Allergic airway inflammation in hypothyroid rats

Background: Hormones play a modulating role in allergic inflammation. Hyper thyroidism may increase the severity of asthma, and hypothyroidism may amel iorate coexistent asthma. The mechanisms regulating this interaction are no t completely understood. Objective: The purpose of this study was to test the hypothesis that thyroi d hormones influence the development of allergic airway inflammation after antigen challenge in rats. Methods: The experimental design included either sensitized or nonsensitize d surgically thyroidectomized and sham-operated rats. Experiments were perf ormed 50 days after surgery. Thyroidectomized rats and sham-operated contro ls were sensitized by subcutaneous injection of ovalbumin (OVA) and Al(OH)( 3) and challenged 14 days later by OVA inhalation. Bronchoalveolar lavages mere performed 24 hours after challenge. Results: Compared with controls, thyroidectomized animals presented markedl y decreased cell yields from bronchoalveolar lavage fluid after OVA challen ge. The impaired response was not related to changes in the number of circu lating leukocytes, Determination of antibody serum concentrations indicated that thyroidectomized rats presented a marked reduction in the level of an ti-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 th yroid hormones influences the development of the inflammatory component of asthma. This is due, at least in part, to a decrease in the production of I gE.