Glucocorticoid Receptor Regulates Expression of L-Selectin and CD11/CD18 on Human Neutrophils

Filep, János G.; Delalandre, Aline; Payette, Yves; Földes-Filep, Éva

doi:10.1161/01.cir.96.1.295

Cited by 137 publications

(94 citation statements)

References 39 publications

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“…This is in agreement with ®ndings in asthmatic patients where glucocorticoid treatment induces a rapid and marked response of the eosinophils [36]. In vitro, glucocorticoids reduced neutrophil adhesion and the expression of CD11b and CD18 on stimulated neutrophils [37]. Intravenous pulse treatment with methylprednisolone in RA decreased peripheral blood neutrophil expression of CD11b…”

Section: Discussionsupporting

confidence: 88%

Enhanced Expression of Integrins and CD66b on Peripheral Blood Neutrophils and Eosinophils in Patients with Rheumatoid Arthritis, and the Effect of Glucocorticoids

Torsteinsdottir¹,

Arvidson

Hällgren

et al. 1999

Scand J Immunol

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The aim of this study was to elucidate signs of granulocyte activation by studying adhesion and phagocytosis receptors on peripheral blood granulocytes from patients with rheumatoid arthritis (RA), and to observe the effect of glucocorticoids. Analyses by flow cytometry showed elevation of the neutrophil and eosinophil expression of the α‐ and β‐chains of the β2‐integrin Mac‐1 (CD11b/CD18) and of the CEA‐gene family member 6 (CGM6, CD66b). Expression of the adhesion receptor antigens CD11a, CD29, CD49d, CD49f and CD44, and the Fcγ receptors II and III, was unaffected. Treatment with low‐dose prednisolone reduced the expression of CD11b on neutrophils and of CD11b, CD18 and CD66b on eosinophils to the same level as that found in healthy controls. Metyrapone treatment increased the surface expression of CD35 and CD49f on eosinophils, but did not affect surface expression on neutrophils. Activation of blood granulocytes may be important for the increased recruitment of neutrophils and eosinophils to the synovial cavity in RA. Treatment with low doses of glucocorticoids in RA normalizes the enhanced expression of the studied adhesion molecules in eosinophils but has minor impact on neutrophil activation. Endogenous glucocorticoid production seems to have minimal or no effect on the expression of adhesion and phagocytosis receptors on circulating granulocytes.

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Section: Discussionsupporting

confidence: 88%

Enhanced Expression of Integrins and CD66b on Peripheral Blood Neutrophils and Eosinophils in Patients with Rheumatoid Arthritis, and the Effect of Glucocorticoids

Torsteinsdottir¹,

Arvidson

Hällgren

et al. 1999

Scand J Immunol

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“…45 Our failure to demonstrate that methylprednisolone reduced myeloperoxidase content in injured spinal cord may reflect the fact that the injuryinduced expression of endothelial cell adhesion molecules is beyond glucocorticoid regulation by 30 min after injury. Alternatively, capillary disruption by the injury may render the endothelial cell unimportant in regulating neutrophil traffic into the injured tissue.…”

Section: Discussionmentioning

confidence: 88%

Effect of postinjury intravenous or intrathecal methylprednisolone on spinal cord excitatory amino-acid release, nitric oxide generation, PGE2 synthesis, and myeloperoxidase content in a pig model of acute spinal cord injury

