S100A8/A9 and Inflammation in Rheumatoid Arthritis
Author Information
Author(s): Sunahori Katsue, Yamamura Masahiro, Yamana Jiro, Takasugi Kouji, Kawashima Masanori, Yamamoto Hiroshi, Chazin Walter J, Nakatani Yuichi, Yui Satoru, Makino Hirofumi
Primary Institution: Okayama University
Hypothesis
The S100A8/A9 heterodimer amplifies proinflammatory cytokine production by macrophages via activation of nuclear factor kappa B and p38 mitogen-activated protein kinase in rheumatoid arthritis.
Conclusion
The S100A8/A9 heterodimer may amplify proinflammatory cytokine responses through activation of NF-κB and p38 MAPK pathways in rheumatoid arthritis.
Supporting Evidence
- S100A8/A9 levels were significantly higher in patients with rheumatoid arthritis compared to those with osteoarthritis.
- S100A8/A9 stimulated the production of proinflammatory cytokines in monocytes and macrophages.
- NF-κB and p38 MAPK pathways were activated by S100A8/A9 stimulation.
Takeaway
S100A8 and S100A9 are proteins that help cause inflammation in rheumatoid arthritis by making immune cells produce more signals that lead to inflammation.
Methodology
The study involved comparing serum and synovial fluid samples from patients with rheumatoid arthritis and osteoarthritis, measuring cytokine levels, and assessing the effects of S100A8/A9 on monocytes and macrophages.
Limitations
The cellular composition of synovial tissue cells was not determined, and the study did not explore the effects of S100A8/A9 in vivo.
Participant Demographics
17 patients with rheumatoid arthritis (14 women, 3 men; mean age 63 years) and 17 patients with osteoarthritis (12 women, 5 men; mean age 65 years).
Statistical Information
P-Value
p<0.0001
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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