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Phenotypic characteristics of human monocytes undergoing transendothelial migration.

Grisar J, Hahn P, Brosch S, Peterlik M, Smolen JS, Pietschmann P - Arthritis Res. (2001)

Bottom Line: We found that monocyte migration led to an enhanced expression of CD11a, CD33, CD45RO, CD54 [intercellular cell-adhesion molecule (ICAM)-1] and human leucocyte antigen-DR.Taken together, the results suggest that local cytokine production activating ECs is sufficient to enhance monocyte migration and that this, in turn, can induce changes consistent with an activated phenotype known to be interactive between antigen-presenting cells and T cells.These results have implications for our pathogenetic insights into rheumatoid arthritis.

View Article: PubMed Central - PubMed

Affiliation: Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Währinger Gürtel 18-20, A-1180 Vienna, Austria. johannes.grisar@akh-wien.ac.at

ABSTRACT
In our study we characterised the immunophenotype of monocytes that migrated through an endothelial cell (EC) monolayer in vitro. We found that monocyte migration led to an enhanced expression of CD11a, CD33, CD45RO, CD54 [intercellular cell-adhesion molecule (ICAM)-1] and human leucocyte antigen-DR. The most striking increase was observed for ICAM-1 when ECs were activated with tumour necrosis factor-alpha and interleukin-1alpha. The results of our study indicate the following: (1) there is a characteristic immunophenotype on the surface of monocytes after transendothelial migration; (2) this phenotype seems to be induced by interactions between monocytes and ECs; and (3) this change is enhanced by the pretreatment of ECs with cytokines. Taken together, the results suggest that local cytokine production activating ECs is sufficient to enhance monocyte migration and that this, in turn, can induce changes consistent with an activated phenotype known to be interactive between antigen-presenting cells and T cells. These results have implications for our pathogenetic insights into rheumatoid arthritis.

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Monocyte migration is increased after the pretreatment of ECs with cytokines. Confluent monolayers of ECs that were formed on collagen gels were simultaneously incubated without cytokines (control) and with tumour necrosis factor-α (TNF-α) (a), interleukin-1α (IL-1α) (b), interferon-γ (IFN-γ) (c) or macrophage inflammatory protein-1α (MIP-1α) (d). The percentages of migrated peripheral blood mononuclear cells (PBMCs) after a migration period of 30 minutes are shown. Statistical significance: (a)P = 0.006; (b)P < 0.001; (c)P = 0.016; (d)P = 0.043.
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Figure 2: Monocyte migration is increased after the pretreatment of ECs with cytokines. Confluent monolayers of ECs that were formed on collagen gels were simultaneously incubated without cytokines (control) and with tumour necrosis factor-α (TNF-α) (a), interleukin-1α (IL-1α) (b), interferon-γ (IFN-γ) (c) or macrophage inflammatory protein-1α (MIP-1α) (d). The percentages of migrated peripheral blood mononuclear cells (PBMCs) after a migration period of 30 minutes are shown. Statistical significance: (a)P = 0.006; (b)P < 0.001; (c)P = 0.016; (d)P = 0.043.

Mentions: It has been reported that cytokines such as TNF-α, IL-1α and IFN-γ and also the chemokine MIP-1α can enhance the transendothelial migration of monocytes [19,20]. We were therefore interested to investigate whether pretreatment of the ECs with these factors would be sufficient to enhance the transendothelial migration of monocytes and/or to induce changes in their expression of surface markers. Figure 2 shows that pretreatment of the endothelium with any of the cytokines led to a consistent and significant increase in the number of migrated mononuclear cells in comparison with simultaneously performed control experiments in which the endothelium was not pretreated. Pretreatment with IL-1α was the most effective, resulting in a 132% increase in migrated cells (P < 0.001). The respective values for the other cytokines were as follows: MIP-1α, 194% (P = 0.043); TNF-α, 193% (P = 0.006); IFN-γ, 136% (P = 0.016).


Phenotypic characteristics of human monocytes undergoing transendothelial migration.

