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Granulocyte macrophage colony stimulating factor induced changes in cellular adhesion molecule expression and adhesion to endothelium: in‐vitro and in‐vivo studies in man
Author(s) -
Devereux S.,
Bull H. A.,
CcmposCosta D.,
Saib R.,
Linch D. C.
Publication year - 1989
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1989.tb04287.x
Subject(s) - granulocyte , in vivo , cell adhesion molecule , granulocyte macrophage colony stimulating factor , endothelium , immunology , in vitro , endothelial stem cell , cell adhesion , biology , cytokine , microbiology and biotechnology , cell , endocrinology , biochemistry
Summary The administration of recombinant human granulocyte‐macrophage colony‐stimulating factor (rhGM‐CSF) causes a transient leucopenia. Radionuclide labelling studies showed this to be due to margination of neutrophils and monocytes predominantly in the pulmonary vasculature. No evidence of complement activation was found. A rapid in‐vivo rise in neutrophil cellular adhesion molecule (CAM) expression was observed paralleling the development of the neutropenia. Neutrophils exposed to rhGM‐CSF in‐vitro showed similar rapid increases in CAM expression. The adherence of chromium‐labelled neutrophils to endothelial cell cultures was modestly but highly significantly increased by rhGM‐CSF, an effect that was reduced by the binding of a monoclonal antibody to the beta chain of neutrophil CAM. The margination of phagocytic cells induced by rhGM‐CSF administration is therefore likely to be due at least in part to increased expression of adhesion promoting glycoproteins. The demargination, however, occurred at a time when neutrophil CAM expression was still high, suggesting that dissociation of the neutrophil‐endothelial cell interaction depends on factors other than downregulation of CAM expression. In‐vivo modulation of phagocyte CAMS and adhesive properties by GM‐CSF may be of importance in the normal inflammatory response.