Variation of adhesion molecule expression on human umbilical vein endothelial cells upon multiple cytokine application

Raab, Markus; Daxecker, Heide; Živanović, Marko; Karimi, Alireza; Griesmacher, Andrea; Mueller, Mathias M.

doi:10.1016/s0009-8981(02)00048-7

Cited by 54 publications

(40 citation statements)

References 18 publications

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“…In addition, TNF-␣ increases P-selectin expression in human pulmonary microvascular EC (38) and in HUVEC (39), but not in human pulmonary artery or dermal EC (38). Our findings together with these reports, indicate that in lung, TNF-␣-induced P-selectin expression may be restricted to microvascular EC (38) and that the expression may be an early event that is not detectable after several hours of TNF-␣ exposure (40). In EC derived from large vessels, TNF-␣ exposure for several hours causes expression of E-selectin and ICAM-1 by inducing ROS-mediated increase in gene expression of these molecules (41,42).…”

Section: P-selectinsupporting

confidence: 51%

Mitochondrial Reactive Oxygen Species Regulate Spatial Profile of Proinflammatory Responses in Lung Venular Capillaries

Parthasarathi

Ichimura

Quadri

et al. 2002

The Journal of Immunology

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Cytokine-induced lung expression of the endothelial cell (EC) leukocyte receptor P-selectin initiates leukocyte rolling. To understand the early EC signaling that induces the expression, we conducted real-time digital imaging studies in lung venular capillaries. To compare receptor- vs nonreceptor-mediated effects, we infused capillaries with respectively, TNF-α and arachidonate. At concentrations adjusted to give equipotent increases in the cytosolic Ca2+, both agents increased reactive oxygen species (ROS) production and EC P-selectin expression. Blocking the cytosolic Ca2+ increases abolished ROS production; blocking ROS production abrogated P-selectin expression. TNF-α, but not arachidonate, released Ca2+ from endoplasmic stores and increased mitochondrial Ca2+. Furthermore, Ca2+ depletion abrogated TNF-α responses partially, but arachidonate responses completely. These differences in Ca2+ mobilization by TNF-α and arachidonate were reflected in spatial patterning in the capillary in that the TNF-α effects were localized at branch points, while the arachidonate effects were nonlocalized and extensive. Furthermore, mitochondrial blockers inhibited the TNF-α- but not the arachidonate-induced responses. These findings indicate that the different modes of Ca2+ mobilization determined the spatial patterning of the proinflammatory response in lung capillaries. Responses to TNF-α revealed that EC mitochondria regulate the proinflammatory process by generating ROS that activate P-selectin expression.

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Section: P-selectinsupporting

confidence: 51%

Mitochondrial Reactive Oxygen Species Regulate Spatial Profile of Proinflammatory Responses in Lung Venular Capillaries

Parthasarathi

Ichimura

Quadri

et al. 2002

The Journal of Immunology

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“…Previous in vitro studies have shown that the adhesion molecules ICAM-1, PECAM-1, and P/E-selectin can be up-regulated by Th1-type cytokines IL-1␤, TNF-␣, and IFN-␥ and downregulated by Th2 cytokines IL-4, IL-10, and IL-6 (70). In the present study, it is therefore possible that during the disease initiation stage of EAU, P/E-selectin and ICAM-1 are up-regulated by Th1-type cytokines (71) and during the late stage of EAU these adhesion molecules are down-regulated by increased Th2-type cytokines (23,24,71).…”

Section: Discussionmentioning

confidence: 99%

Recruitment of IFN-γ-Producing (Th1-Like) Cells into the Inflamed Retina In Vivo Is Preferentially Regulated by P-Selectin Glycoprotein Ligand 1:P/E-Selectin Interactions

