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Synovial stromal cells from rheumatoid arthritis patients attract monocytes by producing MCP-1 and IL-8.

Hayashida K, Nanki T, Girschick H, Yavuz S, Ochi T, Lipsky PE - Arthritis Res. (2001)

Bottom Line: Macrophages that accumulate in the synovium of rheumatoid arthritis patients play an important role in the pathogenesis of this inflammatory disease.However, the mechanism by which macrophages are attracted into the inflamed synovium and accumulate there has not been completely delineated.These results suggest that one of the mechanisms by which macrophages accumulate in the inflamed synovium is by responding to the chemokines produced locally.

View Article: PubMed Central - PubMed

Affiliation: University of Texas, Southwestern Medical Center, Dallas, Texas, USA. lipskyp@mail.nih.gov

ABSTRACT
Macrophages that accumulate in the synovium of rheumatoid arthritis patients play an important role in the pathogenesis of this inflammatory disease. However, the mechanism by which macrophages are attracted into the inflamed synovium and accumulate there has not been completely delineated. The results of this study show that rheumatoid arthritis synovial stromal cells produce the chemokines monocyte chemotactic protein-1 and IL-8, and these have the capacity to attract peripheral monocytes. These results suggest that one of the mechanisms by which macrophages accumulate in the inflamed synovium is by responding to the chemokines produced locally.

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Blocking of monocyte migration induced by supernatant of RA SCL stimulated with TNF-α. Monocyte migration induced by supernatants of RA SCLs (RA6/1 and RA8/3) stimulated with 2 ng/ml TNF-α was assessed using mAbs, which can neutralize specific chemokines or chemokine receptors. Concentrations of mAbs were 10 μg/ml for MCP-1, IL-8, and IP-10, and 50 μg for anti-CCR5 mAb with 5 × 105 SRBC rosette negative cells. Migrating cells were stained with anti-CD-14 mAb, and migrating CD14+cells were counted by flow cytometry. The mean and SEM were calculated from the results of three independent experiments. The paired Student t test was used to assess statistical differences versus the result with control mAb.
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Figure 8: Blocking of monocyte migration induced by supernatant of RA SCL stimulated with TNF-α. Monocyte migration induced by supernatants of RA SCLs (RA6/1 and RA8/3) stimulated with 2 ng/ml TNF-α was assessed using mAbs, which can neutralize specific chemokines or chemokine receptors. Concentrations of mAbs were 10 μg/ml for MCP-1, IL-8, and IP-10, and 50 μg for anti-CCR5 mAb with 5 × 105 SRBC rosette negative cells. Migrating cells were stained with anti-CD-14 mAb, and migrating CD14+cells were counted by flow cytometry. The mean and SEM were calculated from the results of three independent experiments. The paired Student t test was used to assess statistical differences versus the result with control mAb.

Mentions: Anti-MCP-1 mAb and anti-IL-8 mAb significantly inhibited monocyte migration by supernatants of RA SCLs stimulated with TNF-α. Anti-IP-10 mAb and anti-CCR5 mAb did not inhibit monocyte migration significantly (Fig. 8).


Synovial stromal cells from rheumatoid arthritis patients attract monocytes by producing MCP-1 and IL-8.

Hayashida K, Nanki T, Girschick H, Yavuz S, Ochi T, Lipsky PE - Arthritis Res. (2001)

Blocking of monocyte migration induced by supernatant of RA SCL stimulated with TNF-α. Monocyte migration induced by supernatants of RA SCLs (RA6/1 and RA8/3) stimulated with 2 ng/ml TNF-α was assessed using mAbs, which can neutralize specific chemokines or chemokine receptors. Concentrations of mAbs were 10 μg/ml for MCP-1, IL-8, and IP-10, and 50 μg for anti-CCR5 mAb with 5 × 105 SRBC rosette negative cells. Migrating cells were stained with anti-CD-14 mAb, and migrating CD14+cells were counted by flow cytometry. The mean and SEM were calculated from the results of three independent experiments. The paired Student t test was used to assess statistical differences versus the result with control mAb.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC17828&req=5

Figure 8: Blocking of monocyte migration induced by supernatant of RA SCL stimulated with TNF-α. Monocyte migration induced by supernatants of RA SCLs (RA6/1 and RA8/3) stimulated with 2 ng/ml TNF-α was assessed using mAbs, which can neutralize specific chemokines or chemokine receptors. Concentrations of mAbs were 10 μg/ml for MCP-1, IL-8, and IP-10, and 50 μg for anti-CCR5 mAb with 5 × 105 SRBC rosette negative cells. Migrating cells were stained with anti-CD-14 mAb, and migrating CD14+cells were counted by flow cytometry. The mean and SEM were calculated from the results of three independent experiments. The paired Student t test was used to assess statistical differences versus the result with control mAb.
Mentions: Anti-MCP-1 mAb and anti-IL-8 mAb significantly inhibited monocyte migration by supernatants of RA SCLs stimulated with TNF-α. Anti-IP-10 mAb and anti-CCR5 mAb did not inhibit monocyte migration significantly (Fig. 8).

Bottom Line: Macrophages that accumulate in the synovium of rheumatoid arthritis patients play an important role in the pathogenesis of this inflammatory disease.However, the mechanism by which macrophages are attracted into the inflamed synovium and accumulate there has not been completely delineated.These results suggest that one of the mechanisms by which macrophages accumulate in the inflamed synovium is by responding to the chemokines produced locally.

View Article: PubMed Central - PubMed

Affiliation: University of Texas, Southwestern Medical Center, Dallas, Texas, USA. lipskyp@mail.nih.gov

ABSTRACT
Macrophages that accumulate in the synovium of rheumatoid arthritis patients play an important role in the pathogenesis of this inflammatory disease. However, the mechanism by which macrophages are attracted into the inflamed synovium and accumulate there has not been completely delineated. The results of this study show that rheumatoid arthritis synovial stromal cells produce the chemokines monocyte chemotactic protein-1 and IL-8, and these have the capacity to attract peripheral monocytes. These results suggest that one of the mechanisms by which macrophages accumulate in the inflamed synovium is by responding to the chemokines produced locally.

Show MeSH
Related in: MedlinePlus