Characterization of E-selectin expression in vivo with use of a radiolabeled monoclonal antibody

Keelan, Edward; Licence, S. T.; Peters, A. M.; Binns, R. M.; Haskard, D. O.

doi:10.1152/ajpheart.1994.266.1.h279

Cited by 78 publications

(62 citation statements)

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“…Cutaneous inflammatory sites were induced by intradermal injections of IL-1␣ or saline control, as previously described. 28,29 For the dose-response experiments, the animals were lightly sedated for the entire time (3 hours), after which 111…”

Section: Model Of Cutaneous Inflammationmentioning

confidence: 99%

Elevation of Plasma High-Density Lipoprotein Concentration Reduces Interleukin-1–Induced Expression of E-Selectin in an In Vivo Model of Acute Inflammation

et al. 2001

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Background-Although there is strong evidence that plasma HDL levels correlate inversely with the incidence of coronary artery disease, the precise mechanism(s) for the protective effect of HDLs remains unclear. We recently showed that HDLs inhibit endothelial cell expression of cytokine-induced leukocyte adhesion molecules in vitro. Our study therefore sought to test the hypothesis that elevating the level of circulating HDLs would inhibit endothelial cell activation in vivo. Methods and Results-We used a porcine model of inflammation previously established in our laboratory, in which the level of vascular endothelial cell expression of E-selectin in interleukin (IL)-1␣-induced skin lesions was measured by the uptake of a radiolabeled anti-E-selectin antibody (1.2B6). Porcine plasma HDL levels were elevated by use of a bolus injection of reconstituted discoidal HDL (recHDL). These particles resemble nascent HDL particles in shape and contain apolipoprotein A-I as the sole protein and soybean phosphatidylcholine as the sole phospholipid. We found that recHDLs inhibited the expression of IL-1␣-induced E-selectin by porcine aortic endothelial cells in vitro, confirming that the inhibitory effect is conserved with synthetic HDLs and demonstrating that the phenomenon is not restricted to human endothelial cells. In vivo, elevating the circulating level of HDLs Ϸ2-fold led to significant inhibition of basal and IL-1␣-induced E-selectin expression by porcine microvascular endothelial cells. Conclusions-These observations demonstrate the potential anti-inflammatory action of HDLs and provide support for the further investigation of the mechanisms underlying the inhibitory effects of HDLs on endothelial cell activation.

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Section: Model Of Cutaneous Inflammationmentioning

confidence: 99%

Elevation of Plasma High-Density Lipoprotein Concentration Reduces Interleukin-1–Induced Expression of E-Selectin in an In Vivo Model of Acute Inflammation

et al. 2001

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“…In vivo assessment of P-selectin expression was determined using the method described by Keelan et al [25] and modified by Panes et al [26]. The monoclonal antibody RB40.34, a rat immunoglobulin G1 directed against mouse P-selectin (PharMingen, Inc.), was used for the in vivo assessment of P-selectin.…”

Section: Adhesion Molecule Expressionmentioning

confidence: 99%

Intestinal inflammation in adhesion molecule-deficient mice: an assessment of P-selectin alone and in combination with ICAM-1 or E-selectin

McCafferty

Smith

Granger

et al. 1999

Journal of Leukocyte Biology

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Biopsy specimens from patients with inflammatory bowel disease have demonstrated an up-regulation of P-selectin, suggesting a role for P-selectin in intestinal inflammation. We examined the role of P-selectin in experimental intestinal inflammation using mice deficient in P-selectin alone or in combination with either ICAM-1 or E-selectin. Colitis was induced using acetic acid or trinitrobenzene sulfonic acid (TNBS). Damage scores and neutrophil infiltration 24 h post acetic acid were not different between wild-type and P-selectin-or P-selectin/ICAM-1-deficient mice, whereas P/E-selectin-deficient mice had enhanced leukocyte recruitment and damage. At 72 h an attenuation in damage scores and a slight decrease in neutrophil infiltration was observed in the P-and P/ICAM-deficient animals. The P/E-selectin-deficient mice maintained enhanced leukocyte recruitment and damage. In wild-type mice P-selectin expression was elevated 48 and 72 h post acetic acid-induced inflammation. Surprisingly, P-selectin or P-selectin/ICAM-1 deficiency did not improve the inflammation induced by TNBS over 7 days. In fact, increased mortality was observed. Antiadhesion therapy may play only a limited, beneficial role and often a detrimental role in intestinal inflammation. J. Leukoc. Biol. 66: 67-74; 1999.

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“…P-selectin was previously shown to be constitutively expressed on lung endothelium 14 and E-selectin on cutaneous endothelium. 15 However, in response to inflammation, both are up-regulated on endothelial cells regardless of tissue location. 13 The carbohydrate ligands for E-and P-selectins are expressed on various leukocyte subsets, including activated T cells.…”

Section: Introduction To Leukocyte Migration Selectinsmentioning

confidence: 99%

Leukocyte migration and graft-versus-host disease

Wysocki

Panoskaltsis‐Mortari

Blazar

et al. 2005

Blood

290

274

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Graft-versus-host disease (GVHD) remains a significant complication of allogeneic bone marrow transplantation (allo-BMT). Acute GVHD is mediated by immunocompetent donor T cells, which migrate to lymphoid tissues soon after infusion, recognize host alloantigens, and become activated upon interaction with host antigen-presenting cells (APCs). Recent work from our group and others suggests that activated effector T cells exit lymphoid tissues and traffic to mucosal sites and parenchymal target organs such as the gastrointestinal (GI) tract, liver, lung, and skin where they cause tissue damage. The molecular interactions necessary for effector cell migration during GVHD have become the focus of a growing body of research, as these interactions represent potential therapeutic targets. In this review we discuss chemokine and chemokine receptor interactions and adhesion molecules that have been shown to play roles in effector cell migration in experimental GVHD models, and we discuss a potential model for the role of chemokines during the activation phase of GVHD. (Blood. 2005;105: 4191-4199)

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Characterization of E-selectin expression in vivo with use of a radiolabeled monoclonal antibody

Cited by 78 publications

References 0 publications

Elevation of Plasma High-Density Lipoprotein Concentration Reduces Interleukin-1–Induced Expression of E-Selectin in an In Vivo Model of Acute Inflammation

Elevation of Plasma High-Density Lipoprotein Concentration Reduces Interleukin-1–Induced Expression of E-Selectin in an In Vivo Model of Acute Inflammation

Intestinal inflammation in adhesion molecule-deficient mice: an assessment of P-selectin alone and in combination with ICAM-1 or E-selectin

Leukocyte migration and graft-versus-host disease

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