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Differential effect of E-selectin antibodies on neutrophil rolling and recruitment to inflammatory sites

  • Carroll L. Ramos
    ,
  • Eric J. Kunkel
    ,
  • Michael B. Lawrence
    ,
  • Unsu Jung
    ,
  • Dietmar Vestweber
    ,
  • Roland Bosse
*Corresponding author for this work
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Abstract

The selectins are inducible adhesion molecules critically important for the inflammatory response. We investigate here the functional effects of three monoclonal antibodies (MoAbs) raised against murine E-selectin (9A9, 10E6, and 10E9.6) on neutrophil recruitment in vivo, leukocyte roiling and circulating leukocyte concentrations in vivo, and adhesion of myeloid cells to E-selectin transfectants and recombinant E-selectin-IgG fusion protein in vitro. MoAbs 9A9 and 10E6 map to the lectin and epidermal growth factor (EGF)-like domains of murine E-selectin, whereas 10E9.6 binds to the consensus repeat region. 10E9.6 blocked neutrophil recruitment in a model of thioglycollate-induced peritonitis in Balb/c mice by more than 90% but had no effect in C57BL/6 mice. 9A9 and 10E6 blocked neutrophil recruitment in this assay only when combined with a P-selectin antibody, 5H1. Neither 9A9 nor 10E9.6 alone blocked leukocyte rolling in tumor necrosis factor-α-treated venules of Balb/c mice, but 9A9 almost completely inhibited leukocyte rolling when combined with the function-blocking murine P-selectin MoAb, RB40.34. In contrast, 10E9.6 had no effect on leukocyte rolling in RB40.34-treated Balb/c or C57BL/6 mice. 10E9.6 did not affect adhesion of myeloid cells to E- selectin transfectants or attachment, rolling, and detachment of myeloid cells to murine E-selectin-IgG fusion protein. However, adhesion was completely blocked in the same assays by 9A9. Taken together, these results indicate that E-selectin serves a function, other than rolling, that appears to be critically important for neutrophil recruitment to inflammatory sites in Balb/c mice.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 3009-3018 (10 pages)

Journal (Volume, Issue Number)

Blood (Volume 89, Issue 8)

Publication milestones

  • Published - 04/15/1997

Publication status

Published - 04/15/1997

ISSN

0006-4971

Publication IDs

  • Scopus: 0030903421
  • PubMed: 9108422

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Scopus
citations
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1
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Fractional count
10
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0.91
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1
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1

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Citation count
68
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Funding Details

FunderFunding number
NHLBI
R01HL054614