PMID- 19265500
OWN - NLM
STAT- MEDLINE
DCOM- 20090504
LR  - 20090306
IS  - 1557-9077 (Electronic)
IS  - 1050-7256 (Linking)
VI  - 19
IP  - 3
DP  - 2009 Mar
TI  - 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.
PG  - 283-91
LID - 10.1089/thy.2008.0295 [doi]
AB  - 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.
FAU - Kostic, Irena
AU  - Kostic I
AD  - Institute of Pathophysiology, School of Medicine, University of Kragujevac, 
      Kragujevac, Serbia.
FAU - Toffoletto, Barbara
AU  - Toffoletto B
FAU - Fontanini, Elisabetta
AU  - Fontanini E
FAU - Moretti, Massimo
AU  - Moretti M
FAU - Cesselli, Daniela
AU  - Cesselli D
FAU - Beltrami, Carlo A
AU  - Beltrami CA
FAU - Ambesi Impiombato, Francesco S
AU  - Ambesi Impiombato FS
FAU - Curcio, Francesco
AU  - Curcio F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Thyroid
JT  - Thyroid : official journal of the American Thyroid Association
JID - 9104317
RN  - 0 (Annexin A5)
RN  - 0 (DNA, Neoplasm)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Iodides)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9010-34-8 (Thyroglobulin)
SB  - IM
MH  - Annexin A5/biosynthesis
MH  - Cell Cycle/drug effects
MH  - Cell Proliferation/*drug effects
MH  - DNA, Neoplasm/biosynthesis/genetics
MH  - Flow Cytometry
MH  - G2 Phase/drug effects
MH  - HLA-DR Antigens/*biosynthesis
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/*biosynthesis
MH  - Interferon-gamma/*pharmacology
MH  - Iodides/*pharmacology
MH  - Thyroglobulin/*metabolism
MH  - Thyroid Gland/*cytology/drug effects
EDAT- 2009/03/07 09:00
MHDA- 2009/05/05 09:00
CRDT- 2009/03/07 09:00
PHST- 2009/03/07 09:00 [entrez]
PHST- 2009/03/07 09:00 [pubmed]
PHST- 2009/05/05 09:00 [medline]
AID - 10.1089/thy.2008.0295 [doi]
PST - ppublish
SO  - Thyroid. 2009 Mar;19(3):283-91. doi: 10.1089/thy.2008.0295.