Adhesion of Monocyte Very Late Antigen-4 to Endothelial Vascular Cell Adhesion Molecule-1 Induces Interleukin-1β–Dependent Expression of Interleukin-6 in Endothelial Cells

Zohlnhöfer, Dietlind; Brand, Korbinian; Schipek, Katharina; Pogátsa-Murray, Gisela; Schömig, Albert; Neumann, Franz‐Josef

doi:10.1161/01.atv.20.2.353

Cited by 29 publications

(28 citation statements)

References 52 publications

(44 reference statements)

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“…This induction involves NF-kB activation in the stromal cells and requires leukemia cell/stromal cell contact, which is in part mediated by VLA-4/ VCAM-1 interaction. VLA-4/VCAM-1 interaction is reported to activate NF-kB (Zohlnhofer et al 2000), and NF-kB, in turn, up-regulates VCAM-1 (Rajan et al 2008), suggesting a positive feedback loop reinforcing VLA4 þ CML cell binding to the VCAM-1-expressing stromal cells, thereby ensuring PlGF production. Stromal cell-derived PlGF then promotes proliferation and metabolism of the CML cells.…”

Section: Discussionmentioning

confidence: 99%

PlGF: A Multitasking Cytokine with Disease-Restricted Activity

Dewerchin¹,

Carmeliet²

2012

Cold Spring Harbor Perspectives in Medicine

188

176

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Section: Discussionmentioning

confidence: 99%

PlGF: A Multitasking Cytokine with Disease-Restricted Activity

Dewerchin¹,

Carmeliet²

2012

Cold Spring Harbor Perspectives in Medicine

188

176

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“…Furthermore, MK2.7 also reduced the development of arthritis in a collagen-induced arthritis model (57) and inhibited inflammatory cell infiltration into the skin in a keratin-14 IL-4 transgenic mouse atopic dermatitis model (58). The mouse anti-hVCAM-1 Abs 4B9, BBIG-V1, 1G11, and P3H12 block binding of lymphoma cell lines to VCAM-1-expressing endothelial cells (52,59,60). However, these Abs are species specific.…”

Section: Discussionmentioning

confidence: 99%

An Antibody to the Sixth Ig-like Domain of VCAM-1 Inhibits Leukocyte Transendothelial Migration without Affecting Adhesion

Lee

Yoon

et al. 2012

The Journal of Immunology

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VCAM-1 plays a key role in leukocyte trafficking during inflammatory responses. However, molecular mechanisms underlying this function have not been clearly elucidated. In this study, using phage display technology, we developed a rabbit/human chimeric VCAM-1 Ab, termed VCAM-1 domain 6 (VCAM-1-D6), which specifically recognizes aa 511–599 within the sixth Ig-like domain. We report that the VCAM-1-D6 Ab blocked U937 cell transmigration across activated HUVECs but did not alter adhesion of U937 cells to the HUVECs. We also demonstrate that VCAM-1-D6 does not alter TNF-α–stimulated endothelial cell chemokine or cytokine production. Furthermore, through in vivo efficacy testing using a mouse islet allograft model, we demonstrate that VCAM-1-D6 significantly alleviates allograft rejection by blocking leukocyte infiltration to the grafted islets. Taken together, our results suggest that the VCAM-1-D6 Ab may block VCAM-1–mediated inflammation and could be a useful tool in treating inflammatory diseases.

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“…The credibility of these potential mechanisms is presently under investigation. Cellular interactions between monocytes and EC induce early release of proinflammatory cytokines, such as TNF-␣ and IL-1␤ (15,19,30,50). Considering the effects of these cytokines on EC TFA (reference 11 and this study) and the synergistic effect of rIL-1 on TFA of bacterium-infected EC (43), we investigated whether these cytokines mediate TFA induction in our coculture studies.…”

Section: Discussionmentioning

confidence: 99%

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

2001

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In bacterial endocarditis (BE), intravascular infection with Staphylococcus aureus, Streptococcus sanguis, orStaphylococcus epidermidis can lead to formation of a fibrin clot on the inner surface of the heart and cause heart dysfunction. The events that start the coagulation in the early stage of the disease are largely unknown. We have recently shown that human endothelial cells (EC) upon binding and internalization of S. aureus, but not S. sanguis or S. epidermidis, express tissue factor (TF)-dependent procoagulant activity (TFA). The present study shows that infection of EC with these three pathogens induces surface expression of intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) and monocyte adhesion. Subsequent coculture of these cells synergistically enhanced TFA, which was exclusively dependent on TF molecules that were expressed on EC during coculture. TFA induction required direct contact between monocytes and bacterium-infected EC, but the signals for this response were not generated by the binding of monocytes through their ␤ 2 -or ␣ 4 -integrins to ICAM-1 or VCAM-1, respectively, on infected EC. The mechanism by which monocytes induce TFA in bacterium-infected EC was partly mediated by the proinflammatory cytokine interleukin-1 produced by the cells during coculture. Endogenous tumor necrosis factor alpha was not involved. This modulating effect of monocytes on species-and strain-dependent TFA of bacterium-infected EC supports our hypothesis that in an early stage in the pathogenesis of BE, as well as other intravascular infections that lead to detrimental fibrin formation, the coagulation cascade can be activated on the surfaces of EC as a consequence of specific interactions between pathogenic bacteria, EC, and monocytes.

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Adhesion of Monocyte Very Late Antigen-4 to Endothelial Vascular Cell Adhesion Molecule-1 Induces Interleukin-1β–Dependent Expression of Interleukin-6 in Endothelial Cells

Cited by 29 publications

References 52 publications

PlGF: A Multitasking Cytokine with Disease-Restricted Activity

PlGF: A Multitasking Cytokine with Disease-Restricted Activity

An Antibody to the Sixth Ig-like Domain of VCAM-1 Inhibits Leukocyte Transendothelial Migration without Affecting Adhesion

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

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