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Adhesion Molecules Involved in the Interaction of LGL/NK Cells and Human Endothelial Cells Stimulated with Salmonella Bacteria
Author(s) -
PINOLA M.,
SAKSELA E.
Publication year - 1992
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1992.tb03127.x
Subject(s) - cell adhesion molecule , salmonella , adhesion , microbiology and biotechnology , endothelium , biology , chemistry , bacteria , genetics , organic chemistry , endocrinology
Previously we showed that pretreatment of LGL/NK or HUVE cells with Salmonella bacteria augments the adhesion of LGL/NK cells to endothelium. Here we analyse the roles of HUVEC adhesion molecules VCAM‐l, ICAM‐I and E‐selectin, and the counter‐receptors VLA‐4, LFA‐1 and SLe 3 in the increase of LGL/NK adhesion to HUVEC, stimulated with Salmonella Minnesota mR595 bacteria. LPS or TNF‐α. On salmonella ‐stimulated HUVEC, VCAM‐l and ICAM‐1 were the major binding structures involved, and their effect was additive in monoclonal antibody inhibition experiments. We could demonstrate the induction of both structures on cultured HUVEC after 24 h of Salmonella stimulation in flow cytometric analysis. For salmonella ‐stimulaled LGL/NK, the principal binding structure was LFA‐1, Stimulation of LGL/NK cells did not alter the expression of the adhesion structures (subunits CD11a/CD18, CD49d/CD29). as determined by flow cytometric analysis, and thus the increased adherence is presumably produced by an increased avidity of the receptors on LGL/NK cells. Pretreatment of endothelium or lymphocytes with various stimuli, including Salmonella bacteria or LPS, leads to an activation state which provides for characteristic anchorage sites for the increased migration of LGL/NK cells towards the site of inflammation.