Pro- and Anti-inflammatory Cytokine Profiles in Osteoarthritis

Bastiaansen-Jenniskens, Y.M.; Saris, Daniël B.F.; Creemers, Laura B.

doi:10.1007/978-3-319-45803-8_5

Cited by 6 publications

(9 citation statements)

References 77 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among cytokines, low molecular weight chemokines are recognizable with the role of inducing chemotaxis [131]. Both chemokines and cytokines are produced by joint tissues (synovial membrane, cartilage, meniscus, IFP, and bone), glial cells, and sensory neurons; they are found also in SF exerting an important role in OA disease [17, 137–139]. Moreover, there is evidence that some of them are involved not only in inflammation but also in the process of neuropathic pain [131].…”

Section: Ifp-synovial Membrane Mediators Involved In Oa Pathology mentioning

confidence: 99%

Contribution of Infrapatellar Fat Pad and Synovial Membrane to Knee Osteoarthritis Pain

Belluzzi

Stocco

Pozzuoli

et al. 2019

BioMed Research International

132

124

View full text Add to dashboard Cite

Osteoarthritis (OA) is the most common form of joint disease and a major cause of pain and disability in the adult population. Interestingly, there are patients with symptomatic OA displaying pain, while patients with asymptomatic OA that do not experience pain but show radiographic signs of joint damage. Pain is a complex experience integrating sensory, affective, and cognitive processes related to several peripheral and central nociceptive factors besides inflammation. During the last years, the role of infrapatellar fat pad (IFP), other than the synovial membrane, has been investigated as a potential source of pain in OA. Interestingly, new findings suggest that IFP and synovial membrane might act as a functional unit in OA pathogenesis and pain. The present review discuss the role of IFP and synovial membrane in the development of OA, with a particular focus on pain onset and the possible involved mediators that may play a role in OA pathology and pain mechanisms. Inflammation of IFP and synovial membrane may drive peripheral and central sensitization in KOA. Since sensitization is associated with pain severity in knee OA and may potentially contribute to the transition from acute to chronic, persistent pain in knee OA, preventing sensitization would be a potentially effective and novel means of preventing worsening of pain in knee OA.

show abstract

Section: Ifp-synovial Membrane Mediators Involved In Oa Pathology mentioning

confidence: 99%

Contribution of Infrapatellar Fat Pad and Synovial Membrane to Knee Osteoarthritis Pain

Belluzzi

Stocco

Pozzuoli

et al. 2019

BioMed Research International

132

124

View full text Add to dashboard Cite

show abstract

“…Both the progression and debut of OA seems to be linked to cytokines. In the synovial fluid proinflammatory cytokines accumulate together with anti-inflammatory ones forming a combination entitled cytokine network that can modulate the process of degradation of the cartilage matrix [57,58].…”

Section: Mechanism Of Inflammaging and Implications In Oamentioning

confidence: 99%

“…Similarly, interleukin-37 also known as IL 1F7, is associated with OA disease activity being correlated with the suppression of proinflammatory cytokine production such as IL-1β, TNF-α, and IL-6, at the synovial cell level [61]. Possible novel therapeutic targets could be discovered if we take into account other inflammatory, anti-inflammatory, and modulatory cytokines associated with OA rather than the presence of IL-1 and TNF-α, which often show poor correlation with the osteoarthritic joint [58].…”

Section: Mechanism Of Inflammaging and Implications In Oamentioning

confidence: 99%

The Link Between Inflammaging and Degenerative Joint Diseases

Rezuş

Cardoneanu

Burlui

et al. 2019

IJMS

View full text Add to dashboard Cite

Aging is an inevitable process in the human body that is associated with a multitude of systemic and localized changes. All these conditions have a common pathogenic mechanism characterized by the presence of a low-grade proinflammatory status. Inflammaging refers to all the processes that contribute to the occurrence of various diseases associated with aging such as frailty, atherosclerosis, Alzheimer’s disease, sarcopenia, type 2 diabetes, or osteoarthritis. Inflammaging is systemic, chronic, and asymptomatic. Osteoarthritis and many age-related degenerative joint diseases are correlated with aging mechanisms such as the presence of an inflammatory microenvironment and the impaired link between inflammasomes and autophagy. There is a close relationship between chondrocyte activity and local articular environment changes due to cell senescence, followed by secretion of inflammatory mediators. In addition, systemic inflammaging can lead to cartilage destruction, pain, disability, and an impaired quality of life. The purpose of this review is to summarize the main mechanisms implicated in inflammaging and the connection it has with degenerative joint diseases.

