Structure and Function of Intercellular Adhesion Molecule-1

Hogg, Nancy; Bates, Paul A.; Harvey, Jo

doi:10.1159/000319059

Cited by 38 publications

(18 citation statements)

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“…Its soluble forms (sICAM-1), both monomeric and dimeric, are generated by proteolytic cleavage (16)(17)(18)(19). The majority of molecules that bind ICAM-l are leukocyte integrins (LFA-l and Mac-) (20)(21)(22)(23), but also other types of molecules, including fibrinogen, rhinoviruses, and erythrocytes infected by Plasmodium falciparum can bind this molecule (24)(25).…”

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confidence: 99%

Procalcitonin, C-Reactive Protein, Interleukin-6, and Soluble Intercellular Adhesion Molecule-1 as Markers of Postoperative Orthopaedic Joint Prosthesis Infections

Drago

Vassena

Dozio

et al. 2011

Int J Immunopathol Pharmacol

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There is a universally recognized need to identify new, reliable markers of inflammation that can aid in the rapid diagnosis of orthopaedic joint prosthesis infections (OJP-Is). Since prompt diagnosis is key to timely intervention in the course of infection, different molecules have been studied. In this study, we examined three groups of patients: those with prosthesis infection, those without infection, and a third group with previous infection in whom the infection had been cleared. Four presumed markers of infection were tested: procalcitonin (PCT); C-reactive protein (CRP); interleukin-6 (IL-6); and soluble intercellular adhesion molecule-1 (sICAM-1). The results showed that PCT cannot be considered as a good marker of periprosthetic infection as no statistically significant difference in serum PCT levels emerged between patients with infection and controls or patients without infection. In contrast, both sICAM-1 and CRP may be considered as good markers of infection, as measurement of their levels allowed us to distinguish between patients with and without infection, and between patients with infection and those with previous infection, since marker levels quickly returned to baseline values after clearance of the infection. IL-6 was found to be a good marker for inflammation, as it distinguished between patients with infection and the other groups. In the patients with previous infection, the IL-6 values remained high versus the controls but lower and with a statistically significant difference versus the patients with infection. Further studies are needed to determine the cut-off value of IL-6 between patients with infection and those with previous infection.

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confidence: 99%

Procalcitonin, C-Reactive Protein, Interleukin-6, and Soluble Intercellular Adhesion Molecule-1 as Markers of Postoperative Orthopaedic Joint Prosthesis Infections

Drago

Vassena

Dozio

et al. 2011

Int J Immunopathol Pharmacol

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“…fox 24 h. is ihe most likely candidate in mediating the /i;-inlegrin, in particular LFA-1 and CR3-depcndenl adhesion of rIFN--;-stinuilated monocytes [7]. In a preliminary sludy.…”

Section: Discussionmentioning

confidence: 85%

“…LFA-I (CDlla/CDI8) and CR3 (CDllb/ CD18), on monocytes [5.6] that ean interact with counterstructures on EC. among them the immunoglobulin supcrgene family member intercellular adhesion molecule-l (ICAM-I) (CD54) [7]. The increased adherence o\' monocytes to EC stimulated with inflammatory cytokines is more complex, and follows a sequence of events which implicates the cooperation of dislinet adhesion mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Surface molecules involved in the adherence of recombinant interferon-gamma (rIFN-γ)-stimulated human monocytes to vascular endothelial cells

Wang

Beekhuizen

Furth

1994

Clinical and Experimental Immunology

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SUMMARYDuring an inlianimalory reaction, an increased number of circulating monocytes adhere lo the endolhelial cells (EC) of the vessel wall. This process is mediated by molecules located on the surface of monocytes and EC. Locally released Intlammatory mediators can modulate monocyte EC interaction-In an earlier sludy we reported that stimulation ofmonolayers ofcultured venous EC with riFN-y enhanced their adhesiveness for monocyles. The aim of the present study was to investigate ihe effect of rlFN-y on peripheral blood monocyles with regard to the expression of surface molecules and the binding lo non-stimulated or cytokine-stimutaied EC, Flow cytometric analysis demonstrated that monocytes stimulated with 500 U ml rIEN-y for 24 h showed increased expression of CR3 (CDl lb;CDIS), pl50.95 (GDI lc;CD18) and EcyRl (CD64); the expression of LFA-1 (CDl la/CDI 8). L-selectin. CD14 and VLA-4 {CD49d/CD29) did nol change or was slightly reduced. Upon sLimtilation with rlFN--/ monocytes showed an enhanced binding to both nonstimulaled or rIFN-y-stimulaied EC, This was even tnore pronounced when EC had been stimulated with rlL-l5 for 24 h. The increased binding of rI EN-7-stimulalednionocyteslorlL-la-stimulated EC was further analysed. Studies with MoAbs against adhesion molecules on monocyles revealed that the binding of rIFN--,'-stimulated monocyles, hut not thai of non-stimulated monocytes. to rIL-lastimulated EC was inhibited by about 30-60"., with MoAbs against CDl la. CDllb. CDI8. Lselectin or CDI4, MoAbs againsi CDi Ic or CD49d had liltle or no eftect. From Ihese results, we conclude ihat exposure of monoeytes lo rlFN--; enhances their adhesiveness to cytokinc-stimulated EC by a mechanism which involve.s CDIla/CDIX. CDtlbCDI8. CDI4 am! L-selectin on monocytes-

