Surface-related triggering of the neutrophil respiratory burst. Characterization of the response induced by IgG adsorbed to hydrophilic and hydrophobic glass surfaces

Liu, L; Elwing, Hans; Karlsson, Anna; Nimeri, Ghada; Dahlgren, Cláes

doi:10.1046/j.1365-2249.1997.4311329.x

Cited by 36 publications

(37 citation statements)

References 27 publications

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“…2). This contradicts the previously reported rapid inhibition of integrin dependent ROSgeneration on IgG-and complement-opsonized surfaces [22,26].…”

Section: Igg-stimulated Platelets Activate Neutrophils -Wetterö Et Alcontrasting

confidence: 99%

“…The potentiating effect of platelets on the neutrophil oxidase activity resembles the previously reported effect of IgG in normal human serum [22,23]. While the serum triggered neutrophil CL-response was disrupted by drugs that interfere with the actin cytoskeleton (cytochalasin B and jasplakinolide [22,26]), the platelet-induced neutrophil oxidase activity in the presence of IgG-coated particles was unaffected, arguing against a tentative interaction between neutrophil CR3 and platelet GpIIb/IIIa as the main effector mechanism during the amplification process.…”

Section: The Role Of Psgl-1 Is Pronounced Under Stirring Conditionssupporting

confidence: 66%

“…In other studies, the interaction between CR3 and F c -receptors was counteracted by drugs that disrupt the actin dynamics [25], also on IgG-coated artificial surfaces [22,26]. However, we observed that both the actin polymerization inhibitor cytochalasin B and the actin polymerization stabilizer jasplakinolide transiently stimulated the platelet-mediated ROS-production in neutrophils (Fig.…”

Section: Igg-stimulated Platelets Activate Neutrophils -Wetterö Et Almentioning

confidence: 45%

“…Others and we have previously demonstrated that integrin-dependent ROS-production, e.g. by neutrophils that interact with surface-deposited complement activated by IgG, depend on a dynamic actin cytoskeleton for the coupling of CR3 to the NADPH-oxidase [22, 25,26]. We found in the present study that actin filament inhibitors that block de novo expression of integrins [35] had no inhibitory effect on the oxidative burst of neutrophils and platelets that interacted with the IgG-coated surfaces.…”

Section: Discussionmentioning

confidence: 99%

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Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway

2003

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Blood platelets bind rapidly to foreign surfaces and interact with adsorbed proteins and neutrophil granulocytes. We demonstrate by use of luminol-amplified chemiluminescence under stirred and nonstirred conditions that platelets at IgG-coated surfaces amplify the neutrophil extracellular release of reactive oxygen species (ROS). The neutrophil response involved tyrosine phosphorylation, but was only in part induced by neutrophil F c -receptor stimulation. The platelet mediated effects were contact-dependent since the respiratory burst was inhibited when the IgG-stimulated platelets were removed by filtration, but not when they were fixed in paraformaldehyde. Bodipyphallacidin-staining of filamentous actin (F-actin) revealed that an actin-dependent platelet adhesion supported the subsequent adhesion and spreading of neutrophils. The neutrophil ROS-response was lowered when the interaction between platelet P-selectin (CD62P) and neutrophil P-selectin glycoprotein ligand-l (PSGL-1 or CD162) was inhibited. The blocking of L-selectin (CD62L) or blocking of the interaction between platelet glycoprotein (Gp) IIb/IIIa and neutrophil complement receptor 3 (CR3) showed no effect. We conclude that platelet activation on immobilized IgG trigger a contact-dependent "frustrated" phagocytosis by neutrophils, associated with a release of toxic ROS. IgG-stimulated platelets activate neutrophils -Wetterö et al.3

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“…2). This contradicts the previously reported rapid inhibition of integrin dependent ROSgeneration on IgG-and complement-opsonized surfaces [22,26].…”

Section: Igg-stimulated Platelets Activate Neutrophils -Wetterö Et Alcontrasting

confidence: 99%

Section: The Role Of Psgl-1 Is Pronounced Under Stirring Conditionssupporting

confidence: 66%

Section: Igg-stimulated Platelets Activate Neutrophils -Wetterö Et Almentioning

confidence: 45%

Section: Discussionmentioning

confidence: 99%

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Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway

