We found that endotoxemia induced IL-1α expression during the saccular stage of neonatal lung development and was not present in the other neonatal organs or the adult lung.
At postoperative day 7, the sepsis-positive group continued to demonstrate an increase in intestinal permeability, endotoxemia and elastase; a significant difference was observed between the two groups (P = 0.02), whereas there was no significant difference in IL-1, IL-6, and CRP levels.
Endotoxin, a constituent of Gram-negative bacteria, stimulates macrophages to release large quantities of tumor necrosis factor (TNF) and interleukin-1 (IL-1), which can precipitate tissue injury and lethal shock (endotoxemia).