PRO-INFLAMMATORY EFFECTS OF EXPERIMENTAL HYPERTHYROIDISM IN COLON OF MICE (IMMUNOHISTOCYTOCHEMICAL STUDY)

Thyroid hormones can exert responses in various immune cells affecting several inflammation-related processes. The interactions between the endocrine and immune systems have been shown to contribute to pathophysiological conditions. Aim of study - to answer the question if hyper- or/and hypothyroid state can be as provoking factor for inflammation in colon. The study was performed on 60 mature male mice of the inbred line C3H-A. On male mice was reproduced a model of experimental hyperthyroidism and hypothyroidism by oral intake of L-thyroxin and propylthyouracil, accordingly. By the 22nd week of the experiment all animals were sacrificed. The rectum was removed for histo- and immunocytochemical examination. In histological examination in hyperthyroid group the hypertrophy of the mucous membrane of the colon is detected. Simultaneously the frequency of cell mitosis is increased. Among the epithelium glands of the colon can clearly be seen apoptotic bodies. Moderate or expressed infiltration by lymphocytes and plasma cells is elucidated in mucous membrane of colon relatively to mucous membrane of colon of euthyroid group i.e. control one. In hyporthyroid group the hyportrophy of the mucous membrane of the colon was detected. The lymphocytic infiltration is not found. In immunocytochemical examination the frequency of CD20 and CD56 positive cells was significantly higher (>23%) in cytological preparation of membrane mucous of colon from hyperthyroid mice (p<0.01). Meanwhile CD20 and CD56 positive cells were detected in single cases in cytological preparation of membrane mucous of colon from hypothyroid mice. The same observation was done for healthy membrane mucous from control (euthyroid) group. It is possible that the thyroid status is one of the factors modulating the inflammation. This discussion is far from over, because it is unclear whether prolonged hyperthyroidism can actually activate pro-inflammatory reactions, which subsequently, in turn, activate carcinogenesis.