Expression of tumor necrosis factor and c-fos genes in peritoneal macrophages of hypothyroid mice.

It is well documented that hypothyroid patients are more susceptible to microbial infections. In order to study whether this impaired response is due to a decrease in production of antitumor molecules or an impaired ability to transmit information in the macrophage, a hypothyroid animal model was used to study the expression of both tumor necrosis factor gene and c-fos protooncogene in peritoneal macrophages. Inbred mice were rendered hypothyroid by an antithyroid drug, methimazole, and the expression of tumor necrosis factor gene and c-fos protooncogene in peritoneal macrophages were studied. Impairment of c-fos and TNF genes were at both transcriptional and translational levels using northern blot analysis, bioassays, and immunocytochemical staining methods. These results indicate that the reduction in signal transduction and in the production of antitumor molecules may cause the poor defense ability of hypothyroid animals.