Synovial tissue macrophages: friend or foe?

Kurowska‐Stolarska, Mariola; Alivernini, Stefano

doi:10.1136/rmdopen-2017-000527

Cited by 99 publications

(95 citation statements)

References 93 publications

(140 reference statements)

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“…Moreover, defective regulatory T cells are associated with autoimmune disorders, such as RA [46]. Furthermore, macrophages play an active role in the pathogenesis of inflammatory arthritides because of the high expression of pro-inflammatory cytokines and matrix metalloproteinases, and they are APCs for T cells and B cells, representing a source of osteoclast precursors in an inflammatory context [47]. Lymphocytes infiltrate the synovium, where aggregates of T cells and B cells are found, and their absence is associated with remission [48,49].…”

Section: Oxidative Stress and Inflammation In Arthritismentioning

confidence: 99%

Hydrogen Sulfide as Potential Regulatory Gasotransmitter in Arthritic Diseases

Sunzini

Stefano

Chimenti

et al. 2020

IJMS

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The social and economic impact of chronic inflammatory diseases, such as arthritis, explains the growing interest of the research in this field. The antioxidant and anti-inflammatory properties of the endogenous gasotransmitter hydrogen sulfide (H 2 S) were recently demonstrated in the context of different inflammatory diseases. In particular, H 2 S is able to suppress the production of pro-inflammatory mediations by lymphocytes and innate immunity cells. Considering these biological effects of H 2 S, a potential role in the treatment of inflammatory arthritis, such as rheumatoid arthritis (RA), can be postulated. However, despite the growing interest in H 2 S, more evidence is needed to understand the pathophysiology and the potential of H 2 S as a therapeutic agent. Within this review, we provide an overview on H 2 S biological effects, on its role in immune-mediated inflammatory diseases, on H 2 S releasing drugs, and on systems of tissue repair and regeneration that are currently under investigation for potential therapeutic applications in arthritic diseases.

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Section: Oxidative Stress and Inflammation In Arthritismentioning

confidence: 99%

Hydrogen Sulfide as Potential Regulatory Gasotransmitter in Arthritic Diseases

Sunzini

Stefano

Chimenti

et al. 2020

IJMS

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“…Activated macrophages promote a number of proinflammatory mechanisms in the RA synovium through abundant secretion of proinflammatory cytokines; in addition, macrophages induce nitric oxide synthase, present antigen to T and B cells and drive bone resorption [41]. RA synovial CD68 + macrophages correlate strongly with mitochondrial dysfunction and oxidative stress and are inversely related to in-vivo synovial pO2 levels [11,12,20].…”

Section: The Role Of Monocyte and Macrophage Metabolism In Ramentioning

confidence: 99%

Altered metabolic pathways regulate synovial inflammation in rheumatoid arthritis

Fearon

Hanlon

Wade

et al. 2018

Clinical and Experimental Immunology

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Rheumatoid arthritis is characterized by synovial proliferation, neovascularization and leucocyte extravasation leading to joint destruction and functional disability. The blood vessels in the inflamed synovium are highly dysregulated, resulting in poor delivery of oxygen; this, along with the increased metabolic demand of infiltrating immune cells and inflamed resident cells, results in the lack of key nutrients at the site of inflammation. In these adverse conditions synovial cells must adapt to generate sufficient energy to support their proliferation and activation status, and thus switch their cell metabolism from a resting regulatory state to a highly metabolically active state. This alters redox-sensitive signalling pathways and also results in the accumulation of metabolic intermediates which, in turn, can act as signalling molecules that further exacerbate the inflammatory response. The RA synovium is a multi-cellular tissue, and while many cell types interact to promote the inflammatory response, their metabolic requirements differ. Thus, understanding the complex interplay between hypoxia-induced signalling pathways, metabolic pathways and the inflammatory response will provide better insight into the underlying mechanisms of disease pathogenesis. OTHER ARTICLES PUBLISHED IN THIS REVIEW SERIESTranslating immunometabolism: towards curing human diseases by targeting metabolic processes underpinning the immune response. Clinical and Experimental Immunology 2019, 197: 141-142. T cell metabolism in chronic viral infection. Clinical and Experimental Immunology 2019, 197: 143-152. Sculpting tumor microenvironment with immune system: from immunometabolism to immunoediting. Clinical and Experimental Immunology 2019, 197: 153-160. Sensing between reactions -how the metabolic microenvironment shapes immunity.

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“…M2-like macrophages can be induced ex vivo by incubation in the presence of M-CSF supplemented or not with IL-4-IL-13 or of macrophage medium containing human serum AB (SAB) and have diverse functions, ranging from parasite control to immune suppression, wound repair, tissue remodeling, and angiogenesis (11). Some studies have clearly demonstrated that infiltrating synovial macrophages display a proinflammatory profile (2,(12)(13)(14)(15)(16).…”

mentioning

confidence: 99%

Monocyte/Macrophage Abnormalities Specific to Rheumatoid Arthritis Are Linked to miR-155 and Are Differentially Modulated by Different TNF Inhibitors

Paoletti

Rohmer

et al. 2019

The Journal of Immunology

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Proinflammatory macrophages and miR-155 are increased in patients with rheumatoid arthritis (RA). We studied membrane TNF (mTNF) expression on blood monocytes, polarization into macrophages, miR-155 expression, and the effect of anti-TNF on these biomarkers in RA patients. Sixty-seven RA patients and 109 controls (55 healthy, 54 with spondyloarthritis and connective tissue diseases) were studied. Monocytes were isolated and differentiated into macrophages with or without anti-TNF. mTNF expression was increased on monocytes from RA patients, but not from other inflammatory diseases, correlated with disease activity. Under human serum AB or M-CSF, only monocytes from RA had a defect of differentiation into M2-like macrophages and had a propensity for preferential maturation toward M1-like macrophages that contributed to synovial inflammation. This defect was correlated to mTNF expression and was partially reversed by monoclonal anti-TNF Abs but not by the TNF soluble receptor. miR-155 was increased in M2-macrophages except in adalimumab-treated patients. Transfection of healthy monocytes with miR-155 induced a decrease in M2-like markers, and transfection of RA monocytes with antagomir-155 allowed restoration of M2-like polarization. Defect in differentiation of monocytes into M2-like-macrophages linked to increased miR-155 and correlated with increased mTNF on monocytes could play a key role in RA pathogenesis. Monoclonal anti-TNF Abs but not the TNF soluble receptor partially restored this defect.

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Synovial tissue macrophages: friend or foe?

Cited by 99 publications

References 93 publications

Hydrogen Sulfide as Potential Regulatory Gasotransmitter in Arthritic Diseases

Hydrogen Sulfide as Potential Regulatory Gasotransmitter in Arthritic Diseases

Altered metabolic pathways regulate synovial inflammation in rheumatoid arthritis

Monocyte/Macrophage Abnormalities Specific to Rheumatoid Arthritis Are Linked to miR-155 and Are Differentially Modulated by Different TNF Inhibitors

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