Where to Stand with Stromal Cells and Chronic Synovitis in Rheumatoid Arthritis?

Brondello, Jean-Marc; Djouad, Farida

doi:10.3390/cells8101257

Cited by 14 publications

(12 citation statements)

References 75 publications

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“…Hyaluronic acid (HA), a negatively charged, nonsulfated glycosaminoglycan ubiquitous both in synovial fluid and articular cartilage [ 24 , 25 ], was for many years, assumed to be the molecule responsible for cartilage lubrication [ 26 , 27 ]. Clearly, HA plays a major role in joint homeostasis [ 28 , 29 , 30 ]; however, its boundary lubricating ability is poor, as directly determined experimentally by surface force balance (SFB) investigations [ 31 , 32 , 33 ]. Recent studies by Seror et al [ 33 ] and Zhu et al [ 34 ] demonstrated that the friction between two surface-attached HA layers was much reduced (from μ ≈ 0.3 to μ ≈ 0.001) after adding small unilamellar vesicles (SUVs) composed of PC lipids.…”

Section: Introductionmentioning

confidence: 99%

The Role of Hyaluronic Acid in Cartilage Boundary Lubrication

Lin

Liu

Kampf

et al. 2020

Cells

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Hydration lubrication has emerged as a new paradigm for lubrication in aqueous and biological media, accounting especially for the extremely low friction (friction coefficients down to 0.001) of articular cartilage lubrication in joints. Among the ensemble of molecules acting in the joint, phosphatidylcholine (PC) lipids have been proposed as the key molecules forming, in a complex with other molecules including hyaluronic acid (HA), a robust layer on the outer surface of the cartilage. HA, ubiquitous in synovial joints, is not in itself a good boundary lubricant, but binds the PC lipids at the cartilage surface; these, in turn, massively reduce the friction via hydration lubrication at their exposed, highly hydrated phosphocholine headgroups. An important unresolved issue in this scenario is why the free HA molecules in the synovial fluid do not suppress the lubricity by adsorbing simultaneously to the opposing lipid layers, i.e., forming an adhesive, dissipative bridge between them, as they slide past each other during joint articulation. To address this question, we directly examined the friction between two hydrogenated soy PC (HSPC) lipid layers (in the form of liposomes) immersed in HA solution or two palmitoyl–oleoyl PC (POPC) lipid layers across HA–POPC solution using a surface force balance (SFB). The results show, clearly and surprisingly, that HA addition does not affect the outstanding lubrication provided by the PC lipid layers. A possible mechanism indicated by our data that may account for this is that multiple lipid layers form on each cartilage surface, so that the slip plane may move from the midplane between the opposing surfaces, which is bridged by the HA, to an HA-free interface within a multilayer, where hydration lubrication is freely active. Another possibility suggested by our model experiments is that lipids in synovial fluid may complex with HA, thereby inhibiting the HA molecules from adhering to the lipids on the cartilage surfaces.

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Section: Introductionmentioning

confidence: 99%

The Role of Hyaluronic Acid in Cartilage Boundary Lubrication

Lin

Liu

Kampf

et al. 2020

Cells

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“…RRV infection has been shown to promote glycolytic pathways in vitro , however a clear relationship between glycolytic pathways and IL-17 signaling in arthritic disease remains to be established [ 93 ]. In addition, studies have shown that differentiation and proliferation of IL-17–producing Th17 cells from naïve CD4 + T cells requires significant cellular metabolic changes, and these changes are essential in nutrient-poor environments such as the acidic environment found in inflamed RA joints [ 94 , 95 ]. Among genes upregulated in CD45 + cells from IL-17A/F mAb-treated mice, SLC27A1 encodes FATP1 (fatty acid transport protein-1), which helps control lipid and glucose metabolism, and has been associated with anti-inflammatory phenotypes in macrophages by acting as a modulator of oxidative stress [ 96 ], and is highly expressed in skeletal tissues during steady-state [ 97 , 98 ].…”

