Regulatory effects of adrenal gland products in IgG immune complex acute lung injury

Adrenal gland-derived corticosterone and epinephrine are thought to function as endogenous antiinflammatory mediators of inflammatory injury. To determine whether adrenalectomy impacts inflammatory processes associated with IgG immune complex-mediated acute lung injury, adrenalectomized and sham adrenal-ectomized Long Evans rats were treated with IgG or saline intratracheally. IgG immune complex lung injury resulted in a two-fold increase in pulmonary vascular permeability for serum albumin in adrenalectomized rats, compared to adrenal-intact animals. This increase in injury was associated with increases in NF-κB activity in whole lung homogenates, bronchoalveolar lavage fluid TNFα concentrations, pulmonary vascular ICAM-1 expression and whole lung myeloperoxidase activity. Adrenalectomy did not alter nitric oxide content in bronchoalveolar lavage fluid. Adrenalectomized saline-treated rats also had increased ICAM-1 expression and pulmonary vascular permeability, compared to saline-treated adrenal-intact sham animals. These data suggest that adrenal gland-derived mediators regulate either directly or indirectly several parameters of inflammatory signaling and activation in the IgG immune complex-injured lung.