In many cases, evidently inert and nontoxic
biomaterials may trigger procoagulant and inflammatory responses. Because most polymeric
biomaterials accumulate a surface layer of
protein immediately after implantation, these adverse reactions may stem from secondary interactions between the host and this surface layer of adsorbed
proteins. Using
polyester terephthalate (the
polymer from which both
Dacron and Mylar are produced) as a model, we have explored the hypothesis that surface-adsorbed
immunoglobulin might mediate subsequent inflammatory responses. We find, as have others, that
immunoglobulin G (
IgG) does spontaneously adsorb to
polymer surfaces, both in vitro and in vivo. Furthermore,
polymer implants precoated with
IgG do activate human polymorphonuclear neutrophils in vitro and also attract substantial numbers of phagocytes (especially polymorphonuclear neutrophils and macrophages) when implanted in mice. However, when implants are placed in mice having a form of
severe combined immunodeficiency (and, consequently, almost undetectable levels of serum
IgG), a near-normal influx of phagocytic cells ensues. Thus, spontaneously-adsorbed surface
IgG does not appear to be a necessary precedent to inflammatory responses directed against implanted
biomaterials.