Grisar J, Hahn P, Brosch S, Peterlik M, Smolen JS, Pietschmann P - Arthritis Res. (2001)

Monocyte migration is increased after the pretreatment of ECs with cytokines. Confluent monolayers of ECs that were formed on collagen gels were simultaneously incubated without cytokines (control) and with tumour necrosis factor-α (TNF-α) (a), interleukin-1α (IL-1α) (b), interferon-γ (IFN-γ) (c) or macrophage inflammatory protein-1α (MIP-1α) (d). The percentages of migrated peripheral blood mononuclear cells (PBMCs) after a migration period of 30 minutes are shown. Statistical significance: (a)P = 0.006; (b)P < 0.001; (c)P = 0.016; (d)P = 0.043.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC17829&req=5

Figure 2: Monocyte migration is increased after the pretreatment of ECs with cytokines. Confluent monolayers of ECs that were formed on collagen gels were simultaneously incubated without cytokines (control) and with tumour necrosis factor-α (TNF-α) (a), interleukin-1α (IL-1α) (b), interferon-γ (IFN-γ) (c) or macrophage inflammatory protein-1α (MIP-1α) (d). The percentages of migrated peripheral blood mononuclear cells (PBMCs) after a migration period of 30 minutes are shown. Statistical significance: (a)P = 0.006; (b)P < 0.001; (c)P = 0.016; (d)P = 0.043.
Mentions: It has been reported that cytokines such as TNF-α, IL-1α and IFN-γ and also the chemokine MIP-1α can enhance the transendothelial migration of monocytes [19,20]. We were therefore interested to investigate whether pretreatment of the ECs with these factors would be sufficient to enhance the transendothelial migration of monocytes and/or to induce changes in their expression of surface markers. Figure 2 shows that pretreatment of the endothelium with any of the cytokines led to a consistent and significant increase in the number of migrated mononuclear cells in comparison with simultaneously performed control experiments in which the endothelium was not pretreated. Pretreatment with IL-1α was the most effective, resulting in a 132% increase in migrated cells (P < 0.001). The respective values for the other cytokines were as follows: MIP-1α, 194% (P = 0.043); TNF-α, 193% (P = 0.006); IFN-γ, 136% (P = 0.016).

Bottom Line: We found that monocyte migration led to an enhanced expression of CD11a, CD33, CD45RO, CD54 [intercellular cell-adhesion molecule (ICAM)-1] and human leucocyte antigen-DR.Taken together, the results suggest that local cytokine production activating ECs is sufficient to enhance monocyte migration and that this, in turn, can induce changes consistent with an activated phenotype known to be interactive between antigen-presenting cells and T cells.These results have implications for our pathogenetic insights into rheumatoid arthritis.

View Article: PubMed Central - PubMed

Affiliation: Division of Rheumatology, Department of Internal Medicine III, University of Vienna, Währinger Gürtel 18-20, A-1180 Vienna, Austria. johannes.grisar@akh-wien.ac.at

ABSTRACT
In our study we characterised the immunophenotype of monocytes that migrated through an endothelial cell (EC) monolayer in vitro. We found that monocyte migration led to an enhanced expression of CD11a, CD33, CD45RO, CD54 [intercellular cell-adhesion molecule (ICAM)-1] and human leucocyte antigen-DR. The most striking increase was observed for ICAM-1 when ECs were activated with tumour necrosis factor-alpha and interleukin-1alpha. The results of our study indicate the following: (1) there is a characteristic immunophenotype on the surface of monocytes after transendothelial migration; (2) this phenotype seems to be induced by interactions between monocytes and ECs; and (3) this change is enhanced by the pretreatment of ECs with cytokines. Taken together, the results suggest that local cytokine production activating ECs is sufficient to enhance monocyte migration and that this, in turn, can induce changes consistent with an activated phenotype known to be interactive between antigen-presenting cells and T cells. These results have implications for our pathogenetic insights into rheumatoid arthritis.

Show MeSH
Related in: MedlinePlus