show abstract

“…These cytokines are elevated in the synovial fluid, synovial membrane, subchondral bone, and cartilage of patients with OA, and act by both suppressing synthesis of cartilage matrix components and inducing expression of catabolic and degradative enzymes and inflammatory cytokines. [3][4][5] The presence of inflammation within an OA joint provides a challenging environment for articular cartilage repair, as pro-inflammatory cytokines will cause degeneration of native and tissue-engineered cartilage, as well as prevent chondrogenesis of stem cells. 6,7 Thus, a number of approaches have targeted the IL-1 or TNF-α pathways as a therapy for OA [8][9][10][11] or as a means of inhibiting inflammatory effects on tissue-engineered cartilage.…”

Section: Introductionmentioning

confidence: 99%

“…These processes are mediated in part by pro‐inflammatory cytokines, such as interleukin‐1 (IL‐1) and tumor necrosis factor‐α (TNF‐α). These cytokines are elevated in the synovial fluid, synovial membrane, subchondral bone, and cartilage of patients with OA, and act by both suppressing synthesis of cartilage matrix components and inducing expression of catabolic and degradative enzymes and inflammatory cytokines 3‐5 . The presence of inflammation within an OA joint provides a challenging environment for articular cartilage repair, as pro‐inflammatory cytokines will cause degeneration of native and tissue‐engineered cartilage, as well as prevent chondrogenesis of stem cells 6,7 …”

Section: Introductionmentioning

confidence: 99%

The miRNA‐mRNA interactome of murine induced pluripotent stem cell‐derived chondrocytes in response to inflammatory cytokines

et al. 2020

View full text Add to dashboard Cite

Osteoarthritis (OA) is a degenerative joint disease, and inflammation within an arthritic joint plays a critical role in disease progression. Pro‐inflammatory cytokines, specifically IL‐1 and TNF‐α, induce aberrant expression of catabolic and degradative enzymes and inflammatory cytokines in OA and result in a challenging environment for cartilage repair and regeneration. MicroRNAs (miRNAS) are small noncoding RNAs and are important regulatory molecules that act by binding to target messenger RNAs (mRNAs) to reduce protein synthesis and have been implicated in many diseases, including OA. The goal of this study was to understand the mechanisms of miRNA regulation of the transcriptome of tissue‐engineered cartilage in response to IL‐1β and TNF‐α using an in vitro murine induced pluripotent stem cell (miPSC) model system. We performed miRNA and mRNA sequencing to determine the temporal and dynamic responses of genes to specific inflammatory cytokines as well as miRNAs that are differentially expressed (DE) in response to both cytokines or exclusively to IL‐1β or TNF‐α. Through integration of mRNA and miRNA sequencing data, we created networks of miRNA‐mRNA interactions which may be controlling the response to inflammatory cytokines. Within the networks, hub miRNAs, miR‐29b‐3p, miR‐17‐5p, and miR‐20a‐5p, were identified. As validation of these findings, we found that delivery of miR‐17‐5p and miR‐20a‐5p mimics significantly decreased degradative enzyme activity levels while also decreasing expression of inflammation‐related genes in cytokine‐treated cells. This study utilized an integrative approach to determine the miRNA interactome controlling the response to inflammatory cytokines and novel mediators of inflammation‐driven degradation in tissue‐engineered cartilage.

show abstract

Pro- and Anti-inflammatory Cytokine Profiles in Osteoarthritis

Cited by 6 publications

References 77 publications

Contribution of Infrapatellar Fat Pad and Synovial Membrane to Knee Osteoarthritis Pain

Contribution of Infrapatellar Fat Pad and Synovial Membrane to Knee Osteoarthritis Pain

The Link Between Inflammaging and Degenerative Joint Diseases

The miRNA‐mRNA interactome of murine induced pluripotent stem cell‐derived chondrocytes in response to inflammatory cytokines

Contact Info

Product

Resources

About