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Multiple Receptors on Human Monocytes Are Involved in Adhesion to Cultured Human Endothelial Cells
Author(s) -
Carlos Timothy M.,
Dobrina Aldo,
Ross Russell,
Harlan John M.
Publication year - 1990
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.48.5.451
Subject(s) - monocyte , cd18 , umbilical vein , lipopolysaccharide , biology , monoclonal antibody , tumor necrosis factor alpha , receptor , phorbol , microbiology and biotechnology , in vitro , immunology , biochemistry , antibody , protein kinase c , signal transduction
Monocytes exhibit significant basal (unstimulated) adherence to human umbilical vein endothelium (HUVE), which is only partially inhibited by an anti‐CD18 monoclonal antibody (mAb) (60.3). We examined factors modulating the residual, CD18‐independent monocyte binding to HUVE by pretreating monocytes with mAb 60.3 to eliminate CD18‐dependent binding. Basal adherence was reduced from 32% ± 2% to 14% ± 2% with mAb 60.3 (means ± SE of eight experiments; P < 0.01). mAb 60.3‐treated monocytes were incubated with tumor necrosis factor‐γ (TNF‐α), interleukin‐1 (IL‐1), lipopolysaccharide (LPS), N‐formylmethionyl‐leucyl‐phenylalamine (FMLP), or phorbol myristate acetate (PMA). Only PMA affected CD18‐independent binding. Pretreatment with PMA alone reduced adherence to 21% ± 2% (mean ± SE of eight experiments; P < 0.01). In conjunction with mAb 60.3, PMA virtually eliminated monocyte adherence to HUVE (7% ± 1%, mean ± SE of eight experiments; P < 0.01). We also examined CD18‐independent monocyte binding to endothelial‐leukocyte adhesion molecules (E‐LAMs) induced by pretreatment of HUVE with LPS. Monoclonal antibody 60.3‐treated monocytes increased adherence from 14% ± 2% with unstimulated HUVE to 37% ± 2% with LPS‐stimulated HUVE (mean ± SE of four experiments; P < 0.01). Monocytes pretreated with both mAb 60.3 and PMA increased adherence from 5% ± 1% with the unstimulated HUVE to 18% ± 1% with the LPS‐stimulated HUVE (mean ± SE of four experiments; P < 0.01). This result implies the presence of a CD18‐independent and PMA‐insensttive receptor on human monocytes for an E‐LAM induced by LPS. In summary, we have identified two CD18‐independent mechanisms of monocyte adherence to HUVE; a PMA‐sensitive mechanism mediating basal adherence and a PMA‐insensitive mechanism involved in binding to E‐LAMs.