Selectins mediate eosinophil recruitment in vivo: a comparison with their role in neutrophil influx.

Abstract

The role of selectins in mediating eosinophil recruitment in vivo was assessed in a model of lipopolysaccharide (LPS)-induced mouse pleurisy. LPS administration resulted in significant eosinophil influx at 24 hours, whereas neutrophil recruitment to the cavity peaked at 4 hours and persisted for 24 hours. The anti-L-selectin monoclonal antibody (MoAb) MEL-14 effectively inhibited (by 97%) eosinophil influx at 24 hours and also inhibited neutrophil recruitment at both times (75% to 95%). Eosinophil recruitment was partially reduced (54%) by the anti-P-selectin MoAb 5H1 but, in contrast, was unaffected by the anti-E-selectin MoAb 10E6. Neutrophil influx at 4 or 24 hours was not affected by the anti-P- or anti-E-selectin MoAbs. However, coadministration of anti-P-selectin and anti-E-selectin was very effective at inhibiting eosinophil influx at 24 hours (86%) and neutrophil influx at 4 (93%) and 24 hours (92%). These results show that all three selectins play a role in LPS-induced eosinophil and neutrophil recruitment in vivo, although P- and E-selectin show a degree of functional redundancy. The demonstration that P-selectin mediates eosinophil but not neutrophil influx suggests that suppressing the function of this adhesion molecule may be beneficial in blocking eosinophil accumulation in pleural inflammation.

• Authors: G M Henriques, J M Miotla, S B Cordeiro, B A Wolitzky, S T Woolley, P G Hellewell
• Journal: Blood (Blood) Vol. 87 Issue 12 Pg. 5297-304 (Jun 15 1996) ISSN: 0006-4971 [Print] United States
• PMID: 8652845 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antibodies, Monoclonal
• E-Selectin
• Endotoxins
• Lipopolysaccharides
• P-Selectin
• L-Selectin
• endotoxin, Escherichia coli

Topics

• Animals
• Antibodies, Monoclonal (immunology, pharmacology)
• Cell Adhesion (physiology)
• Chemotaxis, Leukocyte (physiology)
• E-Selectin (immunology, physiology)
• Endothelium, Vascular (metabolism, pathology)
• Endotoxins (toxicity)
• Eosinophilia (immunology, pathology)
• Eosinophils (physiology)
• L-Selectin (immunology, physiology)
• Lipopolysaccharides (toxicity)
• Macrophages (immunology)
• Male
• Mice
• Mice, Inbred BALB C
• Neutrophils (physiology)
• P-Selectin (immunology, physiology)
• Pleurisy (chemically induced, immunology, pathology)
• T-Lymphocytes (immunology)