Sentence examples for mediating monocyte adhesion from inspiring English sources

In order to study the effect of chlamydial infection of endothelial cells in mediating monocyte adhesion under shear conditions, we perfused THP-1 monocytes at 1 dyn/cm2, over a monolayer of HAEC that were exposed to infected or uninfected monocyte supernatant.

Earlier studies suggested the involvement of CD62L (L-selectin), as it mediates monocyte adhesion to cytokine-stimulated endothelial monolayers [ 39], and its downregulation was regularly observed during cryopreservation of hematopoietic stem cells and PBMC [ 40, 41].

In the presence of a neutralizing antibody against platelet-derived CXCL12 and blocking antibody against CXCR7 but not CXCR4 or IgG control monocyte adhesion to immobilized platelets was significantly reduced (P<0.05), indicating that CXCR7 primarily mediates monocyte adhesion to immobilized platelets enriched in CXCL12.

In accord with the importance of adhesion molecules in development of arthritis, frozen section binding assays in rheumatoid synovitis demonstrated that, apart from E-selectin and counter receptors for β1/β2 integrins, P-selectin is the predominant adhesion molecule, mediating monocyte binding to inflamed synovial venules [ 23].

PSGL-1 was also chosen as the interaction between P- and E-selectin and PSGL-1 induces changes in integrin function and increased adhesion of monocytes to endothelium in vitro, but to date there is no record of its role in mediating monocyte function in delayed-type hypersensitivity (DTH) inflammation in vivo.

The prominent role of CCR1 and CCR5 can also be related to the deposition of platelet-derived chemokines mediating proatherogenic monocyte adhesion on endothelium (von Hundelshausen et al, 2001).

Monocyte adhesion to cerebral endothelium is mediated by interactions between ICAM-1 and VCAM-1, which have been shown to be up-regulated in CM, 10,11,53 and their corresponding ligands on monocytes, macrophage-1 antigen (MAC-1) (CD11β/CD18), and VLA4 (α4/β1).

Ox-LDL, via upregulation of LOX-1 mediated by angiotensin II and ET-1, induces monocyte adhesion to the endothelium via enhanced expression of P-selectin, ICAM-1, and VCAM-1 [ 149, 150].

In the present study we demonstrate that microparticles of patients after successful cardiopulmonary resuscitation cause enhanced monocyte adhesion to the endothelium that is partly mediated by enhanced expression of the endothelial adhesion molecules ICAM-1 and VCAM-1.

In contrast, FO-based lipid emulsions reduced monocyte adhesion, decreased pro-inflammatory cytokines, and neutrophil recruitment into the alveolar space possibly mediated by ChemR23-signaling.

These findings suggest that in HRMCs, LPS-induced VCAM-1 expression was, at least in part, mediated through a TLR4/MyD88/c-Src/NADPH oxidase/ROS/p38 MAPK-dependent p300 and ATF2 pathway relevant to recruitment of monocyte adhesion to kidney.