Abstract | OBJECTIVE: METHODS: T cell proliferation, cytokine production by T cells stimulated through CD28, CD26, or PMA with or without anti-CD3 Mab, cytokine production by macrophages stimulated with lipopolysaccharide, and transendothelial migration of T cells were analyzed in the presence or absence of various concentrations of RXM. We evaluated the effect of RXM treatment in collagen induced arthritis in mice. RESULTS: RXM did not affect the production of Th1-type and Th2-type cytokines, whereas it specifically inhibited production of proinflammatory cytokines such as tumor necrosis factor-a and interleukin 6 (IL-6) by T cells and macrophages. RXM inhibited T cell migration. We found that RXM treatment of mice with CIA reduced the severity of arthritis and serum level of IL-6, as well as leukocyte migration into the affected joints and destruction of bones and cartilage. CONCLUSION:
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Authors | Yasuyo Urasaki, Mamoru Nori, Satoshi Iwata, Takahiro Sasaki, Osamu Hosono, Hiroshi Kawasaki, Hirotoshi Tanaka, Nam H Dang, Eiji Ikeda, Chikao Morimoto |
Journal | The Journal of rheumatology
(J Rheumatol)
Vol. 32
Issue 9
Pg. 1765-74
(Sep 2005)
ISSN: 0315-162X [Print] Canada |
PMID | 16142877
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cytokines
- Interleukin-6
- Tumor Necrosis Factor-alpha
- Roxithromycin
- Collagen
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Topics |
- Animals
- Arthritis, Experimental
(drug therapy, pathology)
- Biopsy, Needle
- Cell Proliferation
(drug effects)
- Cells, Cultured
- Collagen
- Cytokines
(biosynthesis, drug effects)
- Disease Models, Animal
- Enzyme-Linked Immunosorbent Assay
- Immunohistochemistry
- Interleukin-6
(biosynthesis)
- Macrophages
(cytology, drug effects)
- Male
- Mice
- Mice, Inbred DBA
- Probability
- Roxithromycin
(pharmacology)
- Sensitivity and Specificity
- T-Lymphocytes
(cytology, drug effects)
- Tumor Necrosis Factor-alpha
(biosynthesis, drug effects)
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