Section: Discussionmentioning

confidence: 99%

Interleukin-17 contributes to Ross River virus-induced arthritis and myositis

et al. 2022

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Arthritogenic alphaviruses are mosquito-borne viruses that are a major cause of infectious arthropathies worldwide, and recent outbreaks of chikungunya virus and Ross River virus (RRV) infections highlight the need for robust intervention strategies. Alphaviral arthritis can persist for months after the initial acute disease, and is mediated by cellular immune responses. A common strategy to limit inflammation and pathology is to dampen the overwhelming inflammatory responses by modulating proinflammatory cytokine pathways. Here, we investigate the contribution of interleukin-17 (IL-17), a cytokine involved in arthropathies such as rheumatoid arthritis, in the development RRV-induced arthritis and myositis. IL-17 was quantified in serum from RRV-infected patients, and mice were infected with RRV and joints and muscle tissues collected to analyse cellular infiltrates, tissue mRNA, cytokine expression, and joint and muscle histopathology. IL-17 expression was increased in musculoskeletal tissues and serum of RRV-infected mice and humans, respectively. IL-17–producing T cells and neutrophils contributed to the cellular infiltrate in the joint and muscle tissue during acute RRV disease in mice. Blockade of IL-17A/F using a monoclonal antibody (mAb) reduced disease severity in RRV-infected mice and led to decreased proinflammatory proteins, cellular infiltration in synovial tissues and cartilage damage, without affecting viral titers in inflamed tissues. IL-17A/F blockade triggered a shift in transcriptional profile of both leukocyte infiltrates and musculoskeletal stromal cells by downregulating proinflammatory genes. This study highlights a previously uncharacterized role for an effector cytokine in alphaviral pathology and points towards potential therapeutic benefit in targeting IL-17 to treat patients presenting with RRV-induced arthropathy.

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“…In addition to several autoimmune diseases such as RA, epigenetic modifications have also been shown to increase inflammation in tissues through pro-inflammatory transcription factor nuclear factor kappa B (NF-κB) activation [ 296 , 297 , 298 , 299 , 300 , 301 , 302 , 303 , 304 ]. Furthermore, the epigenetic phenomena underlying the anti-inflammatory potential of diet and lifestyle conditions have resulted in the development of therapeutic actions to alleviate constant inflammation affecting the epigenome.…”

Section: Treatment Strategies In Ramentioning

confidence: 99%

Recent Advances in Understanding the Pathogenesis of Rheumatoid Arthritis: New Treatment Strategies

Mueller

Payandeh

Mohammadkhani

et al. 2021

Cells

104

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Rheumatoid arthritis (RA) is considered a chronic systemic, multi-factorial, inflammatory, and progressive autoimmune disease affecting many people worldwide. While patients show very individual courses of disease, with RA focusing on the musculoskeletal system, joints are often severely affected, leading to local inflammation, cartilage destruction, and bone erosion. To prevent joint damage and physical disability as one of many symptoms of RA, early diagnosis is critical. Auto-antibodies play a pivotal clinical role in patients with systemic RA. As biomarkers, they could help to make a more efficient diagnosis, prognosis, and treatment decision. Besides auto-antibodies, several other factors are involved in the progression of RA, such as epigenetic alterations, post-translational modifications, glycosylation, autophagy, and T-cells. Understanding the interplay between these factors would contribute to a deeper insight into the causes, mechanisms, progression, and treatment of the disease. In this review, the latest RA research findings are discussed to better understand the pathogenesis, and finally, treatment strategies for RA therapy are presented, including both conventional approaches and new methods that have been developed in recent years or are currently under investigation.

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Where to Stand with Stromal Cells and Chronic Synovitis in Rheumatoid Arthritis?

Cited by 14 publications

References 75 publications

The Role of Hyaluronic Acid in Cartilage Boundary Lubrication

The Role of Hyaluronic Acid in Cartilage Boundary Lubrication

Interleukin-17 contributes to Ross River virus-induced arthritis and myositis

Recent Advances in Understanding the Pathogenesis of Rheumatoid Arthritis: New Treatment Strategies

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