Manivannan

Jiang

et al. 2004

The Journal of Immunology

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Although there is evidence that altering the Th1/Th2 balance toward Th2 cells may be important in the resolution of Th1-type autoimmune disease, adoptive transfer of Th2 cells is not effective in protecting against Th1-type disease and may cause disease. Therefore, we examined the recruitment of Th1- and Th2-like cells into the retina in the murine autoimmune disease experimental autoimmune uveoretinitis. CD4 T cells were polarized in vitro to IFN-γ-producing Th1-like cells and non-IFN-γ-producing Th2-like cells, labeled, and adoptively transferred. Trafficking to the retina in vivo was evaluated by scanning laser ophthalmoscopy and infiltration by confocal microscopy. There were more rolling and adherent Th1-like cells and they rolled more slowly than did Th2-like cells. Th1-like cells were preferentially recruited into the retinal parenchyma at both initiation and resolution. Surface P-selectin glycoprotein ligand 1 (PSGL-1) and LFA-1 were up-regulated on both populations but were expressed at higher levels on Th1-like cells. Up-regulation of CD44 expression was higher on Th2-like cells. P-selectin, E-selectin, and ICAM-1 are up-regulated on postcapillary venules in the retina. Pretreatment of Th1-like cells with anti-PSGL-1 inhibited rolling and infiltration of Th1-like cells but not Th2-like cells, providing direct in vivo evidence for the inability of Th2 to respond to P/E-selectin despite increased expression of PSGL-1. Anti-LFA-1 pretreatment inhibited infiltration of both Th1- and Th2-like cells, but more so Th-1. We suggest that random trafficking of activated T cells (both Th1 and Th2) across the blood-retina barrier is mediated by CD44:CD44R and LFA-1:ICAM-1, whereas preferential recruitment of Th1 cells is mediated by PSGL-1:P/E-selectin.

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“…Macrophage activation via IFN-c receptors (IFN-cR) appears to be extremely important, resulting in increased microbicidal activity, increased MHC class I and MHC class II expression as well as induction of iNOS expression and NO production (reviewed in [10,11]). IFN-c also has a potent effect on endothelium, leading to increased adhesion molecule expression [12,13] and the induction of chemokine expression [14]. This effect is synergistic with TNF-a, another type-1 cytokine.…”

Section: Introductionmentioning

confidence: 99%

Interferon‐γ limits Th1 lymphocyte adhesion to inflamed endothelium: A nitric oxide regulatory feedback mechanism

Norman¹,

Zbytnuik²,

Kubes³

2008

Eur J Immunol

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AustraliaCD4 + T helper (Th1 and Th2) cell localization to a site of inflammation is important for the development, maintenance and regulation of an immune response. The factors that regulate Th1 and Th2 cell recruitment into tissue are not fully understood. The aim of the present study was to examine the effect of different cytokine microenvironments on the recruitment of Th1 and Th2 lymphocytes into tissue. Fluorescently labelled Th1 or Th2 lymphocyte-endothelial interactions were observed via intravital microscopy of the cytokine-treated cremaster muscle. Our results show that TNF-a alone is sufficient to maximally recruit Th1 cells. Surprisingly, treatment with TNF-a + IFN-c significantly decreased Th1 adhesion and emigration in comparison to TNF-a treatment alone. The decreased adhesion of Th1 cells in response to TNF-a + IFN-c reflected a decreased ability to bind to ICAM-1 and was iNOS-dependent. This phenomenon was not observed with Th2 cells. These results suggest that IFN-c may play a key immunomodulatory role in the recruitment of different T lymphocyte subsets. Indeed, blockade of IFN-c or iNOS function during the Th1-mediated contact hypersensitivity response resulted in an acceleration and exacerbation of the late-phase inflammatory response.

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Variation of adhesion molecule expression on human umbilical vein endothelial cells upon multiple cytokine application

Cited by 54 publications

References 18 publications

Mitochondrial Reactive Oxygen Species Regulate Spatial Profile of Proinflammatory Responses in Lung Venular Capillaries

Mitochondrial Reactive Oxygen Species Regulate Spatial Profile of Proinflammatory Responses in Lung Venular Capillaries

Recruitment of IFN-γ-Producing (Th1-Like) Cells into the Inflamed Retina In Vivo Is Preferentially Regulated by P-Selectin Glycoprotein Ligand 1:P/E-Selectin Interactions

Interferon‐γ limits Th1 lymphocyte adhesion to inflamed endothelium: A nitric oxide regulatory feedback mechanism

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