Adhesion Molecules Involved in the Interaction of LGL/NK Cells and Human Endothelial Cells Stimulated with Salmonella Bacteria

Abstract

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-1, ICAM-1 and E-selectin, and the counter-receptors VLA-4, LFA-1 and SLex in the increase of LGL/NK adhesion to HUVEC, stimulated with Salmonella Minnesota mR595 bacteria, LPS or TNF-alpha. On Salmonella-stimulated HUVEC, VCAM-1 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-stimulated 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.

Human Intestinal Microvascular Endothelial Cells Express Toll-Like Receptor 5: A Binding Partner for Bacterial Flagellin

“…Eventually, enteroinvasive pathogens will enter the intestinal microcirculation, resulting in systemic infection and causing septic illness. Intestinal Salmonella infection in vivo is characterized by a marked inflammatory infiltration of the lamina propria (1), and infection of human endothelial cells with Salmonella has been shown to be a potent inductor of ICAM-1 and other endothelial adhesion molecules (2). In vitro studies with human endothelial cells have indicated that bacterial LPS are potent inductors of endothelial adhesion molecules by triggering the proinflammatory signal transduction response via the transcription factor NF-B (3).…”

Expansion of large granular lymphocytes following Pseudomonas infection in a patient with adult-onset Still's disease

“…Several reports have demonstrated that the proliferation of LGL is caused by stimulation by bacteria. [16][17][18][19][20][21] However, in this case, Pseudomonas infection was only limited to a local area involving the bulbar conjunctiva, and the portal site appeared to be corneal infection with contaminated contact lenses. Moreover, it has been reported that expanded LGL observed during bacterial infection are mostly associated with NK phenotypes, [16][17][18][19][20][21] while in this case they were predominantly composed of CD8(+) T cells with a small fraction of CD56(+) cells.…”

“…[16][17][18][19][20][21] However, in this case, Pseudomonas infection was only limited to a local area involving the bulbar conjunctiva, and the portal site appeared to be corneal infection with contaminated contact lenses. Moreover, it has been reported that expanded LGL observed during bacterial infection are mostly associated with NK phenotypes, [16][17][18][19][20][21] while in this case they were predominantly composed of CD8(+) T cells with a small fraction of CD56(+) cells. Our patient required a prompt initiation of treatment due to the risk of blindness by pressure secondary to severe orbital cellulitis, and hence, did not have time to undergo complete examinations including Ga scintigram, although general examination including chest X-ray and abdominal sonogram detected no other foci of suspected infection or lymph node swelling.…”

Human NK Cells Expressing α4β1/β7 Adhere to VCAM‐1 Without Preactivation

“…and Leu4 (anti-CD3) from Becton-Dlckinson. For the surface marker analysis, the NK and T cells were isolated as described above and the immunofluorescence staining was performed as a standard procedure [5]. Flow cylometry was then performed by means of a fluorescence-activated cell sorter (FACScan.…”

“…NK cell adhesion to stimulated endothelium is mediated both by the LFA-I/ ICAM-I counterpair, and the leucocyte /H-integrin VLA-4 (a4/il). which recognizes the VCAM-1 expressed on endothelium [2,5]. Nevertheless, NK cell adhesion to endothelium cannot be abrogated by blocking these pathways, which suggests that other receptor-ligand counterpairs might also be involved.…”