Binding of Efb fromStaphylococcus aureusto Fibrinogen Blocks Neutrophil Adherence

Receptors are commonly defined in terms of number per cell, affinity for ligand, chemical structure, mode of attachment to the cell surface, and mechanism of signal transduction. We propose to show that knowledge of spatial distribution of receptors on the cell surface can provide additional clues to their function and components of functional control.L-selectin and Mac-1 denote two receptor populations on the neutrophil surface that mediate neutrophil-endothelial cell adherence interactions and provide for targeting of neutrophil recruitment to sites of inflammation. We have studied the spatial distributions of these receptors using LVSEM and backscatter imaging of isolated human neutrophils stained with mouse anti-receptor (primary) antibody and goat anti-mouse (secondary) antibody conjugated to 12 nm colloidal gold. This combination of techniques provides for three-dimensional analysis of the expression of these receptors on different surface membrane domains of the neutrophil: the ruffles and microvilli that project from the cell surface, and the cell body between these projecting structures.

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Neutrophils do not bind to or phagocytize human immune complexes formed with influenza virus

Blood ◽

10.1182/blood.v82.5.1639.1639 ◽

1993 ◽

Vol 82 (5) ◽

pp. 1639-1646 ◽

Cited By ~ 3

Author(s):

DR Ratcliffe ◽

J Michl ◽

EB Cramer

Keyword(s):

Influenza Virus ◽

Sialic Acid ◽

Epithelial Cells ◽

Binding Site ◽

Immune Complexes ◽

Human Neutrophils ◽

Sialic Acid Binding ◽

Infected Cells ◽

Neutrophil Adherence ◽

Human Immune

Abstract Neutrophils appear to form the first line of defense against influenza virus, yet it is unclear how these leukocytes recognize influenza- infected cells. While demonstrating that neutrophils adhere specifically to the sialic acid-binding site on the hemagglutinin molecule (HA) on the surface of influenza-infected (WSN[H1N1]) epithelial cells and not to other viral or epithelial cell antigens, it was observed that human neutrophils do not recognize immune complexes formed with influenza virus. Intact antibodies (mouse monoclonal antibodies [MoAbs] IgG1 and IgG2b, human immune heat-inactivated serum [predominantly IgG1], and IgG purified from human immune serum) that block the sialic acid-binding site on HA significantly reduced (> 80%) neutrophil adherence to influenza-infected epithelial cells. Binding and phagocytosis of free influenza virions and neutrophil agglutination by influenza virus were completely prevented by these antibodies. Intact and F(ab')2 fragments of mouse MoAbs to other viral epitopes caused increased neutrophil adherence to infected cells. This binding was eliminated by F(ab'2) fragments of MoAbs against the sialic acid- binding site on HA, but not by saturating amounts of MoAbs, which block the neutrophil Fc receptors. Thus, it appears that human neutrophils show little ability to bind via their Fc receptors to the immune complexes formed with antibody and either influenza-infected epithelial cells or the free virion. These findings are in contrast to the general dogma, and are the first example of antibody opsonization reducing, rather than enhancing, neutrophil binding and phagocytosis of a pathogen.

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Neutrophil chemotaxis, random migration, and adherence in patients with hyperthyroidism

Acta Endocrinologica ◽

10.1530/acta.0.1210817 ◽

1989 ◽

Vol 121 (6) ◽

pp. 817-820 ◽

Cited By ~ 5

Author(s):

B. Wolach ◽

B. Lebanon ◽

A. Jedeikin ◽

M. S. Shapiro ◽

L. Shenkman

Keyword(s):

Thyroid Function ◽

Chemotactic Activity ◽

Neutrophil Chemotaxis ◽

Phagocytic Cells ◽

Random Migration ◽

Significant Difference ◽

Neutrophil Adherence ◽

Hyperthyroid Patients ◽

Normal Controls ◽

Neutrophil Chemotactic Activity

Abstract. We have examined neutrophil adherence, chemotactic activity, and random migration in 35 hyperthyroid patients with Graves' disease and 106 normal volunteers. No statistically significant differences were found between granulocyte adherence of 17 hyperthyroid subjects (67 ± 15.6%) and 81 healthy volunteers (63.1 ± 17%). In 3 thyrotoxic patients, impaired neutrophil adherence was found, which resolved when thyroid function returned to normal. The neutrophil chemotactic activity of 32 normal controls was 107.5 ± 21.4 cells, and the random migration 36 ± 15.5 cells. No statistically significant difference was demonstrated in 13 hyperthyroid patients who had a neutrophil chemotactic activity of 102 ± 14.6 cells and a random migration of 31.2 ± 13.2 cells. Defective chemotactic activity and random migration was found in 2 patients. Neutrophil functions returned to normal in one of the two subjects who were re-evaluated when thyroid function recovered. In summary, 14% of hyperthyroid patients had impaired leukocyte functions. However, severe pyogenic infections are quite rare in hyperthyroid patients, indicating that the observed alterations in function of phagocytic cells are not clinically important.

