Does lung microenvironment contribute to the resistance of alveolar macrophages to develop tolerance to endotoxin*?
Our results support the conclusion that at homeostasis in the lungs, constitutive expression of granulocyte-macrophage colony-stimulating factor, interleukin-18, interferon-γ and possibly interleukin-15, and a cross-talk between B lymphocytes and alveolar macrophages create a microenvironment specific to the lungs that prevents alveolar macrophages from becoming tolerant to endotoxin.
In a swine model of catastrophic blunt hepatic injury, abdominal insufflation significantly decreased blood loss and mortality.