Lung responses to hypothyroidism, hyperthyroidism, and lipopolysaccharide challenge in rats.
Huffman LJ; Judy DJ; Rao KMK; Frazer DG; Goldsmith WT
J Toxicol Environ Health, A 2000 Dec; 61(7):623-639
The objectives of this investigation were to study the effects of hypo- and hyperthyroidism on some factors involved in lung injury under basal conditions (air exposure) and during an inflammatory response induced by inhalation exposure to lipopolysaccharide (LPS; 100 microg/ml; 3 h) in adult rats. Thyroid status was altered by thyroidectomy or thyroxine injections for 15 d. Hyperthyroidism alone caused a greater degree of lung cell damage, an increase in the permeability of the alveolar-capillary barrier, a rise in the total number of phagocytic cells obtained by bronchoalveolar lavage (BAL), and enhanced nitric oxide (NO) release by phagocytic cells relative to that in euthyroid control animals. Hypothyroidism alone was associated with opposite effects. Exposure of animals to LPS produced inflammatory responses, which included significant increases in lung cell damage, permeability of the alveolar-capillary barrier, number of phagocytic cells obtained by BAL, and NO production by the phagocytic cells. In general, hyperthyroidism enhanced the effects of LPS, while hypothyroidism reduced LPS-induced responses. These results suggest that thyroid status alone can affect some of the factors involved in lung injury and also modulate some of the inflammatory effects of LPS. Hyperthyroidism tends to enhance lung injury, while hypothyroidism seems to reduce lung injury.
Lung disorders; Pulmonary system disorders; Respiratory system disorders; Inhalation studies; Exposure levels; Laboratory animals; Animals; Animal studies; Phagocytic activity; Phagocytes; Thyroid gland disorders; Endocrine system disorders; Endocrinology
Linda Huffman, PhD, M/S 2015, NIOSH, 1095 Willowdale Road, Morgantown, WV 26505, USA
Journal of Toxicology and Environmental Health, Part A: Current Issues