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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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Related in: MedlinePlus

Blocking of monocyte migration induced by RA SCL supernatants with blocking anti-chemokine or chemokine receptor mAbs. Monocyte migration induced by supernatants of RA SCLs (RA6/1 and RA8/3) 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 nine independent experiments. The paired Student t test was used to assess statistical differences versus the result with control mAb.
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Figure 5: Blocking of monocyte migration induced by RA SCL supernatants with blocking anti-chemokine or chemokine receptor mAbs. Monocyte migration induced by supernatants of RA SCLs (RA6/1 and RA8/3) 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 nine independent experiments. The paired Student t test was used to assess statistical differences versus the result with control mAb.

Mentions: Blocking experiments were carried out using mAbs to determine the chemokines that contribute to monocyte migration induced by RA SCLs (Fig. 5). Anti-MCP-1 and anti-IL-8 mAbs decreased monocyte migration significantly, with the effect of anti-MCP-1 being consistently greater than that of anti-IL-8. Anti-CCR5 blocking mAb did not effect monocyte migration. The anti-CCR5 mAb did have blocking activity, however, since migration of T cells induced by RANTES (500 ng/ml) was blocked by 95% (data not shown).


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 RA SCL supernatants with blocking anti-chemokine or chemokine receptor mAbs. Monocyte migration induced by supernatants of RA SCLs (RA6/1 and RA8/3) 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 nine independent experiments. The paired Student t test was used to assess statistical differences versus the result with control mAb.
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Related In: Results  -  Collection

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

Figure 5: Blocking of monocyte migration induced by RA SCL supernatants with blocking anti-chemokine or chemokine receptor mAbs. Monocyte migration induced by supernatants of RA SCLs (RA6/1 and RA8/3) 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 nine independent experiments. The paired Student t test was used to assess statistical differences versus the result with control mAb.
Mentions: Blocking experiments were carried out using mAbs to determine the chemokines that contribute to monocyte migration induced by RA SCLs (Fig. 5). Anti-MCP-1 and anti-IL-8 mAbs decreased monocyte migration significantly, with the effect of anti-MCP-1 being consistently greater than that of anti-IL-8. Anti-CCR5 blocking mAb did not effect monocyte migration. The anti-CCR5 mAb did have blocking activity, however, since migration of T cells induced by RANTES (500 ng/ml) was blocked by 95% (data not shown).

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