A novel β1‐dependent adhesion pathway on neutrophils: a mechanism invoked by dihydrocytochalasin B or endothelial transmigration

It is generally accepted that the β2‐integrin is restricted to mononuclear leukocytes. The objective of this study was to determine whether neutrophils can also express β1‐integrin (specifically α4β1) and whether this can support neutrophil adhesion to endothelial cells and to extracellular matrix. We stimulated neutrophils with dihydrocytochalasin B (DHCB) and various chemotactic stimuli and observed that chemotactic stimuli induced neutrophil adhesion via β2‐integrin (CD18), whereas DHCB and either fMLP, PAF, or IL‐8 induced adhesion to endothelium or protein‐coated plastic that was not inhibitable by and‐CD18 antibody, β2‐integrin‐deficient cells, which did not respond to chemotactic stimuli alone, also adhered avidly in the presence of chemotactic stimuli and DHCB. The induced neutrophil adhesion was inhibited by antibody to β1‐ or α‐integrin chains, but only if an anti‐α2‐integrin antibody was also present. Flow cytometry revealed increased expression of both β1 and α4 in the presence of fMLP plus DHCB. Transendothelial migration of neutrophils induced by chemotactic stimuli alone also increased expression of β1 and α4. Transmigration across deendothelialized membranes induced a similar β1 expression on neutrophils suggesting that events other than an endothelial signal elicited β1‐integrin expression. Transmigration‐induced β1‐dependent expression translated into only modest adhesion to protein‐coated plastic. These data suggest that both a pharmacological (DHCB) and a physiological (transmigration) stimulus can invoke expression of α4 and β1 on human neutrophils to mediate adhesion.—Kubes, P., Niu, X.‐F., Smith, C. W., Kehrli, M. E., Jr., Reinhardt, P. H., Woodman, R. C. A novel β1‐dependent adhesion pathway on neutrophils: a mechanism invoked by dihydrocytochalasin B or endothelial transmigration. FASEB J. 1103‐1111 (1995)

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