Increased PSGL‐1 expression on granulocytes from allergic‐asthmatic subjects results in enhanced leukocyte recruitment under flow conditions

Allergic asthma is increasing in incidence and severity in many industrial countries. Leukocyte recruitment into the airways of affected individuals contributes to the severity of the disease. In this study, whole blood from normal, allergic, asthmatic, or allergic‐asthmatic subjects was perfused over immobilized adhesion molecules using an in vitro flow chamber system to determine if there were differences in leukocyte recruitment in these patient populations. Leukocytes from allergic‐asthmatic subjects showed a threefold increase in recruitment on P‐selectin as compared with normal controls. In both patient populations, the accumulated cells were exclusively neutrophils and eosinophils. Increased granulocyte recruitment was specific for P‐selectin, as neither purified E‐selectin nor vascular cell adhesion molecule‐1 (VCAM‐1) supported enhanced leukocyte recruitment from allergic‐asthmatics. Leukocyte accumulation on P‐selectin was completely blocked by an anti‐P‐selectin or anti‐P‐selectin glycoprotein ligand‐1 (PSGL‐1) monoclonal antibody. Flow cytometry revealed that neutrophils and eosinophils from allergic‐asthmatic subjects had increased expression of PSGL‐1, whereas expression of another adhesion molecule, L‐selectin, was unchanged. PSGL‐1 expression on peripheral blood mononuclear cells of allergic‐asthmatic patients was unaffected. The increased PSGL‐1 expression on granulocytes from allergic‐asthmatic patients also led to enhanced leukocyte recruitment on interleukin‐4‐stimulated human umbilical vein endothelial cells, which express P‐selectin and VCAM‐1. Thus, increased PSGL‐1 expression on granulocytes from allergic‐asthmatic subjects resulted in increased leukocyte recruitment on P‐selectin under flow conditions.

• Publication year

  2002

• Venue

  Journal of Leukocyte Biology

• Publication date

  2002-10-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1189/jlb.72.4.702PMID 12377939
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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