Interleukin-6 messenger RNA expression and interleukin-6 protein secretion in cells isolated from normal human bone: Regulation by interleukin-1

Linkhart, Thomas A.; Linkhart, Susan G.; MacCharles, Daniel C.; Long, Dana L.; Strong, Donna D.

doi:10.1002/jbmr.5650061204

Cited by 102 publications

(21 citation statements)

References 53 publications

(2 reference statements)

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“…The pro-inflammatory cytokines; TNF-α, IL-1β and IL-6 have been shown not only to coordinate the hematopoietic and immune systems, but also to contribute to bone repair by regulating osteoclastogenesis and the early recruitment and differentiation of osteoblastic lineage cells [20], [21], [22], [23], [24], [25], [26], [27], [28], [29]. Therefore, we have analyzed the effect of targeted disruption of Darc on the expression of these three inflammatory cytokines in bone fracture.…”

Section: Resultsmentioning

confidence: 99%

Duffy Antigen Receptor for Chemokines Regulates Post-Fracture Inflammation

2013

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There is now considerable experimental data to suggest that inflammatory cells collaborate in the healing of skeletal fractures. In terms of mechanisms that contribute to the recruitment of inflammatory cells to the fracture site, chemokines and their receptors have received considerable attention. Our previous findings have shown that Duffy antigen receptor for chemokines (Darc), the non-classical chemokine receptor that does not signal, but rather acts as a scavenger of chemokines that regulate cell migration, is a negative regulator of peak bone density in mice. Furthermore, because Darc is expressed by inflammatory and endothelial cells, we hypothesized that disruption of Darc action will affect post-fracture inflammation and consequently will affect fracture healing. To test this hypothesis, we evaluated fracture healing in mice with targeted disruption of Darc and corresponding wild type (WT) control mice. We found that fracture callus cartilage formation was significantly greater (33%) at 7 days post-surgery in Darc-KO compared to WT mice. The increased cartilage was associated with greater Collagen (Col) II expression at 3 days post-fracture and Col-X at 7 days post-fracture compared to WT mice, suggesting that Darc deficiency led to early fracture cartilage formation and differentiation. We then compared the expression of cytokine and chemokine genes known to be induced during inflammation. Interleukin (Il)-1β, Il-6, and monocyte chemotactic protein 1 were all down regulated in the fractures derived from Darc-KO mice at one day post-fracture, consistent with an altered inflammatory response. Furthermore, the number of macrophages was significantly reduced around the fractures in Darc-KO compared to WT mice. Based on these data, we concluded that Darc plays a role in modulating the early inflammatory response to bone fracture and subsequent cartilage formation. However, the early cartilage formation was not translated with an early bone formation at the fracture site in Darc-KO compared to WT mice.

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Section: Resultsmentioning

confidence: 99%

Duffy Antigen Receptor for Chemokines Regulates Post-Fracture Inflammation

2013

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“…IL-1 is also considered to be a powerful inducer of Interleukin-6 (IL-6) production; it overlaps with IL-6 and Tumor Necrosis Factor-(TNF-) in their actions ( Figure 5) [11]. IL-6 has an increased amount after 24 hrs [12]. It regulates immune responses in inflammation sites [13], and it has an autocrine/paracrine activity stimulating osteoclast formation and bone-resorbing activity of preformed osteoclasts [14].…”

Section: Proinflammatory Cytokines: Interleukin-1 (Il-1 ) Interleukimentioning

confidence: 99%

Biomarkers of Periodontal Tissue Remodeling during Orthodontic Tooth Movement in Mice and Men: Overview and Clinical Relevance

d’Apuzzo¹,

Nucci²,

Jamilian³

et al. 2017

Periodontitis - A Useful Reference

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Biologically active substances are expressed by cells within the periodontium in response to mechanical stimuli from orthodontic appliances. Several possible biomarkers representing biological modifications during specific phenomena as simile-inflammatory process, bone resorption and formation, periodontal ligament changes, and vascular and neural responses are proposed. Citations to potentially published trials were conducted by searching PubMed, Cochrane databases, and scientific textbooks. Additionally, hand searching and contact with experts in the area were undertaken to identify potentially relevant published and unpublished studies. Selection criteria were as follows: animal models involving only mice and rats undergoing orthodontic treatment; collection of gingival crevicular fluid (GCF) as a noninvasively procedure for humans; no other simultaneous treatment that could affect experimental orthodontic movement. The data suggest that knowledge of the remodeling process occurring in periodontal tissues during orthodontic and orthopedic therapies may be a clinical usefulness procedure leading to proper choice of mechanical stress to improve and to shorten the period of treatment, avoiding adverse consequences. The relevance for clinicians of evaluating the rate of some substances as valid biomarkers of periodontal effects during orthodontic movement, by means of two models of study, mice and men, is underlined.

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“…The ability of IL-6 to stimulate bone resorption in vitro is variable and depends on the assay system [1,77,109,115]. The reasons for this variability are not known.…”

Section: In the Nucleustranscriptional Regulationmentioning

confidence: 99%

Genetics and Mutations Affecting Osteoclast Development and Function

Kacena¹,

Lorenzo²

2005

Bone Resorption

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source of osteoclast precursors. It was possible to culture these cells with stromal cell lines or primary osteoblasts to induce the formation of multinucleated, TRAP + bone-resorbing osteoclast-like cells [177]. These authors also demonstrated that cell contact between the hematopoietic osteoclast precursor and the mesenchymal stromal/osteoblastic cell was required for osteoclast formation. These experiments formed the basis for the seminal work that demonstrated the requirement for interaction between the receptor activator of nuclear factor (NF)-kB (RANK)-receptor and the activator of NF-kB ligand (RANKL) for osteoclast precursors to differentiate terminally into functional osteoclast-like cells, a phenomenon that is aided by the presence of macrophage colonystimulating factor (M-CSF) [5,97,200]. RANK is a member of the superfamily of TNF receptors; it is expressed on B and T cells, dendritic cells, osteoclast precursors, and mature osteoclasts [5]. RANKL is a type II transmembrane protein, expressed on stromal cells, osteoblasts, and T cells [97,194,200].It has taken more than 30 years for bone biologists to understand how osteoclasts develop, become active and function. Modern molecular biology has made it possible to manipulate specific genes. The identification of spontaneous mutations and the ability to engineer overexpression or deletion of specific genes have brought valuable insights into how those genes affect the organism. This genetic approach has been used successfully in defining osteoclast biology.

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Interleukin-6 messenger RNA expression and interleukin-6 protein secretion in cells isolated from normal human bone: Regulation by interleukin-1

Cited by 102 publications

References 53 publications

Duffy Antigen Receptor for Chemokines Regulates Post-Fracture Inflammation

Duffy Antigen Receptor for Chemokines Regulates Post-Fracture Inflammation

Biomarkers of Periodontal Tissue Remodeling during Orthodontic Tooth Movement in Mice and Men: Overview and Clinical Relevance

Genetics and Mutations Affecting Osteoclast Development and Function

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