Interleukin 17A: a Janus-faced regulator of osteoporosis.

Absorptiometry, Photon Animals Cancellous Bone / pathology Disease Models, Animal Enzyme-Linked Immunosorbent Assay Female Femur / diagnostic imaging Humans Interleukin-17 / physiology Mice Mice, Knockout Osteogenesis / drug effects Osteoporosis / diagnostic imaging Osteoporosis, Postmenopausal / etiology Ovariectomy / adverse effects Real-Time Polymerase Chain Reaction Receptors, Interleukin-17 / physiology X-Ray Microtomography

Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
30 03 2020
Historique:
received: 20 12 2019
accepted: 14 03 2020
entrez: 2 4 2020
pubmed: 2 4 2020
medline: 1 12 2020
Statut: epublish

Résumé

Interleukin (IL)-17A is a well-described mediator of bone resorption in inflammatory diseases, and postmenopausal osteoporosis is associated with increased serum levels of IL-17A. Ovariectomy (OVX) can be used as a model to study bone loss induced by estrogen deficiency and the role of IL-17A in osteoporosis development has previously been investigated using various methods to inhibit IL-17A signaling in this model. However, the studies show opposing results. While some publications reported IL-17A as a mediator of OVX-induced osteoporosis, others found a bone-protective role for IL-17 receptor signaling. In this study, we provide an explanation for the discrepancies in previous literature and show for the first time that loss of IL-17A has differential effects on OVX-induced osteoporosis; with IL-17A being important for cortical but not trabecular bone loss. Interestingly, the decrease in trabecular bone after OVX in IL-17A knock-out mice, was accompanied by increased adipogenesis depicted by elevated leptin levels. Additionally, the bone marrow adipose tissue expanded, and the bone-turnover decreased in ovariectomized mice lacking IL-17A compared to ovariectomized WT mice. Our results increase the understanding of how IL-17A signaling influences bone remodeling in the different bone compartments, which is of importance for the development of new treatments of post-menopausal osteoporosis.

Identifiants

DOI: 10.1038/s41598-020-62562-2 PMID: 32231224 PMC: PMC7105470
pubmed: 32231224
doi: 10.1038/s41598-020-62562-2
pii: 10.1038/s41598-020-62562-2
pmc: PMC7105470
doi:

Substances chimiques

Il17a protein, mouse 0
Interleukin-17 0
Receptors, Interleukin-17 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

