Protective effect of low dose intra-articular cadmium on inflammation and joint destruction in arthritis.
Paola BonaventuraGuillaume CourbonAline LambouxFabien LavocatHubert MarotteFrancis AlbarèdePierre MiossecPublished in: Scientific reports (2017)
Synovium hyperplasia characterizes joint diseases, such as rheumatoid arthritis (RA). The cytotoxic effect of low-dose Cadmium (Cd) was tested in vitro and ex vivo on synoviocytes, the mesenchymal key effector cells of inflammation and proliferation in arthritis. The anti-inflammatory and anti-proliferative effects of Cd were tested in vivo by intra-articular injection in the adjuvant induced arthritis rat joints, where the clinical scores and the consequences of arthritis were evaluated. Cell death through apoptosis was highly induced by Cd in inflammatory synoviocytes (80% reduction of cell viability, p < 0.01). TNF plus IL-17 cytokine combination induced a two-fold increase of Cd cell content by enhancing the ZIP-8 importer and the MT-1 homeostasis regulator expression. Addition of Cd reduced IL-6 production in TNF plus IL-17-activated synoviocytes (up to 83%, p < 0.05) and in ex-vivo synovium biopsies (up to 94%, p < 0.01). Cd-injection in rat joints improved arthritis, reducing clinical scores (arthritic score reduced from 4 to 2, p < 0.01), inflammatory cell recruitment (up to 50%, p < 0.01) and protecting from bone/cartilage destruction. This proof of concept study is supported by the limited Cd spread in body reservoirs, with low-dose Cd providing a safe risk/benefit ratio, without toxic effects on other cell types and organs.
Keyphrases
- rheumatoid arthritis
- low dose
- oxidative stress
- cell death
- nk cells
- cell cycle arrest
- disease activity
- single cell
- high dose
- induced apoptosis
- anti inflammatory
- endoplasmic reticulum stress
- cell therapy
- ankylosing spondylitis
- diabetic rats
- high glucose
- poor prognosis
- bone marrow
- mesenchymal stem cells
- dendritic cells
- heavy metals
- postmenopausal women
- binding protein
- type iii