Document Detail


Influence of iodide excess and interferon-gamma on human primary thyroid cell proliferation, thyroglobulin secretion, and intracellular adhesion molecule-1 and human leukocyte antigen-DR expression.
MedLine Citation:
PMID:  19265500     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The effect of iodide on thyroid cell proliferation and function in vivo or in cultured thyroid cells has been previously reported and is still controversial. The aim of this study was to clarify these conflicting results by examining if prolonged high iodide exposition with or without interferon (IFN)-gamma has an effect on human primary thyroid cell proliferation, thyroglobulin (Tg) production, and intercellular adhesion molecule-1 (ICAM-1) and human leukocyte antigen (HLA)-DR expression. METHODS: Primary human thyroid cells were used. Cells were cultured in Coon's modified Ham's F-12 medium supplemented with 5% fetal calf serum in monolayer conditions to induce proliferation and were aggregated for molecular expression and Tg production analysis. HLA-DR and ICAM-1 expression were measured by flow cytometry and Tg by immunometric assay. RESULTS: Potassium iodide (KI) was more potent in arresting primary human thyroid cell proliferation as compared to sodium iodide and the effect was mediated by its action at G0/G1 and G2/M phases of the cell cycle. There were no signs of apoptosis or necrosis. An excess of KI alone did not change the expression of HLA-DR and Tg production, but gradually increased ICAM-1. Low-dose IFN-gamma and excess KI in combination transiently inhibited HLA-DR expression, while ICAM-1 was expressed at a higher level than with IFN-gamma alone. Tg production was moderately increased with low-dose IFN-gamma. However, a combination of high-dose KI with low-dose IFN-gamma significantly decreased Tg secretion, compared with IFN-gamma alone. CONCLUSIONS: Augmented ICAM-1 in the presence of iodide excess and low-dose IFN-gamma could induce secretion of proinflammatory cytokines and lymphocytic infiltration in the thyroid gland. Decreased Tg production in the presence of KI excess and IFN-gamma could explain the development of hypothyroidism after adding iodide in a diet of subjects that already have lymphocytic infiltration and/or mild inflammation in the thyroid gland.
Authors:
Irena Kostic; Barbara Toffoletto; Elisabetta Fontanini; Massimo Moretti; Daniela Cesselli; Carlo A Beltrami; Francesco S Ambesi Impiombato; Francesco Curcio
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Thyroid : official journal of the American Thyroid Association     Volume:  19     ISSN:  1557-9077     ISO Abbreviation:  Thyroid     Publication Date:  2009 Mar 
Date Detail:
Created Date:  2009-03-06     Completed Date:  2009-05-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9104317     Medline TA:  Thyroid     Country:  United States    
Other Details:
Languages:  eng     Pagination:  283-91     Citation Subset:  IM    
Affiliation:
Institute of Pathophysiology, School of Medicine, University of Kragujevac, Kragujevac, Serbia.
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MeSH Terms
Descriptor/Qualifier:
Annexin A5 / biosynthesis
Cell Cycle / drug effects
Cell Proliferation / drug effects*
DNA, Neoplasm / biosynthesis,  genetics
Flow Cytometry
G2 Phase / drug effects
HLA-DR Antigens / biosynthesis*
Humans
Intercellular Adhesion Molecule-1 / biosynthesis*
Interferon-gamma / pharmacology*
Iodides / pharmacology*
Thyroglobulin / metabolism*
Thyroid Gland / cytology*,  drug effects
Chemical
Reg. No./Substance:
0/Annexin A5; 0/DNA, Neoplasm; 0/HLA-DR Antigens; 0/Iodides; 126547-89-5/Intercellular Adhesion Molecule-1; 82115-62-6/Interferon-gamma; 9010-34-8/Thyroglobulin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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