title: The influence of plasma proteins and platelets on oxygen radical production and F-actin distribution in neutrophils adhering to polymer surfaces.
abstract: It is well known that blood cell interactions with artificial surfaces might have deleterious effects on host tissue, however, the mechanisms involved are far from understood. In this study, neutrophil-platelet interaction on uncoated or protein-coated polymer surfaces was investigated. Cell spreading, reorganization of actin filaments and release of oxygen metabolites (measured as luminol-amplified chemiluminescence) were used as criteria for cell activation on positively charged, hydrophilic 1,2-diaminocyclohexane, and negatively charged, hydrophobic hexamethylene-disiloxane. The model surfaces were made by radio frequency plasma discharge polymerization. Neutrophil contact with the uncoated polymers induced a prolonged generation of oxygen radicals. Precoating of the polymer surfaces with human serum albumin (HSA) or fibrinogen, markedly reduced neutrophil activation, whereas coating with human immunoglobulin G (IgG), a well-known opsonin, resulted in significantly higher levels of cell activation. Consequently, protein coating overruled the activating effects of the polymer surfaces. The presence of unstimulated or thrombin-stimulated platelets markedly increased the reactivity of neutrophils against fibrinogen- and IgG-coated surfaces. However, neutrophils remained relatively unreactive in the presence of platelets on HSA-treated surfaces. Comparison of the different types of surfaces used, reveals a correlation between the degree of cell spreading, reorganization of the actin cytoskeleton and the amount of oxygen radicals produced. Our results suggest that the acute inflammatory reaction on a biomaterial surface is highly dependent on the nature and composition of the first adsorbed protein layer and the extent of platelet activation.
authors.affiliation: Department of Health and Environment, Faculty of Health Sciences, Linköping University, Sweden.
authors.forename: Ghada
authors.initials: G
authors.lastname: Nimeri
authors.forename: Lena
authors.initials: L
authors.lastname: Ohman
authors.forename: Hans
authors.initials: H
authors.lastname: Elwing
authors.forename: Jonas
authors.initials: J
authors.lastname: Wetterö
authors.forename: Torbjörn
authors.initials: T
authors.lastname: Bengtsson
mesh_terms: D000199:Actins / Q000378:metabolism*; D001792:Blood Platelets / Q000166:cytology* / Q000378:metabolism; D002448:Cell Adhesion; D005340:Fibrinogen / Q000378:metabolism; D005609:Free Radicals; D006098:Granulocytes / Q000378:metabolism; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism; D007249:Inflammation; D008163:Luminescent Measurements; D009504:Neutrophils / Q000166:cytology* / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D010949:Plasma / Q000378:metabolism*; D011108:Polymers / Q000378:metabolism; D012709:Serum Albumin / Q000378:metabolism; D013997:Time Factors
chemical_list: D000199:Actins; D005609:Free Radicals; D007074:Immunoglobulin G; D011108:Polymers; D012709:Serum Albumin; D005340:Fibrinogen; D010100:Oxygen