selectin was investigated in lung specimens obtained at autopsy from sepsis-associated fatalities (n = 6), possible sepsis-associated fatalities (n = 7), non-sepsis group I (death due to unnatural causes, e.g. trauma, electrocution, drowning, hanging n = 17) and non-sepsis group II fatalities (death due to natural causes, e.g. myocardial infarction, intracerebral bleeding n = 7). E-selectin was detected in paraffin sections using the ABC technique and the expression was scored semiquantitatively by evaluating the intensity and incidence of positively stained endothelium of the interstitial pulmonary microvasculature. E-selectin was strongly expressed in all cases of the definite sepsis group, in 29% of the possible sepsis-associated fatalities and in only 4% of the cases in the non-sepsis groups I and II. In comparison to all other study groups, E-selectin expression in the definite sepsis group differed significantly (p < 0.05). Cases with inflammatory and mechanical lung tissue alterations from the control groups showed no positive immunohistochemical reaction for E-selectin; therefore, false positive results should not be expected in non-sepsis cases. Our findings suggest that the immunohistochemical detection of an intense expression of E-selectin in lung tissue may prove to be a valuable diagnostic tool in the forensic post-mortem elucidation of death due to sepsis.