Asakawa H, Miyagawa J, Kobayashi T, Hanafusa T, Kuwajima M, Matsuzawa Y
Second Department of Internal Medicine, Osaka University Medical School, Japan.
Immunopharmacology. 1996 Sep;34(2-3):131-7. doi: 10.1016/0162-3109(96)00126-9.
Interleukin (IL-1), an inflammatory cytokine that is detected in the thyroid tissues of patients with autoimmune thyroiditis, is believed to be involved in the disease process. To clarify the role of IL-1 in the development of autoimmune thyroiditis, we investigated the effects of interleukin-1 beta (IL-1 beta) on the morphology of human thyrocytes in monolayer culture as well as the effect on thyroid peroxidase (TPO) content of these cells. Human normal thyrocytes were cultured with IL-1 beta for 4 days in the presence and absence of TSH. In morphologic studies, cultured cells were fixed for examination by scanning electron microscopy and for immunofluorescent staining of acting filaments. IL-1 produced striking morphologic changes in the cultured thyrocytes, including the cytoplasmic retraction and dissociation and/or depolymerization of actin filaments. These changes were unrelated to TSH stimulation. For detection of TPO, cultured cells were stained by an immunofluorescent technique and analyzed by fluorescence photometry. IL-1 reduced the TPO content and inhibited the TSH-induced increase in TPO in a concentration-dependent manner. These morphological changes and the reduction in TPO content of cultured thyrocytes suggest that IL-1 modulates the pathophysiology of autoimmune thyroiditis.