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YOJIRO KAWABE, KATSUMI EGUCHI, CHIKAKO SHIMOMURA, MASANOBU MINE, TOSHIO OTSUBO, YUKITAKA UEKI, HIROSHI TEZUKA, HIDETO NAKAO, ATSUSHI KAWAKAMI, KIYOSHI MIGITA, SHUNICHI YAMASHITA, MAYUMI MATSUNAGA, NAOFUMI ISHIKAWA, KUNIHIKO ITO, SHIGENOBU NAGATAKI, Interleukin-1 Production and Action in Thyroid Tissue, The Journal of Clinical Endocrinology & Metabolism, Volume 68, Issue 6, 1 June 1989, Pages 1174–1183, https://doi.org/10.1210/jcem-68-6-1174
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Abstract
This study was undertaken to determine the effects of interleukin-1 (IL-1) on human thyroid epithelial cells (thyrocytes) and whether thyrocytes produce IL-1. The supernatants of cultured peripheral blood monocytes stimulated with lipopolysaccharide (LPS) increased [3H]thymidine incorporation into thyrocytes from normal subjects and patients with Graves’ disease. The IL-1 levels of cultured supernatants of monocytes were measured by a thymocyte costimulation assay and a solid phase sandwich immunoenzymometric assay. The supernatants of monocyte cultures stimulated with LPS contained significant amounts of IL-1 bioactivity and IL-lα and IL-1β immunoactivity. Recombinant IL-1β (rIL-1β) also stimulated [3H]thymidine incorporation into thyrocytes from normal subjects and patients with Graves’ disease, and it increased the proportion of thyrocytes in the S phase of the cell cycle. Furthermore, thyrocytes stimulated with rIL-1β for 24 h produced significant amounts of prostaglandin E2. Indomethacin inhibited completely the rIL-lβ-stimulated protaglandin E2 production and increased markedly [3H]thymidine incorporation. IL-1-like activity also was detected in the cultured supernatants of lipopolysaccharide (LPS)-stimulated thyrocytes from Graves’ and normal thyroid glands, but the amount of IL-1-like activity secreted by thyrocytes was significantly less than that secreted by circulating monocytes. The kinetics of the release of IL-1-like activity by thyrocytes were similar to those of its production by circulating monocytes. Pretreatment of thyrocytes with interferon-α failed to enhance the release of IL-1-like activity. Moreover, IL-lα or IL-1β immunoreactivity could not be detected in the supernatants of LPS-stimulated thyrocytes, despite the presence of IL-1-like bioactivity. No IL-lα mRNA was detected in unstimulated thyrocytes or thyrocytes stimulated with LPS and phorbol myristate acid. These findings demonstrate that thyrocytes produce an IL-1-like substance(s), but not IL-1, when stimulated by LPS. We conclude that IL-1 may regulate the proliferation of thyrocytes and that local production of IL-1 by infiltrating monocytes may contribute to the development of goiter in patients with autoimmune thyroid diseases.