5692

Références

Ducy, P., Schinke, T. & Karsenty, G. The osteoblast: a sophisticated fibroblast under central surveillance. Science 289, 1501–1504, https://doi.org/10.1126/science.289.5484.1501 (2000).
doi: 10.1126/science.289.5484.1501 pubmed: 10968779 pmcid: 10968779
Teitelbaum, S. L. Bone Resorption by Osteoclasts. Science 289, 1504–1508, https://doi.org/10.1126/science.289.5484.1504 (2000).
doi: 10.1126/science.289.5484.1504 pubmed: 10968780 pmcid: 10968780
Albright, F., Smith, P. H. & Richardson, A. M. Postmenopausal osteoporosis: its clinical features. JAMA 116, 2465–2474, https://doi.org/10.1001/jama.1941.02820220007002 (1941).
doi: 10.1001/jama.1941.02820220007002
Effects of hormone therapy on bone mineral density: results from the postmenopausal estrogen/progestin interventions (PEPI) trial. The Writing Group for the PEPI. Jama 276, 1389–1396 (1996).
Jin, J. Hormone Therapy for Primary Prevention of Chronic Conditions in Postmenopausal WomenHormone Therapy for Prevention of Chronic Conditions in Postmenopausal WomenHormone Therapy for Prevention of Chronic Conditions in Postmenopausal Women. JAMA 318, 2265–2265, https://doi.org/10.1001/jama.2017.18440 (2017).
doi: 10.1001/jama.2017.18440 pubmed: 29234809 pmcid: 29234809
Hofbauer, L. C. et al. Estrogen stimulates gene expression and protein production of osteoprotegerin in human osteoblastic cells. Endocrinology 140, 4367–4370, https://doi.org/10.1210/endo.140.9.7131 (1999).
doi: 10.1210/endo.140.9.7131 pubmed: 10465311 pmcid: 10465311
Imai, Y. et al. Estrogens maintain bone mass by regulating expression of genes controlling function and life span in mature osteoclasts. Ann. N. Y. Acad. Sci. 1173(Suppl 1), E31–39, https://doi.org/10.1111/j.1749-6632.2009.04954.x (2009).
doi: 10.1111/j.1749-6632.2009.04954.x pubmed: 19751412 pmcid: 19751412
Fujiwara, Y. et al. RANKL produced by osteocytes is required for the increase in B cells and bone loss caused by estrogen deficiency in mice. Journal of Biological Chemistry, https://doi.org/10.1074/jbc.M116.742452 (2016).
Cummings, S. R. et al. Denosumab for Prevention of Fractures in Postmenopausal Women with Osteoporosis. N. Engl. J. Med. 361, 756–765, https://doi.org/10.1056/NEJMoa0809493 (2009).
doi: 10.1056/NEJMoa0809493 pubmed: 19671655 pmcid: 19671655
Charatcharoenwitthaya, N., Khosla, S., Atkinson, E. J., McCready, L. K. & Riggs, B. L. Effect of Blockade of TNF-α and Interleukin-1 Action on Bone Resorption in Early Postmenopausal Women. J. Bone Miner. Res. 22, 724–729, https://doi.org/10.1359/jbmr.070207 (2007).
doi: 10.1359/jbmr.070207 pubmed: 17295604 pmcid: 17295604
Zheng, S. X. et al. Increase in cytokine production (IL-1β, IL-6, TNF-α but not IFN-γ, GM-CSF or LIF) by stimulated whole blood cells in postmenopausal osteoporosis. Maturitas 26, 63–71, https://doi.org/10.1016/S0378-5122(96)01080-8 (1997).
doi: 10.1016/S0378-5122(96)01080-8 pubmed: 9032749 pmcid: 9032749
Pacifici, R. et al. Effect of surgical menopause and estrogen replacement on cytokine release from human blood mononuclear cells. Proc. Natl Acad. Sci. 88, 5134–5138, https://doi.org/10.1073/pnas.88.12.5134 (1991).
doi: 10.1073/pnas.88.12.5134 pubmed: 2052592 pmcid: 2052592
Zhang, J. et al. Changes of serum cytokines-related Th1/Th2/Th17 concentration in patients with postmenopausal osteoporosis. Gynecol. Endocrinol. 31, 183–190, https://doi.org/10.3109/09513590.2014.975683 (2015).
doi: 10.3109/09513590.2014.975683 pubmed: 25384921 pmcid: 25384921
Gumus, P. et al. Gingival crevicular fluid, serum levels of receptor activator of nuclear factor-kappaB ligand, osteoprotegerin, and interleukin-17 in patients with rheumatoid arthritis and osteoporosis and with periodontal disease. J. Periodontol. 84, 1627–1637, https://doi.org/10.1902/jop.2013.120595 (2013).
doi: 10.1902/jop.2013.120595 pubmed: 23327689 pmcid: 23327689
Lubberts, E. et al. IL-17 promotes bone erosion in murine collagen-induced arthritis through loss of the receptor activator of NF-kappa B ligand/osteoprotegerin balance. J. Immunol. 170, 2655–2662 (2003).