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“…The expression of adhesion molecules can be induced by TNF-α [38] . The adhesion molecule ICAM-1 mediates firm adhesion between leukocytes and endothelial cells and contributes to the migration of leukocytes from postcapillary venues into the reperfused tissue [42,43] . ICAM-1 initiates adhesion and transendothelial migration of circulating leukocytes [42] .…”

Section: Discussionmentioning

confidence: 99%

“…The adhesion molecule ICAM-1 mediates firm adhesion between leukocytes and endothelial cells and contributes to the migration of leukocytes from postcapillary venues into the reperfused tissue [42,43] . ICAM-1 initiates adhesion and transendothelial migration of circulating leukocytes [42] . Evidence has also suggested that IL-10 may have a therapeutic potential in acute and chronic inflammatory disease [44] .…”

Section: Discussionmentioning

confidence: 99%

Kynurenic acid attenuates multiorgan dysfunction in rats after heatstroke

Hsieh

Chen

Yeh³

et al. 2011

Acta Pharmacol Sin

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IntroductionHeatstroke is defined as a form of excessive hyperthermia (>40 °C) associated with a systemic inflammatory response that leads to multi-organ dysfunction in which central nervous system (CNS) disorders such as delusion, convulsion and coma predominate [1] . Our recent results have demonstrated that heatstroke rodents display hypotension, systemic inflammatory responses, hypothalamic ischemia and neuronal damage, and multi-organ dysfunction [2][3][4] .Kynurenic acid (KYNA) or its metabolic precursor L-kynurenine may be of therapeutic value in neurodegenerative diseased models [5,6] . For example, systemically administered high doses of KYNA had a neuroprotective effect in the gerbil model of global ischemia [7] . Both the homocysteine-induced impairment of endothelial cells [8] and the motility and inflammatory activation in the early phase of acute experimental colitis in the rat [9] were significantly reduced by administration of KYNA. The aim of this study was to investigate whether the heatstroke induced hypotension, systemic inflammatory responses, hypothalamic ischemia and damage, and multiorgan dysfunction could be attenuated by KYNA preconditioning. Accordingly, the temporal profiles of the apoptotic cell numbers of spleen, kidney, liver, lung, and hypothalamus, Kynurenic acid attenuates multiorgan dysfunction in rats after heatstroke Aim: To assess whether systemic delivery of kynurenic acid improves the outcomes of heatstroke in rats. Methods: Anesthetized rats were divided into 2 major groups and given vehicle solution (isotonic saline 0.3 mL/kg rat weight) or kynurenic acid (30-100 mg in 0.3 mL saline/kg) 4 h before the start of thermal experiments. They were exposed to an ambient temperature of 43 ºC for 68 min to induce heatstroke. Another group of rats were exposed to room temperature (26 ºC) and used as normothermic controls. Their core temperatures, mean arterial pressures, serum levels of systemic inflammatory response molecules, hypothalamic values of apoptotic cells and neuronal damage scores, and spleen, liver, kidney and lung values of apoptotic cells were determined. Results: The survival time values during heatstroke for vehicle-treated rats were decreased from the control values of 475-485 min to new values of 83-95 min. Treatment with KYNA (30-100 mg/kg, iv) 4 h before the start of heat stress significantly and dose-dependently decreased the survival time to new values of 152-356 min (P<0.05). Vehicle-treated heatstroke rats displayed hypotension, hypothalamic neuronal degeneration and apoptosis, increased serum levels of tunor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and interleukin-10 (IL-10), and spleen, liver, kidney, and lung apoptosis. KYNA preconditioning protected against hypotension but not hyperthermia and attenuated hypothalamic neuronal degeneration and apoptosis during heatstroke. KYNA preconditioning attenuated spleen, kidney, liver, and lung apoptosis and up-regulated serum IL-10 levels but down-regulated serum TNF-α and ICAM-1 lev...

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Structure and Function of Intercellular Adhesion Molecule-1

Cited by 38 publications

References 0 publications

Procalcitonin, C-Reactive Protein, Interleukin-6, and Soluble Intercellular Adhesion Molecule-1 as Markers of Postoperative Orthopaedic Joint Prosthesis Infections

Procalcitonin, C-Reactive Protein, Interleukin-6, and Soluble Intercellular Adhesion Molecule-1 as Markers of Postoperative Orthopaedic Joint Prosthesis Infections

Surface molecules involved in the adherence of recombinant interferon-gamma (rIFN-γ)-stimulated human monocytes to vascular endothelial cells

Kynurenic acid attenuates multiorgan dysfunction in rats after heatstroke

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