Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

Vandooren, Bernard; Noordenbos, Troy; Ambarus, Carmen A.; Krausz, Sarah; Cantaert, Tineke; Yeremenko, Nataliya; Boumans, Maartje; Lutter, René; Tak, Paul P.; Baeten, Dominique

doi:10.1002/art.24406

Cited by 148 publications

(92 citation statements)

References 56 publications

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“…This E2-potentiated M1 activation could contribute to the perpetuation of joint inflammation and tissue breakdown. The importance of M1 activation was previously revealed in a clinical study where the synovial fluid levels of M1-derived cytokines were well correlated with joint inflammation in RA (39). Therefore, the promotion and accumulation of M1 macrophages by estrogen in inflamed joints may be an important mechanism underlying the sex differences of TMD and RA.…”

Section: Discussionmentioning

confidence: 78%

Estradiol Promotes M1-like Macrophage Activation through Cadherin-11 To Aggravate Temporomandibular Joint Inflammation in Rats

Kou¹,

et al. 2015

The Journal of Immunology

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Macrophages play a major role in joint inflammation. Estrogen is involved in rheumatoid arthritis and temporomandibular disorders. However, the underlying mechanism is still unclear. This study was done to verify and test how estrogen affects M1/M2-like macrophage polarization and then contributes to joint inflammation. Female rats were ovariectomized and treated with increasing doses of 17β-estradiol for 10 d and then intra-articularly injected with CFA to induce temporomandibular joint (TMJ) inflammation. The polarization of macrophages and expression of cadherin-11 was evaluated at 24 h after the induction of TMJ inflammation and after blocking cadherin-11 or estrogen receptors. NR8383 macrophages were treated with estradiol and TNF-α, with or without blocking cadherin-11 or estrogen receptors, to evaluate the expression of the M1/M2-like macrophage-associated genes. We found that estradiol increased the infiltration of macrophages with a proinflammatory M1-like predominant profile in the synovium of inflamed TMJ. In addition, estradiol dose-dependently upregulated the expressions of the M1-associated proinflammatory factor inducible NO synthase (iNOS) but repressed the expressions of the M2-associated genes IL-10 and arginase in NR8383 macrophages. Furthermore, estradiol mainly promoted cadherin-11 expression in M1-like macrophages of inflamed TMJ. By contrast, blockage of cadherin-11 concurrently reversed estradiol-potentiated M1-like macrophage activation and TMJ inflammation, as well as reversed TNF-α–induced induction of inducible NO synthase and NO in NR8383 macrophages. The blocking of estrogen receptors reversed estradiol-potentiated M1-like macrophage activation and cadherin-11 expression. These results suggested that estradiol could promote M1-like macrophage activation through cadherin-11 to aggravate the acute inflammation of TMJs.

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Section: Discussionmentioning

confidence: 78%

Estradiol Promotes M1-like Macrophage Activation through Cadherin-11 To Aggravate Temporomandibular Joint Inflammation in Rats

Kou¹,

et al. 2015

The Journal of Immunology

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“…Second, differences in spontaneous osteoclastogenesis appear to be related to the culture conditions, suggesting a critical role of extrinsic factors, rather than an intrinsic increase in osteoclast precursors, in the peripheral blood monocyte population (5,8). The extent to which the in vitro expression of these factors reflects the in vivo situation in the inflamed joint remains in question (16,17).…”

Section: Discussionmentioning

confidence: 99%

In vitro spontaneous osteoclastogenesis of human peripheral blood mononuclear cells is not crucially dependent on T lymphocytes

Vandooren¹,

Melis²,

Veys³

et al. 2009

Arthritis & Rheumatism

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Objective. In vitro spontaneous osteoclastogenesis from peripheral blood mononuclear cells (PBMCs) is increased in diseases with excessive bone loss. The purpose of this study was to reassess the role of T lymphocytes in this process.Methods. Fresh or cryopreserved PBMCs obtained from healthy subjects and from patients with rheumatoid arthritis, psoriatic arthritis, and nonpsoriatic spondylarthritis were cultured at high density and stained for tartrate-resistant acid phosphatase (TRAP). Resorption of mineralized matrix was assessed by a dentin disc assay. CD14؉ monocytes and CD3؉ T cells were selected using magnetically labeled antibodies.Results. Numerous multinucleated, TRAP؉, dentin-resorbing osteoclasts developed spontaneously from fresh PBMCs from healthy individuals. This process was abrogated by T cell depletion and was restored by exogenous macrophage colony-stimulating factor (M-CSF) and RANKL, indicating the important role of T cells in spontaneous osteoclastogenesis in vitro. Using physiologic freezing and thawing as a model for the activation of PBMCs, spontaneous osteoclastogenesis was significantly increased in cryopreserved versus fresh cells. Under these conditions, spontaneous osteoclastogenesis was not dependent on T lymphocytes, since it was not influenced by T cell depletion and persisted in purified CD14؉ cell cultures supplemented with M-CSF and RANKL. In contrast to studies with fresh PBMCs, spontaneous osteoclastogenesis under these conditions did not appear to be clearly different between healthy subjects and patients with arthritis.Conclusion. Spontaneous osteoclastogenesis in vitro is dependent on T lymphocytes or on the direct activation of monocytic cells, depending on the test conditions. This variability warrants better validation of the relevance of this functional test for in vivo osteoclastogenesis.

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“…The cellular and molecular pathways responsible for the differences and commonalities between these two types of arthritis remain largely unknown. Based on a series of systematic synovial studies, we recently proposed that joint inflammation in SpA may be driven mainly by cells of the innate immune system, including specific macrophage subsets and granulocytes, whereas molecular pathways related to (auto)antigen-specific T and B lymphocyte activation predominate in RA synovitis (1)(2)(3)(4)(5)(6)(7)(8)(9)(10).…”

mentioning

confidence: 99%

Interleukin‐17–positive mast cells contribute to synovial inflammation in spondylarthritis

Noordenbos

Yeremenko

Gofita

et al. 2011

Arthritis & Rheumatism

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159

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Absence of a classically activated macrophage cytokine signature in peripheral spondylarthritis, including psoriatic arthritis

Cited by 148 publications

References 56 publications

Estradiol Promotes M1-like Macrophage Activation through Cadherin-11 To Aggravate Temporomandibular Joint Inflammation in Rats

Estradiol Promotes M1-like Macrophage Activation through Cadherin-11 To Aggravate Temporomandibular Joint Inflammation in Rats

In vitro spontaneous osteoclastogenesis of human peripheral blood mononuclear cells is not crucially dependent on T lymphocytes

Interleukin‐17–positive mast cells contribute to synovial inflammation in spondylarthritis

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