doi: 10.4049/jimmunol.170.5.2655 pubmed: 12594294 pmcid: 12594294
Tyagi, A. M. et al. Enhanced immunoprotective effects by anti-IL-17 antibody translates to improved skeletal parameters under estrogen deficiency compared with anti-RANKL and anti-TNF-alpha antibodies. J. Bone Min. Res. 29, 1981–1992, https://doi.org/10.1002/jbmr.2228 (2014).
doi: 10.1002/jbmr.2228
Tyagi, A. M. et al. Estrogen deficiency induces the differentiation of IL-17 secreting Th17 cells: a new candidate in the pathogenesis of osteoporosis. PLoS One 7, e44552, https://doi.org/10.1371/journal.pone.0044552 (2012).
doi: 10.1371/journal.pone.0044552 pubmed: 3438183 pmcid: 3438183
Li, J.-Y. et al. Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics. J. Clin. Investigation 126, 2049–2063, https://doi.org/10.1172/JCI86062 (2016).
doi: 10.1172/JCI86062
DeSelm, C. J. et al. IL-17 mediates estrogen-deficient osteoporosis in an Act1-dependent manner. J. Cell. Biochem. 113, 2895–2902, https://doi.org/10.1002/jcb.24165 (2012).
doi: 10.1002/jcb.24165 pubmed: 22511335 pmcid: 22511335
Goswami, J., Hernandez-Santos, N., Zuniga, L. A. & Gaffen, S. L. A bone-protective role for IL-17 receptor signaling in ovariectomy-induced bone loss. Eur. J. Immunol. 39, 2831–2839, https://doi.org/10.1002/eji.200939670 (2009).
doi: 10.1002/eji.200939670 pubmed: 19731364 pmcid: 19731364
Nakae, S. et al. Antigen-specific T cell sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral responses. Immunity 17, 375–387 (2002).
doi: 10.1016/S1074-7613(02)00391-6 pubmed: 12354389 pmcid: 12354389
Windahl, S. H., Vidal, O., Andersson, G., Gustafsson, J. A. & Ohlsson, C. Increased cortical bone mineral content but unchanged trabecular bone mineral density in female ERβ–/– mice. J. Clin. Investigation 104, 895–901, https://doi.org/10.1172/JCI6730 (1999).
doi: 10.1172/JCI6730
Movérare-Skrtic, S. et al. Osteoblast-derived WNT16 represses osteoclastogenesis and prevents cortical bone fragility fractures. Nature Medicine 20, 1279, doi:10.1038/nm.3654 https://www.nature.com/articles/nm.3654#supplementary-information (2014).
Toyosawa, S. et al. Histochemistry of tartrate-resistant acid phosphatase and carbonic anhydrase isoenzyme II in osteoclast-like giant cells in bone tumours. Virchows Archiv. A, Pathological Anat. histopathology 418, 255–261, https://doi.org/10.1007/bf01606064 (1991).
doi: 10.1007/bf01606064
Masuzawa, T. et al. Estrogen deficiency stimulates B lymphopoiesis in mouse bone marrow. J. Clin. Invest. 94, 1090–1097, https://doi.org/10.1172/jci117424 (1994).
doi: 10.1172/jci117424 pubmed: 8083350 pmcid: 8083350
Kong, Y.-Y. et al. OPGL is a key regulator of osteoclastogenesis, lymphocyte development and lymph-node organogenesis. Nature 397, 315–323, https://doi.org/10.1038/16852 (1999).
doi: 10.1038/16852 pubmed: 9950424 pmcid: 9950424
Rissanen, J. P. et al. Short-term changes in serum PINP predict long-term changes in trabecular bone in the rat ovariectomy model. Calcif. tissue Int. 82, 155–161, https://doi.org/10.1007/s00223-007-9101-6 (2008).
doi: 10.1007/s00223-007-9101-6 pubmed: 18219436 pmcid: 18219436
Zúñiga, L. A. et al. IL-17 regulates adipogenesis, glucose homeostasis, and obesity. J. immunology 185, 6947–6959, https://doi.org/10.4049/jimmunol.1001269 (2010).
doi: 10.4049/jimmunol.1001269
Lancha, A., Frühbeck, G. & Gómez-Ambrosi, J. Peripheral signalling involved in energy homeostasis control. Nutr. Res. Rev. 25, 223–248, https://doi.org/10.1017/S0954422412000145 (2012).
doi: 10.1017/S0954422412000145 pubmed: 23174510 pmcid: 23174510
Li, J. Y. et al. Sex steroid deficiency-associated bone loss is microbiota dependent and prevented by probiotics. J. Clin. Invest. 126, 2049–2063, https://doi.org/10.1172/jci86062 (2016).
doi: 10.1172/jci86062 pubmed: 27111232 pmcid: 27111232
DeSelm, C. J. et al. IL-17 mediates estrogen-deficient osteoporosis in an Act1-dependent manner. J. Cell Biochem. 113, 2895–2902, https://doi.org/10.1002/jcb.24165 (2012).