2003

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“…IgG was covalently bound to APTES + GA surfaces through a similar incubation. IgG immobilized by both procedures has proven able to activate the classical pathway of complement [29,30] and to induce leukocyte frustrated phagocytosis in vitro [31,32].…”

Section: Preparation Of Igg-coated Surfacesmentioning

confidence: 99%

On the binding of complement to solid artificial surfaces in vitro

et al. 2002

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Since the realization of a complement activation capacity by artificial surfaces upon contact with blood, a common belief has evolved that charged nucleophilic surface groups such as amine (-NH 2 ) and hydroxyl (-OH) react with and eventually bind to the internal thioester in complement factor 3 (C3). A covalent ester or amide linkage is thereby supposed to form between C3b and the surface itself. In this report,we present complement surface binding data by null-ellipsometry for two nucleophilic surfaces (-NH 2 and -OH), for surfaces with immunoglobulin G (IgG) covalently bound, and for IgG spontaneously pre-adsorbed to hydrophobic silicon. The results reveal that the plasma proteins that were deposited during complement activation became eluted by sodium dodecyl sulfate (SDS). Hence the direct covalent binding between C3 and solid nucleophilic surfaces seems to be only of moderate importance, at least during shorter serum incubations. This strongly suggests that the prevalent covalent linkage model between solid artificial surfaces and C3b is not accurate.Instead we suggest a more pronounced role for C3 associations to other adsorbed proteins and/or electrostatic and hydrophobic protein-surface interactions.

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Inflammatory cell recruitment, distribution, and chemiluminescence response at IgG precoated- and thiol functionalized gold surfaces

Källtorp

Askendal

Thomsen

et al. 1999

J. Biomed. Mater. Res.

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The role of complement activation by artificial surfaces relative to inflammatory response is not well understood. This study was performed to evaluate the inflammatory cell recruitment, distribution, and ex vivo metabolic activation of surfaces with different plasma protein adsorption and complement activation properties in vitro. The implants were (1) pure gold (reference), (2) albumin-precoated (3) IgG-precoated gold, and (4) 3-mercapto-1, 2-propanediol [mercaptoglycerol (MG)] and (5) glutathione (GSH) immobilized to gold. The implant disks were inserted subcutaneously in rats for 24 h, and the number of inflammatory cells that were recruited to the implant adjacent to the surrounding fluid phase (exudate) and the surfaces were quantified by DNA measurements. The oxidative burst was analyzed ex vivo using spontaneous and phorbol myristate acetate (PMA)-stimulated, luminol-enhanced chemiluminescence (CL). The in vitro surface-induced anti-rat C3 binding was evaluated by ellipsometry and antibody techniques after plasma incubations for 1 and 30 min. The ellipsometric results showed that immobilized mercaptoglycerol and IgG-coated, but not the immobilized glutathione or the reference Au, bound anti-C3. The in vivo results revealed that the largest amount of cells was associated with the IgG-coated surfaces, followed by immobilized GSH and MG, albumin-coated, and gold surfaces, respectively. No spontaneous ex vivo luminol-enhanced CL was recorded from the cells irrespective of surface functionality or localization. A down-regulation of surface-associated and exudate leukocyte CL was observed ex vivo, irrespective of surface functionality. The results do not indicate a clear relationship between the degree of complement activation in vitro and leukocyte recruitment and adhesion in vivo for differently functionalized surfaces.

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Surface-related triggering of the neutrophil respiratory burst. Characterization of the response induced by IgG adsorbed to hydrophilic and hydrophobic glass surfaces

Cited by 36 publications

References 27 publications

Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway

Platelets stimulated by IgG-coated surfaces bind and activate neutrophils through a selectin-dependent pathway

On the binding of complement to solid artificial surfaces in vitro

Inflammatory cell recruitment, distribution, and chemiluminescence response at IgG precoated- and thiol functionalized gold surfaces

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