Human fibrinogen gel formed by the action of a cell surface polysaccharide obtained from a Staphylococcus.

An alkali-stable polysaccharide (called compact-colony forming active substance; substance 1) obtained from the cell surface of a strain of Staphylococcus epidermidis caused gel formation of human fibrinogen, with no release of fibrinopeptides. Substance 1 possessed neither esterase nor caseinolytic activities; no inhibition of gel formation was shown by dinitrofluorophosphate. Heparin and galactose prevented gel formation of fibrinogen with substance 1. With the addition of early- and late-fibrinogen or fibrin degradation products into the fibrinogen sample, no prolongation of the gel formation time was observed. This substance is, therefore, assumed to nonenzymatically induce gel formation with fibrinogen, a process resembling paracoagulation.