doi: 10.1002/jcb.24165 pubmed: 22511335 pmcid: 22511335
Cua, D. J. & Tato, C. M. Innate IL-17-producing cells: the sentinels of the immune system. Nat. Rev. Immunology 10, 479–489, https://doi.org/10.1038/nri2800 (2010).
doi: 10.1038/nri2800 pubmed: 20559326 pmcid: 20559326
Takaki-Kuwahara, A. et al. CCR6+ group 3 innate lymphoid cells accumulate in inflamed joints in rheumatoid arthritis and produce Th17 cytokines. Arthritis Res. Ther. 21, 198, https://doi.org/10.1186/s13075-019-1984-x (2019).
doi: 10.1186/s13075-019-1984-x pubmed: 31470891 pmcid: 31470891
Gustafsson, K. L. et al. ERalpha expression in T lymphocytes is dispensable for estrogenic effects in bone. J. Endocrinol. 238, 129–136, https://doi.org/10.1530/joe-18-0183 (2018).
doi: 10.1530/joe-18-0183 pubmed: 29848607 pmcid: 29848607
Nakae, S., Nambu, A., Sudo, K. & Iwakura, Y. Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. J. Immunol. 171, 6173–6177, https://doi.org/10.4049/jimmunol.171.11.6173 (2003).
doi: 10.4049/jimmunol.171.11.6173 pubmed: 14634133 pmcid: 14634133
Fan, Y. et al. Parathyroid Hormone Directs Bone Marrow Mesenchymal Cell Fate. Cell Metab. 25, 661–672, https://doi.org/10.1016/j.cmet.2017.01.001 (2017).
doi: 10.1016/j.cmet.2017.01.001 pubmed: 28162969 pmcid: 28162969
Muto, A. et al. Lineage-committed osteoclast precursors circulate in blood and settle down into bone. J. Bone Min. Res. 26, 2978–2990, https://doi.org/10.1002/jbmr.490 (2011).
doi: 10.1002/jbmr.490
von Vietinghoff, S. & Ley, K. IL-17A Controls IL-17F Production and Maintains Blood Neutrophil Counts in Mice. J. Immunology 183, 865, https://doi.org/10.4049/jimmunol.0804080 (2009).
doi: 10.4049/jimmunol.0804080
Takeda, S. et al. Leptin Regulates Bone Formation via the Sympathetic Nervous System. Cell 111, 305–317, https://doi.org/10.1016/S0092-8674(02)01049-8 (2002).
doi: 10.1016/S0092-8674(02)01049-8
Ducy, P. et al. Leptin Inhibits Bone Formation through a Hypothalamic Relay: A Central Control of Bone Mass. Cell 100, 197–207, https://doi.org/10.1016/S0092-8674(00)81558-5 (2000).
doi: 10.1016/S0092-8674(00)81558-5 pubmed: 10660043 pmcid: 10660043
Lee, N. J., Wong, I. P., Baldock, P. A. & Herzog, H. Leptin as an endocrine signal in bone. Curr. Osteoporos. Rep. 6, 62–66, https://doi.org/10.1007/s11914-008-0011-y (2008).
doi: 10.1007/s11914-008-0011-y pubmed: 18778565 pmcid: 18778565
Kajimura, D. et al. Adiponectin regulates bone mass via opposite central and peripheral mechanisms through FoxO1. Cell Metab. 17, 901–915, https://doi.org/10.1016/j.cmet.2013.04.009 (2013).
doi: 10.1016/j.cmet.2013.04.009 pubmed: 23684624 pmcid: 23684624
Liu, Y., Tang, G. Y., Tang, R. B., Peng, Y. F. & Li, W. Assessment of bone marrow changes in postmenopausal women with varying bone densities: magnetic resonance spectroscopy and diffusion magnetic resonance imaging. Chin. Med. J. 123, 1524–1527 (2010).
pubmed: 20819505 pmcid: 20819505
Schwartz, A. V. et al. Vertebral bone marrow fat associated with lower trabecular BMD and prevalent vertebral fracture in older adults. J. Clin. Endocrinol. Metab. 98, 2294–2300, https://doi.org/10.1210/jc.2012-3949 (2013).
doi: 10.1210/jc.2012-3949 pubmed: 23553860 pmcid: 23553860
Griffith, J. F. et al. Bone marrow fat content in the elderly: a reversal of sex difference seen in younger subjects. J. Magnetic Reson. Imaging 36, 225–230, https://doi.org/10.1002/jmri.23619 (2012).
doi: 10.1002/jmri.23619
Blanco, F. J. et al. Secukinumab in Active Rheumatoid Arthritis: A Phase III Randomized, Double-Blind, Active Comparator– and Placebo-Controlled Study. Arthritis Rheumatol. 69, 1144–1153, https://doi.org/10.1002/art.40070 (2017).
doi: 10.1002/art.40070 pubmed: 28217871 pmcid: 28217871
Paine, A. & Ritchlin, C. Altered Bone Remodeling in Psoriatic Disease: New Insights and Future Directions. Calcif. Tissue Int. 102, 559–574, https://doi.org/10.1007/s00223-017-0380-2 (2018).
doi: 10.1007/s00223-017-0380-2 pubmed: 29330560 pmcid: 29330560

