BACKGROUND: Hormones play a modulating role in allergic inflammation. Hyperthyroidism may increase the severity of asthma, and hypothyroidism may ameliorate coexistent asthma. The mechanisms regulating this interaction are not completely understood. OBJECTIVE: The purpose of this study was to test the hypothesis that thyroid hormones influence the development of allergic airway inflammation after antigen challenge in rats. METHODS: The experimental design included either sensitized or nonsensitized surgically thyroidectomized and sham-operated rats. Experiments were performed 50 days after surgery. Thyroidectomized rats and sham-operated controls were sensitized by subcutaneous injection of ovalbumin (OVA) and Al(OH)(3) and challenged 14 days later by OVA inhalation. Bronchoalveolar lavages were performed 24 hours after challenge. RESULTS: Compared with controls, thyroidectomized animals presented markedly decreased cell yields from bronchoalveolar lavage fluid after OVA challenge. The impaired response was not related to changes in the number of circulating leukocytes. Determination of antibody serum concentrations indicated that thyroidectomized rats presented a marked reduction in the level of anti-OVA IgE compared with controls, without significant differences in IgG(1) and IgG(2a) serum concentrations. Reversal of the impaired responses was attained by 16-day treatment of hypothyroid animals with thyroxine, but not by 1- or 3-day treatment. CONCLUSION: The data presented suggest that the continuing deficiency of thyroid hormones influences the development of the inflammatory component of asthma. This is due, at least in part, to a decrease in the production of IgE.
BACKGROUND: Hormones play a modulating role in allergic inflammation. Hyperthyroidism may increase the severity of asthma, and hypothyroidism may ameliorate coexistent asthma. The mechanisms regulating this interaction are not completely understood. OBJECTIVE: The purpose of this study was to test the hypothesis that thyroid hormones influence the development of allergic airway inflammation after antigen challenge in rats. METHODS: The experimental design included either sensitized or nonsensitized surgically thyroidectomized and sham-operated rats. Experiments were performed 50 days after surgery. Thyroidectomized rats and sham-operated controls were sensitized by subcutaneous injection of ovalbumin (OVA) and Al(OH)(3) and challenged 14 days later by OVA inhalation. Bronchoalveolar lavages were performed 24 hours after challenge. RESULTS: Compared with controls, thyroidectomized animals presented markedly decreased cell yields from bronchoalveolar lavage fluid after OVA challenge. The impaired response was not related to changes in the number of circulating leukocytes. Determination of antibody serum concentrations indicated that thyroidectomized rats presented a marked reduction in the level of anti-OVA IgE compared with controls, without significant differences in IgG(1) and IgG(2a) serum concentrations. Reversal of the impaired responses was attained by 16-day treatment of hypothyroid animals with thyroxine, but not by 1- or 3-day treatment. CONCLUSION: The data presented suggest that the continuing deficiency of thyroid hormones influences the development of the inflammatory component of asthma. This is due, at least in part, to a decrease in the production of IgE.