The final RF model resulted in five variables for SS (Penetrating Abdominal Trauma Index, serum epidermal growth factor, monocyte chemoattractant protein-1, interleukin-6, and eotaxin) and four variables for OSI (Penetrating Abdominal Trauma Index, serum epidermal growth factor, monocyte chemoattractant protein-1, and interleukin-8).
C-reactive protein (CRP), interleukin (IL)-6, IL-8 and procalcitonin (PCT) consistently predict bacteraemia and severe sepsis; other outcomes have highly heterogeneous results.
Baseline lHSP72 was higher in SS (p < 0.03), and mHSP72 in SIRS (p < 0.02), compared to H. Only HS induced l/mHSP72/mRNA HSP72; LPS induced IL-6, IL-8, IL-10, and MCP-1.
Genotypes GG of rs2569190 (the CD14 gene) and AT of rs4073 (the IL8 gene) were associated with a significantly increased risk of developing severe sepsis (p = 0.05 and p = 0.01).
In conclusion, LPS stimulation of endothelial cells causes activation of the IL-8-Nox1 axis, enhances the production of ROS, and ultimately contributes to the progression of severe sepsis.