Abstract

The effects of hyaluronate on rabbit neutrophil adhesion were studied using a variety of techniques. Exogenous hyaluronate inhibited neutrophil aggregation under conditions of both turbulent flow and constant shear rate. Hyaluronate also inhibited neutrophil adhesion to glass. Inhibition was dose-dependent above 100 micrograms ml-1 and a minimum molecular weight for hyaluronate of 1 x 10(4) was required. These effects were not simply the result of increased bulk viscosity of the hyaluronate-containing medium, nor did they appear to be mediated by putative cell-surface receptor mechanisms. Instead, physical factors such as hindrance and/or changes in the interfacial free-energy exchange at the cell surface due to the unusual hydrodynamic properties of the hyaluronate molecule were considered to be more important. Since neutrophil migration in vivo occurs through hyaluronate-rich connective tissue matrices, the relevance of these findings for processes such as inflammation and wound healing is clear.