Interleukin-33 stimulates formation of functional osteoclasts from human CD14+ monocytes

Mun, Se Hwan; Ko, Na Young; Kim, Hyuk Soon; Kim, Jie Wan; Kim, Do Kyun; Kim, Aram; Lee, Seung Hyun; Kim, Yong‐Gil; Lee, Chang Keun; Lee, Seoung Hoon; Kim, Bo Kyung; Beaven, Michael A.; Kim, Young Mi; Choi, Wahn Soo

doi:10.1007/s00018-010-0410-y

Cited by 84 publications

(79 citation statements)

References 38 publications

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“…This phenomenon may also explain the lack of an inhibitory effect of IL-33 on osteoclast development from human peripheral blood CD14 + cells as observed by us and by others (35,36). This finding is in agreement with an increasing number of studies suggesting the existence of various subsets of human and murine circulating monocytes that differ in their cytokine profile, migratory properties, surface markers, and function.…”

Section: Discussionsupporting

confidence: 80%

IL-33 Shifts the Balance from Osteoclast to Alternatively Activated Macrophage Differentiation and Protects from TNF-α–Mediated Bone Loss

Zaiss

Kurowska‐Stolarska

Böhm

et al. 2011

The Journal of Immunology

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IL-33 is a new member of the IL-1 family, which plays a crucial role in inflammatory response, enhancing the differentiation of dendritic cells and alternatively activated macrophages (AAM). Based on the evidence of IL-33 expression in bone, we hypothesized that IL-33 may shift the balance from osteoclast to AAM differentiation and protect from inflammatory bone loss. Using transgenic mice overexpressing human TNF, which develop spontaneous joint inflammation and cartilage destruction, we show that administration of IL-33 or an IL-33R (ST2L) agonistic Ab inhibited cartilage destruction, systemic bone loss, and osteoclast differentiation. Reconstitution of irradiated hTNFtg mice with ST2−/− bone marrow led to more bone loss compared with the chimeras with ST2+/+ bone marrow, demonstrating an important endogenous role of the IL-33/ST2L pathway in bone turnover. The protective effect of IL-33 on bone was accompanied by a significant increase of antiosteoclastogenic cytokines (GM-CSF, IL-4, and IFN-γ) in the serum. In vitro IL-33 directly inhibits mouse and human M-CSF/receptor activator for NF-κB ligand-driven osteoclast differentiation. IL-33 acts directly on murine osteoclast precursors, shifting their differentiation toward CD206+ AAMs via GM-CSF in an autocrine fashion. Thus, we show in this study that IL-33 is an important bone-protecting cytokine and may be of therapeutic benefit in treating bone resorption.

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Section: Discussionsupporting

confidence: 80%

IL-33 Shifts the Balance from Osteoclast to Alternatively Activated Macrophage Differentiation and Protects from TNF-α–Mediated Bone Loss

Zaiss

Kurowska‐Stolarska

Böhm

et al. 2011

The Journal of Immunology

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“…Besides the already described TNF-α and IL-32, IL-33 induces osteoclastogenesis from human monocytes, by activating MAPKs, NF-κB and Syk/PLCγ pathways independently of RANKL [76]. IL-15 directly promotes differentiation of rodent OCPs to preosteoclasts in vitro, through the MAPKs and NF-κB pathways, but also upregulates RANKL expression in synovial fibroblasts [77].…”

Section: Effect Of Arthritic Mediators On Osteoclast Progenitorsmentioning

confidence: 92%

Induction of osteoclast progenitors in inflammatory conditions: key to bone destruction in arthritis

Šućur

Katavić

Kelava

et al. 2014

International Orthopaedics (SICOT)

