The non-obese diabetic (NOD) mouse: an animal model for autoimmune thyroiditis.

The NOD mouse, an ideal model for insulin-dependent diabetes mellitus, is also useful to study the pathogenesis of autoimmune thyroiditis. Spontaneous thyroiditis greatly varies in frequency among NOD colonies, but Hashimoto-like thyroiditis can be induced in two experimental models: goiter involution after iodide administration and immunization by TSH receptor, described hereunder.

What could mice tell us about goiter or other benign thyroid diseases?

Several lines of research have been developed by using mice as animal models, including goiter development and involution, nodules formation and congenital hypothyroidism. They are reviewed and discussed as potential tools to better understand the thyroid pathophysiology.

Two-step development of Hashimoto-like thyroiditis in genetically autoimmune prone non-obese diabetic mice: effects of iodine-induced cell necrosis.

The administration of a high iodide dose (HID; 10 micrograms/day) to goitrous mice is known to induce thyroid cell necrosis and inflammation, which, in most strains, is transient. In this study, we analyzed the effects of iodide in autoimmune prone non-obese diabetic (NOD) mice. Control NOD mice fed a standard diet (MID; 1 microgram I/day) or HID did not spontaneously develop thyroiditis. In NOD mice previously made goitrous, HID provoked thyroid cell necrosis and diffuse inflammation within 4 days. Inflammatory cells consisted of MHC-class II+ antigen-presenting cells, CD4+ T helper cells and CD8+ T suppressor/cytotoxic cells. After 96 days of treatment with HID, thyroiditis similar to Hashimoto's disease was obtained in 100% of the animals, with destruction of thyroid follicles, large clusters of T and B cells, and antithyroid antibodies in the plasma. When treating goitrous mice with MID, no cell necrosis was observed and no autoimmune thyroiditis was obtained. The early iodide-induced cell necrosis and inflammation may thus be considered as an important factor in the induction and persistence of autoimmune thyroiditis in individuals carrying a genetic susceptibility to autoimmune disease.

AIDS-associated cryptococcosis in Bujumbura, Burundi: an epidemiological study.

Cryptococcus neoformans var. neoformans was isolated from domestic dust in 54% of houses occupied or recently occupied by AIDS+ cryptococcosis patients and in 20% of control houses randomly chosen in Bujumbura, Burundi. It was not isolated from wards of similar patients in the University Hospital. This seems to prove that patients could not contaminate their own environment and that the presence of C. neoformans var. neoformans had another origin. In 40% of the cases, patients admitted contact with pigeons in the city and pigeon coops are frequently positive. We are convinced that the pigeon coops of the city play a part in the contamination of HIV+/AIDS patients; however, some patients denied any contact with pigeons and in these cases, the only possible source of contamination identified thus far is domestic dust, although the origin of the yeast remains unknown.

PIP: Researchers took 800 samples from the environment in Bujumbura, Burundi to examine the role of Cryptococcus neoformans var. neoformans in HIV positive/AIDS patients. Specifically they took 375 dust samples from 25 houses of 24 AIDS patients with cryptococcosis (1 patient had 2 homes). 5 of the these patients lived in 1 area. So the researchers also took control samples from the same area. They also obtained contact plate samples from 10 internal medicine wards (4 with AIDS/Cryptococcosis patients, 2 AIDS patients who did not have cryptococcosis, and 4 vacant wards) in Kamenge University Hospital. The researchers isolated C. neoformans var. neoformans in the dust of 54% of the homes either occupied or recently occupied by the patients and in the dust of 20% of the control homes. Further 40% of the patients reported contact with pigeons. In fact, the researchers were able to sample the avian source of 25% (6) of all patients. They detected high doses of C. neoformans in 5 of the 6 pigeon coops. In those patients who did not report contact with pigeons, the researchers assumed these patients contracted cryptococcosis from spores in domestic dust. No spores were evident in the hospital wards including those with AIDS patients with cryptococcosis. Even though the researchers experiments with dissemination of spores did not reveal the extent of contamination they expected, they were sure that pigeon coops do play a contributory role in contaminating HIV positive and AIDS patients. Further they were concerned that AIDS patients who have received successful cryptococcosis treatment could be reinfected by returning to a home contaminated with dust harboring spores.