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Dopamicue Somatostatin Corticosteroids https://theses.gla.ac.uk/ Theses Digitisation: https://www.gla.ac.uk/myglasgow/research/enlighten/theses/digitisation/ This is a digitised version of the original print thesis. Copyright and moral rights for this work are retained by the author A copy can be downloaded for personal non-commercial research or study, without prior permission or charge This work cannot be reproduced or quoted extensively from without first obtaining permission in writing from the author The content must not be changed in any way or sold commercially in any format or medium without the formal permission of the author When referring to this work, full bibliographic details including the author, title, awarding institution and date of the thesis must be given Enlighten: Theses https://theses.gla.ac.uk/ [email protected] Role of Bioaetive Peptides In Autoimmune Thyroid Disease Thesis Submitted To The Faculty of Medicine University of Glasgow For The Degree of Doctor of Philosophy By Gholam Reza Moshtaghi Kashanian Department of Pathological Biochemistry Gartnavel General Hospital Glasgow June 1996 ProQuest Number: 10391489 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a com plete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. uest ProQuest 10391489 Published by ProQuest LLO (2017). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States C ode Microform Edition © ProQuest LLO. ProQuest LLO. 789 East Eisenhower Parkway P.Q. Box 1346 Ann Arbor, Ml 48106- 1346 ri> / o n Y GLASGOW>W I u n i v e r s;rrr i t t LIBRAKT SUMMARY The thyroid gland is the target of the commonest forms of autoimmune disease. Development of goitre, with an increase in the number of thyrocytes and other cells in the thyroid, is one of manifestation of thyroid autoimmunity in some cases. The enlargement of the gland is not simply the effect of stimulation of the thyrocytes with TSH (Hashimoto’s disease), or with thyroid stimulating antibodies (Graves’ disease), but involves many other factors, including cell to cell signalling among the various populations of cells in the gland by cytokines or other mediators. Another consequence of disease is the generation of new blood vessels and infiltration of a variety of mononuclear ceils which form aggregates or are diffusely distributed between and within the thyroid follicles. It seems likely that the mononuclear cells migrate from peripheral blood into thyroid tissue where they are retained by interaction with other cells including thyroid epithelial cells by means of cytokines released locally. The interaction of cytokines and growth factors with thyrocytes could also influence their functional pattern. Finally, the thyroid gland is richly innervated by nerves of different types (adrenergic, cholinergic, and peptidergic) which terminate close to blood vessels and follicular cells. It is likely, therefore, that neurotransmitters released locally may directly influence the activity of the follicular cells. Previous studies showed that a soluble form of the interleukin-2 receptor (sIL- 2R) is present in increased quantities in serum of patients with Graves' disease. Less information is available for the cytokines production among these patients, and the role of neuropeptides in the gland is not clear. The aim of this study was to determine the role of some of these bioactive peptides in Graves' disease. The concentration of soluble IL-2 receptor was increased in serum of the patients with Graves' disease (7.5 fold compared to healthy controls). Experiments on stimulation of blood cells in vitro showed that part of the increase in production of SÏL-2R is due to the elevation of thyroid hormones, while reduction of IL-2 production may be a second factor. In addition, the concentration of sIL-2R depends on other, unknown factors in the plasma, because dilution of whole blood with medium caused an increase in sIL-2R production. Stimulation of diluted (1:11 diluted with medium) whole blood of patients with untreated Graves' disease with a mixture of LPS/PHA caused a release of IL-2 and IL-4 that was significantly higher than from the reference group, after 72 h. The production of IL - 6 was also higher than from the reference group, after 4 h. The production of INF-y depended on the stimulator applied, but incubation of I unstimulated whole blood of the patients released less INF-y than control. Finally, TNF-a production of whole blood of the patients was higher than the reference group after 4 h, and was lower than the reference group after 72 h. These results may indicate that cytokine production by immune cells has a different pattern compared with healthy controls. The