@article{779297f7f7e74658a47a4380c065c2cc,
title = "Circulating IL-17A levels in postmenopausal women with primary hyperparathyroidism: Mediators of Inflammation",
abstract = "Background. Primary hyperparathyroidism (PHPT) is a common cause of secondary osteoporosis in postmenopausal women. Th17 lymphocytes and the released cytokine IL-17A play an important role in bone metabolism. Th17 cells have been shown to be activated by PTH, and peripheral blood T cells from patients affected with PHPT express higher levels of IL-17A mRNA than controls. Aim. To investigate circulating levels of IL-17A and the ratio RANKL/OPG, as markers of osteoclastogenesis, in 50 postmenopausal PHPT women compared with postmenopausal osteoporotic non-PHPT women (n=20). Results. Circulating levels of IL-17A were similarly detectable in most PHPT and non-PHPT osteoporotic women (12.9 (8.4-23.1) vs. 11.3 (8.3-14.3) pg/ml, median (range interquartile), P=0.759), at variance with premenopausal women where IL-17A was undetectable. In PHPT women, any significant correlations could be detected between circulating IL-17A levels and PTH levels. Nonetheless, significant negative correlations between circulating IL-17A and ionized calcium levels (r=-0.294, P=0.047) and urine calcium excretions (r=-0.300, P=0.045) were found. Moreover, PHPT women were characterized by positive correlations between IL-17A levels and femur neck (r=0.364, P=0.021) and total hip (r=0.353, P=0.015) T-scores. Circulating IL-17A levels did not show any significant correlation with sRANKL, OPG, and sRANKL/OPG ratio in PHPT women. Conclusions. In postmenopausal PHPT women, circulating IL-17A levels were similar to those detected in postmenopausal non-PHPT women, showing a disruption of the relationship observed in postmenopausal osteoporosis among circulating PTH, sRANKL, OPG, IL-17A, and bone demineralization in postmenopausal PHPT women. The data support an osteogenic effect of IL-17A in postmenopausal PHPT women. {\textcopyright} 2020 E. Dozio et al.",
keywords = "calcium, calcium ion, interleukin 17, osteoclast differentiation factor, parathyroid hormone, serum albumin, aged, Article, bone density, bone marrow, calcium urine level, clinical article, controlled study, densitometry, female, femoral neck, human, osteoclastogenesis, parathyroid hormone blood level, postmenopause, postmenopause osteoporosis, primary hyperparathyroidism, T lymphocyte",
author = "E. Dozio and E. Passeri and E. Vianello and S. Palmieri and C. Eller-Vainicher and {Corsi Romanelli}, M. and S. Corbetta",
note = "Export Date: 23 February 2021 CODEN: MNFLE Correspondence Address: Corbetta, S.; Endocrinology and Diabetology Service, Italy; email: sabrina.corbetta@unimi.it Chemicals/CAS: calcium, 7440-70-2, 14092-94-5; calcium ion, 14127-61-8; osteoclast differentiation factor, 200145-93-3; parathyroid hormone, 12584-96-2, 68893-82-3, 9002-64-6; serum albumin, 9048-46-8 Funding text 1: This work was supported by the Italian Ministry of Health. References: Eller-Vainicher, C., Cairoli, E., Zhukouskaya, V.V., Prevalence of subclinical contributors to low bone mineral density and/or fragility fracture (2013) European Journal of Endocrinology, 169 (2), pp. 225-237; Li, Y., Toraldo, G., Li, A., B cells and T cells are critical for the preservation of bone homeostasis and attainment of peak bone mass in vivo (2007) Blood, 109 (9), pp. 3839-3848; Tyagi, A.M., Srivastava, K., Mansoori, M.N., Trivedi, R., Chattopadhyay, N., Singh, D., Estrogen deficiency induces the differentiation of IL-17 secreting Th17 cells: A new candidate in the pathogenesis of osteoporosis (2012) PLoS One, 7 (9); Weitzmann, M.N., Pacifici, R., Parathyroid diseases and T cells (2017) Current Osteoporosis Reports, 15 (3), pp. 135-141; Terauchi, M., Li, J.Y., Bedi, B., T lymphocytes amplify the anabolic activity of parathyroid hormone through Wnt10b signaling (2009) Cell Metabolism, 10 (3), pp. 229-240; Li, J.