Auteurs

J M Scheffler (JM)

Krefting Research Center, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. julia.scheffler@gu.se.
Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. julia.scheffler@gu.se.

L Grahnemo (L)

Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

C Engdahl (C)

Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Centre for Bone and Arthritis Research, Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

C Drevinge (C)

Krefting Research Center, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

K L Gustafsson (KL)

Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

C Corciulo (C)

Krefting Research Center, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

L Lawenius (L)

Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

Y Iwakura (Y)

Research Institute for Biomedical Sciences, Tokyo University of Science, Chiba, Japan.

K Sjögren (K)

Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

M K Lagerquist (MK)

Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

H Carlsten (H)

Centre for Bone and Arthritis Research, Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

C Ohlsson (C)

Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Department of Drug Treatment, Sahlgrenska University Hospital, Gothenburg, Sweden.

U Islander (U)

Krefting Research Center, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

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Classifications MeSH

questionsmedicales.fr › Techniques d'investigation › Techniques de chimie analytique › Photométrie › Densitométrie › Absorptiométrie photonique › Interleukin 17A: a Janus-faced regulator of...
questionsmedicales.fr › Eucaryotes › Animaux › Interleukin 17A: a Janus-faced regulator of...
questionsmedicales.fr › Tissus › Tissu conjonctif › Os et tissu osseux › Os spongieux › Interleukin 17A: a Janus-faced regulator of...
questionsmedicales.fr › Techniques d'investigation › Modèles théoriques › Modèles biologiques › Modèles animaux de maladie humaine › Interleukin 17A: a Janus-faced regulator of...
questionsmedicales.fr › Techniques d'investigation › Techniques de sonde moléculaire › Dosage immunologique › Techniques d'immunoadsorption › Test ELISA › Interleukin 17A: a Janus-faced regulator of...
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questionsmedicales.fr › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Cytokines › Interleukines › Interleukine-17 › Interleukin 17A: a Janus-faced regulator of...
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questionsmedicales.fr › Procédures de chirurgie opératoire › Procédures de chirurgie urogénitale › Procédures de chirurgie gynécologique › Ovariectomie › Interleukin 17A: a Janus-faced regulator of...
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