RESUMO
Background: Hormones play a modulating role in allergicinflammation. Hyperthyroidism may increase the severity ofasthma, and hypothyroidism may ameliorate coexistent asthma.The mechanisms regulating this interaction are not completelyunderstood.Objective: The purpose of this study was to test the hypothesisthat thyroid hormones influence the development of allergicairway inflammation after antigen challenge in rats.Methods: The experimental design included either sensitizedor nonsensitized surgically thyroidectomized and sham-operatedrats. Experiments were performed 50 days after surgery.Thyroidectomized rats and sham-operated controls were sensitizedby subcutaneous injection of ovalbumin (OVA) andAl(OH)3 and challenged 14 days later by OVA inhalation.Bronchoalveolar lavages were performed 24 hours after challenge.Results: Compared with controls, thyroidectomized animalspresented markedly decreased cell yields from bronchoalveolarlavage fluid after OVA challenge. The impaired responsewas not related to changes in the number of circulating leukocytes.Determination of antibody serum concentrations indicatedthat thyroidectomized rats presented a marked reductionin the level of anti-OVA IgE compared with controls, withoutsignificant differences in IgG1 and IgG2a serum concentrations.Reversal of the impaired responses was attained by 16-day treatment of hypothyroid animals with thyroxine, but notby 1- or 3-day treatment.Conclusion: The data presented suggest that the continuingdeficiency of thyroid hormones influences the development ofthe inflammatory component of asthma. This is due, at least inpart, to a decrease in the production of IgE. (J Allergy ClinImmunol 1999;104:595-600.).