effects of methimazole, thyroid hormones, and TSH on cytokines production were also investigated. These compounds did not affect the production of IL-2 and IL-4, while they decreased the production of IL-6 , INF-y, and TNF-a. This shows that high concentrations of TSH (in Hashimoto’s disease), and thyroid hormones (in Graves' disease) could influence the production of IL-6 , INF-y, and TNF-a. Furthermore, it also shows that methimazole directly influences the production of these cytokines. The effects of various growth factors, cytokines, and neuropeptides on iodine uptake and growth of rat FRTL-5 thyroid epithelial cells were investigated. In the absence of TSH, the iodine uptake of thyrocytes was increased by ÏGF- 1 (in the presence of insulin), TGF, IL-6 , INF-y, neuropeptide Y, low doses of VIP and tachykinins, high doses of iodine, and thyroid hormones. On the other hand, iodine uptake was decreased by FGF, high doses of LPS, VIP, and tachykinins, and SNAP. The growth of cells was increased by insulin, IGF, FGF, low doses of VIP, high doses of thyroid hormones, inorganic iodine, and SNAP. The growth of cells was decreased by high doses of VIP. In the presence of TSH, the iodine uptake of thyrocytes was increased by insulin, IGF, TGF, endothelin-1, low doses of IL-I and LPS, IL-6 , INF-y, PACAP, low doses of VIP and tachykinins, high doses of SNAP, and noradrenaline. On the other hand, iodine uptake was decreased by inorganic iodine, thyroid hormones, FGF, high dose of IL-1, LPS, and tachykinins, and low doses of SNAP. The growth of cells was increased by high doses of thyroid hormones, insulin, IGF, FGF, endothelin-1, low doses of LPS, IL-6 , and low doses of VIP. The growth of thyrocytes was decreased by IL-4, INF-y, high doses of VIP, and PACAP. The pattern of iodine uptake and growth of cells changed when the cells were treated with high concentrations of thyroid hormones and TSH, before and during stimulation with the growth factor, cytokine, or neuropeptide. In most cases the hormones antagonised the action of the peptides. The stimulatory effects of IGF-1, TGF-p, endothelin-1, interferon-y, PACAP and VIP on iodine uptake were all reduced. In addition, thyroid hormones prevented the inhibitory effects of IL-1 and LPS. However, there was a large potentiation of the increase in iodine uptake caused by noradrenaline. The actions on growth rate were similar. The stimulatory effects of endothelin-1 and LPS were reduced, as were the inhibitory effects of TGF-(5, IL-4 I and interferon-y. The only exceptions were slight growth stimulatory effects in the presence of VIP and neuromedin-U. Combination of IL-1 with some of the growth factors, cytokines, and neuropeptides revealed that the effects of IL-1 were inhibitory. This may have implications for the situation in autoimmune disease or inflammation, where there is evidence for the presence of IL-1 within the gland. The effects were greater in the presence of TSH, so IL-1 may act to limit the growth and activity of the thyroid in both Hashimoto's and Graves’ diseases. Combination of some of the stimulators with noradrenaline also revealed that noradrenaline is directly involved in the pathogenic mechanisms of hyperthyroidism, and not just in eliciting the symptoms. il Î % I ; I I'll _____ _____ __ ACK NOWLEDGEMENT This is the opportunity to thanks those who supported me to carry out this work, without whose admirable contribution completion of the present thesis would be impossible. Roses are attractive, but their beauties are the result of the attention that was taken by a responsible gardener. Like the beauty of roses, the present thesis is the result of the invaluable contribution of time and admirable guidance of Dr. David Shapiro. This thesis could not have been finished without his precious source of guidance and his friendly attitude. I am grateful to him, and would like to express my heartfelt gratitude to him. I also would like to thank Professor Percy Robb for giving me the opportunity to work in his department. Blood samples from the patients with Graves' disease were provided by Professor John Connell. I am grateful to him and would like to thank him for his co­ operation. A good environment is necessary for a research worker to carry out his work in best possible form. This environment was provided for me by the members of Biochemistry Department. I would like to thank them all, especially Dr. M. H. Dominiczak for his friendly attitude during my stay in this department. It is my duty to express my gratitude to the patients and those healthy volunteers who have given blood for my research, whose contribution led to completion of this work.
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