Lung responses to hypothyroidism, hyperthyroidism, and lipopolysaccharide challenge in rats

The objectives of this investigation were to study the effects of hypo- and hyperthyroidism on some factors involved in lung injury under basal condit ions (air exposure) and during an inflammatory response induced by inhalati on exposure to lipopolysaccharide (LPS; 100 mug/ml; 3 h) in adult rats. Thy roid status was altered by thyroidectomy or thyroxine injections for 15 d. Hyperthyroidism alone caused a greater degree of lung cell damage, an incre ase in the permeability of the alveolar-capillary barrier, a rise in the to tal number of phagocytic cells obtained by bronchoalveolar lavage (BAL), an d enhanced nitric oxide (NO) release by phagocytic cells relative to that i n euthyroid control animals. Hypothyroidism alone was associated with oppos ite effects. Exposure of animals to LPS produced inflammatory responses, wh ich included significant increases in lung cell damage, permeability of the alveolar-capillary barrier, number of phagocytic cells obtained by BAL, an d NO production by the phagocytic cells. In general, hyperthyroidism enhanc ed the effects of LPS, while hypothyroidism reduced LPS-induced responses. These results suggest that thyroid status alone can affect some of the fact ors involved in lung injury and also modulate some of the inflammatory effe cts of LPS. Hyperthyroidism tends to enhance lung injury, while hypothyroid ism seems to reduce lung injury.