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The inflammatory milieu favors recruitment and activation of osteoclasts, and leads to bone destruction as a serious complication associated with arthritis and with other inflammatory processes.The frequency and activity of osteoclast progenitors (OCPs) correspond to arthritis severity, and may be used to monitor disease progression and bone resorption, indicating the need for detailed characterization of the discrete OCP subpopulations. Collectively, current studies suggest that the most potent murine bone marrow OCP population can be identified among lymphoid negative population within the immature myeloid lineage cells, as B220 -CD3 -CD11b -/lo CD115 + CD117 + CX3CR1 + and possibly also Ter119 -CD11c -CD135 lo Ly6C + RANK -. In the peripheral blood OCP population bears the monocytoid phenotype B220 -CD3 -NK1.1 -CD11b + Ly-6C hi CD115 + CX3CR1 + , presumably expressing RANK in committed OCPs. Much less is known about human OCPs and their regulation in arthritis, but the circulating OCP subset is, most probably, comprised among the lymphoid negative population (CD3 -CD19 -CD56 -), within immature monocyte subset (CD11b + CD14 + CD16 -), expressing receptors for M-CSF and RANKL (CD115 + RANK + ). Our preliminary data confirmed positive association between the proportion of peripheral blood OCPs, defined as CD3 -CD19 -CD56 -CD11b + CD14 + , and the disease activity score (DAS28) in the follow-up samples from patient with psoriatic arthritis receiving anti-TNF therapy. In addition, we reviewed cytokines and chemokines which, directly or indirectly, activate OCPs and enhance their differentiation potential, thus mediating osteoresorption.Control of the activity and migratory behavior of OCPs as well as the identification of crucial bone/joint chemotactic mediators represent promising therapeutic targets in arthritis.Keyword: osteoclast progenitors, arthritis, inflammation, cytokines, chemokines, osteoresorption 3 Inflammation induced bone lossBone is a highly dynamic tissue important for its mechanical and metabolic functions, and characterized by rapid response to numerous physical, endocrine and paracrine stimuli in physiological and pathological conditions. Among others signals, osteoresorptive mediators (such as interleukin (IL)-1, IL-6, IL-15, IL-17, IL, 21, IL-33, tumor necrosis factor (TNF)-α and receptor activator of nuclear factor-κB ligand (RANKL), CCL2, CXCL12) produced by inflammatory/immune cells create conditions that promote maturation and function of osteoclasts [1][2][3][4]. Bone resorption and osteolysis are the prominent features and causes of substantial morbidity in inflammatory processes associated with arthritis as well as with localized bacterial infections of bone and adjacent tissues, peri-prosthetic loosening, vasculitis, connective tissue diseases, chronic viral infections and inflammatory bowel diseases [5][6][7][8]. Bone resorption in arthritisInflammatory arthritides comprise a heterogeneous group of joint disorders that are characterized by chronic inflammatory response as we...

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“…Interestingly, IL-33 is not able to affect osteoclast development when added to committed immature osteoclasts, suggesting that IL-33 acts on the very early step of cell commitment. This phenomenon may also explain the lack of an inhibitory effect of IL-33 on osteoclast development from human peripheral blood CD14 + cells [ 18,19 ] .…”

Section: Interleukin-33mentioning

confidence: 92%

Effects of the Interleukin-1 Cytokine Family on Bone

Schett

2012

Osteoimmunology

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IntroductionCytokines are major regulators of bone homeostasis and in fl uence the function of both osteoblasts and osteoclasts. For instance, receptor activator of NF-kB ligand (RANKL) is a member of the tumor necrosis factor (TNF) family and an essential mediator of osteoclastogenesis. Apart from RANKL, proin fl ammatory cytokines modulate osteoclast differentiation, amongst them TNF-a is a potent stimulator of osteoclastogenesis. Other proin fl ammatory cytokines like IL-17 and IL-11 are also stimulators of bone resorption by inducing osteoclast differentiation, whereas others such as interferon-(IFN)-g and IL-12 suppress osteoclastogenesis and balance enhanced bone resorption. In this chapter, we focus on the IL-1 of cytokine family and summarize their role on bone homeostasis. Members of the IL-1 cytokine family are involved in multiple cellular functions including the innate and adaptive immune system. They are key mediators of in fl ammation and govern the complex processes of cell traf fi cking, cytokine and matrix enzyme release, fever responses, and metabolic changes during in fl ammatory disease. Interleukin-1The pro-in fl ammatory cytokine IL-1 is induced by TNF-a and was fi rst described as factor acting on T and B cells driving immune responses [ 1 ] . Since then, it became evident that IL-1 is one of the key players during acute in fl ammation and produced by multiple cell lineages including macrophages, lymphocytes as well as mesenchymal cells.

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Interleukin-33 stimulates formation of functional osteoclasts from human CD14+ monocytes

Cited by 84 publications

References 38 publications

IL-33 Shifts the Balance from Osteoclast to Alternatively Activated Macrophage Differentiation and Protects from TNF-α–Mediated Bone Loss

IL-33 Shifts the Balance from Osteoclast to Alternatively Activated Macrophage Differentiation and Protects from TNF-α–Mediated Bone Loss

Induction of osteoclast progenitors in inflammatory conditions: key to bone destruction in arthritis

Effects of the Interleukin-1 Cytokine Family on Bone

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