Clinical and basic studies have suggested that interleukin 2 (IL-2) plays an important role for the development of pulmonary edema. However, its precise mechanism is still undetermined. For the resolution of pulmonary edema, alveolar fluid clearance is essential, and this clearance is known to be dependent of ion transport ability of alveolar epithelial cells. In this study, we determined the effects of IL-2 on alveolar fluid clearance.
Isotonic 5% albumin solutions with pharmacological treatments were instilled into the distal airways in the isolated rat lungs. The lungs were inflated with 100% oxygen at 8cm H2O and placed in a humid incubator at 37°C. Alveolar fluid clearance was estimated by the progressive increase in the albumin concentration over 1h.
Seven male S-D rats were used in each group. IL-2 stimulation caused dose-dependent increase in alveolar fluid clearance (Control, IL-2 (50U/ml), IL-2 (5000U/ml), vs. IL-2 (10000U/ml): 15.8±1.8%, 15.3±1.5%, 21.8±1.0%, vs. 24.6±1.7: P<0.05). Terbutaline (β adrenergic receptor agonist) caused significant increase in alveolar fluid clearance (27.8±1.1%), and this increase was inhibited by propranolol (β adrenergic receptor blocker). In contrast, propronolol did not inhibit the IL-2 stimulation.
This study indicates that IL-2 increases alveolar fluid clearance in the isolated rat lungs. Because the stimulatory effect by IL-2 is not inhibited by propranolol, IL-2 may increase alveolar fluid clearance via non-β adrenergic receptor mediated pathway.
Intravenous administration of IL-2 has been shown to cause pulmonary edema. However, our results suggest that IL-2 stimulates transalveolar fluid transport for clearance of excess edema fluid. This study was supported by Grant for Promoted Research from Kanazawa Medical University (S2003-8).
Makoto Sugita, None.