-Y., D'Amelio, P., Robinson, J., IL-17A is increased in humans with primary hyperparathyroidism and mediates PTH-induced bone loss in mice (2015) Cell Metabolism, 22 (5), pp. 799-810; Baeten, D., Sieper, J., Braun, J., Secukinumab, an interleukin-17A inhibitor, in ankylosing spondylitis (2015) The New England Journal of Medicine, 373 (26), pp. 2534-2548; Basu, R., Hatton, R.D., Weaver, C.T., The Th17 family: Flexibility follows function (2013) Immunological Reviews, 252 (1), pp. 89-103; Komatsu, N., Takayanagi, H., Autoimmune arthritis: The interface between the immune system and joints (2012) Advances in Immunology, 115, pp. 45-71; Li, J.-Y., Yu, M., Tyagi, A.M., IL-17 receptor signaling in Osteoblasts/Osteocytes mediates PTH-induced bone loss and enhances osteocytic RANKL production (2019) Journal of Bone and Mineral Research, 34 (2), pp. 349-360; Adamopoulos, I.E., Chao, C.C., Geissler, R., Interleukin-17A upregulates receptor activator of NF-kappaB on osteoclast precursors (2010) Arthritis Research &Therapy, 12 (1), p. R29; Simonet, W.S., Lacey, D.L., Dunstan, C.R., Osteoprotegerin: A novel secreted protein involved in the regulation of bone density (1997) Cell, 89 (2), pp. 309-319; Chabaud, M., Fossiez, F., Taupin, J.L., Miossec, P., Enhancing effect of il-1, il-17, and TNF-α on macrophage inflammatory protein-3α production in rheumatoid arthritis: Regulation by soluble receptors and th2 cytokines (1998) Journal of Immunology, 167 (10), pp. 6015-6020; Tesmer, L.A., Lundy, S.K., Sarkar, S., Fox, D.A., Th17 cells in human disease (2008) Immunological Reviews, 223, pp. 87-113; Agarwal, S., Misra, R., Aggarwal, A., Interleukin 17 levels are increased in juvenile idiopathic arthritis synovial fluid and induce synovial fibroblasts to produce proinflammatory cytokines and matrix metalloproteinases (2008) The Journal of Rheumatology, 35 (3), pp. 515-519; Schofield, C., Fischer, S.K., Towsend, M.J., Characterization of IL-17AA and IL-17FF in rheumatoid arthritis and multiple sclerosis (2016) Bioanalysis, 8 (22), pp. 2317-2327; Miller, J.P., Izon, D., DeMuth, W., Gerstein, R., Bhandoola, A., Allman, D., The earliest step in B lineage differentiation from common lymphoid progenitors is critically dependent upon interleukin 7 (2002) The Journal of Experimental Medicine, 196 (5), pp. 705-711; Ponzetti, M., Rucci, N., Updates on osteoimmunology: What's new on the cross-talk between bone and immune system (2019) Frontiers in Endocrinology, 10, p. 236; McCauley, L.K., Rosol, T.J., Merryman, J.I., Capen, C.C., Parathyroid hormone-related protein binding to human Tcell lymphotropic virus type I-infected lymphocytes (1992) Endocrinology, 130 (1), pp. 300-306; Molnar, I., Bohaty, I., Somogyin{\`e}-Vari, E., IL-17A-mediated sRANK ligand elevation involved in postmenopausal osteoporosis (2014) Osteoporosis International, 25 (2), pp. 783-786; Ginaldi, L., De Martinis, M., Ciccarelli, F., Interleukin-33 serum levels in postmenopausal women with osteoporosis (2019) Scientific Reports, 9 (1), pp. 1-7; De Martinis, M., Sirufo, M.M., Ginaldi, L., Osteoporosis: Current and emerging therapies targeted to immunological checkpoints (2019) Current Medicinal Chemistry, 26; Xiao, L., Xiao, Y., The autophagy in osteoimmonology: Self-eating, maintenance, and beyond (2019) Frontiers in Endocrinology, 10, p. 490; Korn, T., Mitsdoerffer, M., Croxford, A.L., IL-6 controls Th17 immunity in vivo by inhibiting the conversion of conventional T cells into Foxp3+ regulatory T cells (2008) Proceedings of the National Academy of Sciences of the United States of America, 105 (47), pp. 18460-18465; Kimura, A., Naka, T., Kishimoto, T., IL-6-dependent and-independent pathways in the development of interleukin 17-producing T helper cells (2007) Proceedings of the National Academy of Sciences of the United States of America, 104 (29), pp. 12099-12104; Nackchbandi, I.A., Lang, R., Kinder, B., Insogna, K.L., The role of the receptor activator of nuclear factor-kappaB ligand/osteoprotegerin cytokine system in primary hyperparathyroidism (2008) The Journal of Clinical Endocrinology and Metabolism, 93 (3), pp. 967-973",
year = "2020",
doi = "10.1155/2020/3417329",
language = "English",
volume = "2020",
journal = "Mediators Inflamm.",
issn = "0962-9351",
publisher = "Hindawi Limited",
}