ArticlePloS one2018
Collagen V oral administration decreases inflammation and remodeling of synovial membrane in experimental arthritis.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Immunotherapeutic potential of collagen V oral administration in mBSA/CFA-induced arthritis.PloS one · 2024Article
- Article
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Because collagen type V (Col V) can be exposed in tissue injury, we hypothesized that oral administration of this collagen species modulates the inflammation and remodeling of experimental synovitis, avoiding joint destruction, and that the modulation may differ according to the temporal administration. Arthritis (IA, n = 20) was induced in Lewis rats by intraarticular (ia) injection of 500 μg of methylated bovine serum albumin (mBSA) emulsified in complete Freund's adjuvant (CFA) (10 μl) followed by an intraarticular booster of mBSA (50 μg) in saline (50 μl) administered at 7 and 14 days. The control group received saline (50 μl, ia). After the first intraarticular injection, ten IA animals were supplemented via gavage with Col V (500 μg/300 μl) daily for 30 days (IA/Suppl). The control group received saline (50 μL) and Col V supplement in the same way (Suppl). Col V oral administration in IA/Suppl led to 1) inhibited edema and severe inflammatory cell infiltration, 2) decreased collagen fiber content, 3) decreased collagen type I, 4) inhibited lymphocyte subpopulations and macrophages, 5) inhibited IL-1β, IL-10, IL-17 and TNF-α production and 6) increased expression of caspase-9 in the synovial tissue. In conclusion, Col V supplementation decreased synovial inflammation and the fibrotic response, possibly by increased the apoptosis of inflammatory cells.
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