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Exposure to febrile temperature modifies endothelial cell response to tumor necrosis factor-α

Journal of Applied Physiology ◽

10.1152/jappl.2001.90.1.90 ◽

2001 ◽

Vol 90 (1) ◽

pp. 90-98 ◽

Cited By ~ 30

Author(s):

Jeffrey D. Hasday ◽

Douglas Bannerman ◽

Sirhan Sakarya ◽

Alan S. Cross ◽

Ishwar S. Singh ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Gm Csf ◽

Tnf Α ◽

Neutrophil Adherence ◽

Endothelial Cell Response ◽

Factor Α ◽

Necrosis Factor

Fever is an important regulator of inflammation that modifies expression and bioactivity of cytokines, including tumor necrosis factor (TNF)-α. Pulmonary vascular endothelium is an important target of TNF-α during the systemic inflammatory response. In this study, we analyzed the effect of a febrile range temperature (39.5°C) on TNF-α-stimulated changes in endothelial barrier function, capacity for neutrophil binding and transendothelial migration (TEM), and cytokine secretion in human pulmonary artery endothelial cells (EC). Permeability for [14C]BSA tracer was increased by treatment with TNF-α, and this effect was augmented by incubating EC at 39.5°C. Treating EC with 2.5 U/ml TNF-α stimulated an increase in subsequent neutrophil adherence and TEM. Incubating EC at 39.5°C caused a 30% increase in TEM but did not modify the enhancement of neutrophil adherence or TEM by TNF-α treatment. Analysis of cytokine expression in EC cultures exposed to TNF-α at either 37° or 39.5°C revealed three patterns of temperature and TNF-α responsiveness. Granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL)-8 were not detectable in untreated EC but were increased after TNF-α exposure, and this increase was enhanced at 39.5°C. IL-6 expression was also increased with TNF-α exposure, but IL-6 expression was lower in 39.5°C EC cultures. Transforming growth factor-β1was constitutively expressed, and its expression was not influenced either by TNF-α or exposure to 39.5°C. These data demonstrate that clinically relevant shifts in body temperature might cause important changes in the effects of proinflammatory cytokines on the endothelium.

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Endotoxin-Induced Neutrophil Adherence to Endothelium: Relationship to CD11b/CD18 and L-Selectin Expression and Matrix Disruption

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1994.tb39799.x ◽

1994 ◽

Vol 725 (1) ◽

pp. 173-182 ◽

Cited By ~ 8

Author(s):

ADAM FINN ◽

STEPHEN STROBEL ◽

MICHAEL LEVIN ◽

NIGEL KLEIN

Keyword(s):

Neutrophil Adherence

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Inhibition of Neutrophil Adherence and Movement by Acute Cigarette Smoke Exposure

Experimental Lung Research ◽

10.3109/01902149209031709 ◽

1992 ◽

Vol 18 (6) ◽

pp. 813-827 ◽

Cited By ~ 39

Author(s):

C. Selby ◽

E. Drost ◽

D. Brown ◽

S. Howie ◽

W. Macnee

Keyword(s):

Cigarette Smoke ◽

Smoke Exposure ◽

Cigarette Smoke Exposure ◽

Neutrophil Adherence

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Inhibition of Neutrophil Adherence to Antibody by Daspone: A Possible Therapeutic Mechanism of Dapsone in the Treatment of IgA Dermatoses

Journal of Investigative Dermatology ◽

10.1111/1523-1747.ep12471811 ◽

1993 ◽

Vol 100 (4) ◽

pp. 349-355 ◽

Cited By ~ 59

Author(s):

V.u. Thuong-Nguyen ◽

Donald P. Kadunce ◽

John D. Hendrix ◽

W Ray Gammon ◽

John J. Zone

Keyword(s):

Therapeutic Mechanism ◽

Neutrophil Adherence

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Suppression of tumor necrosis factor-alpha-induced neutrophil adherence responses by essential oils

Mediators of Inflammation ◽

10.1080/09629350310001633342 ◽

2003 ◽

Vol 12 (6) ◽

pp. 323-328 ◽

Cited By ~ 39

Author(s):

Shigeru Abe ◽

Naho Maruyama ◽

Kazumi Hayama ◽

Hiroko Ishibashi ◽

Shigeharu Inoue ◽

...

Keyword(s):

Essential Oils ◽

Tumor Necrosis ◽

Neutrophil Activation ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Neutrophil Adherence ◽

Factor Alpha ◽

Anti Inflammatory ◽

Necrosis Factor

Background:In aromatherapy, essential oils are used as anti-inflammatory remedies, but experimental studies on their action mechanisms are very limited.Aims:To assess their anti-inflammatory activities, effects of essential oils on neutrophil activation were examinedin vitro.Methods:Neutrophil activation was measured by tumor necrosis factor-alpha (TNF-α)-induced adherence reaction of human peripheral neutrophils.Results:All essential oils tested at 0.1% concentration suppressed TNF-α-induced neutrophil adherence, and, in particular, lemongrass, geranium and spearmint oils clearly lowered the reaction even at 0.0125%. Similar inhibitory activities for the neutrophil adherence were obtained by their major constituent terpenoids: citral, geraniol, citronellol and carvone. In contrast, very popular essential oils, tea tree oil and lavender oil, did not display the inhibitory activity at the concentration.Conclusion:Thus, some essential oils used as anti-inflammatory remedies suppress neutrophil activation by TNF-α at a low concentration (0.0125-0.025%)in vitro.

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