Bernards

Akers

2006

Spinal Cord

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Objectives: To determine whether postinjury methylprednisolone could reduce the generation of known mediators of secondary neurological injury. Methods: Intrathecal microdialysis probes were used to sample cerebrospinal fluid (CSF) for measurement of PGE 2 , glutamate, and citrulline (a byproduct of nitric oxide generation), before and after spinal cord injury in anesthetized pigs. The spinal cord was removed at the end of the study for measurement of myeloperoxidase and methylprednisolone concentrations. Animals were randomly allocated to receive intravenous methylprednisolone (30 mg/kg bolus then 3.4 mg/kg/h), intrathecal methylprednisolone (5 mg bolus then 5 mg/h), or saline, beginning 30 min after the spinal cord was injured by using a modification of the Allen weight drop technique. Results: Spinal cord injury significantly increased the amount of glutamate, PGE 2 , myeloperoxidase, and citrulline, recovered from the CSF dialysates. However, neither intravenous nor intrathecal methylprednisolone administered after injury had any effect on the magnitude of the increase in any of the measured biochemicals. Intrathecal methylprednisolone administration produced a spinal cord methylprednisolone concentration that was eight times greater, and a plasma concentration that was 32 times less, than that achieved with intravenous administration. Conclusions: Contrary to earlier animal studies in which methylprednisolone was administered either before or immediately after spinal cord injury, we found no effect of intravenous or intrathecal methylprednisolone on any of the parameters measured when administered 30 min postinjury.

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“…6,7 The inflammation in early myocardial ischemia is characterized by infiltration with leukocytes, 31,32 a process involving the expression of L-selectin, CD11/CD18-complex, and adhesion molecules (for review, see Gumina et al 33 and Jordan et al 34 ). Glucocorticoids decrease the expression of L-selectin and CD11/CD18 on leukocytes 11,12 and the expression of endothelial-leukocyte adhesion molecule-1 and the intercellular adhesion molecule-1. 9 Accordingly, in the present study, nonspecific antiinflammatory treatment with methylprednisolone before coronary microembolization prevented leukocyte infiltration.…”

Section: Discussionmentioning

confidence: 98%

Glucocorticoid Treatment Prevents Progressive Myocardial Dysfunction Resulting From Experimental Coronary Microembolization

et al. 2004

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Background-The frequency and importance of microembolization in patients with acute coronary syndromes and during coronary interventions have recently been appreciated. Experimental microembolization induces immediate ischemic dysfunction, which recovers within minutes. Subsequently, progressive contractile dysfunction develops over several hours and is not associated with reduced regional myocardial blood flow (perfusion-contraction mismatch) but rather with a local inflammatory reaction. We have now studied the effect of antiinflammatory glucocorticoid treatment on this progressive contractile dysfunction. Methods and Results-Microembolization was induced by injecting microspheres (42-m diameter) into the left circumflex coronary artery. Anesthetized dogs were followed up for 8 hours and received placebo (nϭ7) or methylprednisolone 30 mg/kg IV either 30 minutes before (nϭ7) or 30 minutes after (nϭ5) microembolization. In addition, chronically instrumented dogs received either placebo (nϭ4) or methylprednisolone (nϭ4) 30 minutes after microembolization and were followed up for 1 week. In acute placebo dogs, posterior systolic wall thickening was decreased from 20.0Ϯ2.1% (meanϮSEM) at baseline to 5.8Ϯ0.6% at 8 hours after microembolization. Methylprednisolone prevented the progressive myocardial dysfunction. Increased leukocyte infiltration in the embolized myocardium was prevented only when methylprednisolone was given before microembolization. In chronic placebo dogs, progressive dysfunction recovered from 5.0Ϯ0.7% at 4 to 6 hours after microembolization back to baseline (19.1Ϯ1.6%) within 5 days. Again, methylprednisolone prevented the progressive myocardial dysfunction. Conclusions-Methylprednisolone, even when given after microembolization, prevents progressive contractile dysfunction.

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Glucocorticoid Receptor Regulates Expression of L-Selectin and CD11/CD18 on Human Neutrophils

Cited by 137 publications

References 39 publications

Enhanced Expression of Integrins and CD66b on Peripheral Blood Neutrophils and Eosinophils in Patients with Rheumatoid Arthritis, and the Effect of Glucocorticoids

Enhanced Expression of Integrins and CD66b on Peripheral Blood Neutrophils and Eosinophils in Patients with Rheumatoid Arthritis, and the Effect of Glucocorticoids

Effect of postinjury intravenous or intrathecal methylprednisolone on spinal cord excitatory amino-acid release, nitric oxide generation, PGE2 synthesis, and myeloperoxidase content in a pig model of acute spinal cord injury

Glucocorticoid Treatment Prevents Progressive Myocardial Dysfunction Resulting From Experimental Coronary Microembolization

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