Neuraminidase‐induced Thrombocytopenia in Rats

Abstract

Summary. The purpose of this study was to elucidate the effect of neuraminidase on circulating platelets in rats and the pathogenesis of this effect. Injection of bacterial, purified bacterial and viral neuraminidase caused thrombocytopenia of various degrees. Thrombocytopenia was less pronounced in rats given viral neuraminidase and in splenectomized animals. A dose‐response effect was seen only with purified bacterial neuraminidase injected intravenously. Ultrastructural studies of blood platelets were performed after injection of neuraminidase. Fifteen minutes after injecting neuraminidase, before a definite fall in the count, platelets showed evidence of structural damage such as irregular shapes, centripetal migration and fusion of granules and bleb formation. The structural alterations were progressive, reaching a maximum at about 2–4 hr. At no time were large platelet aggregates observed in the circulating blood. Four hours after injection of neuraminidase, when the platelet count dropped significantly, many platelets had normal ultrastructurc. By 24 hr, the majority of circulating platelets appeared normal; however, the splenic sinusoids and macrophages contained platelets with the same structural abnormalities seen in the circulation 15 min to 2 hr after injection of neuraminidase. We conclude that neuraminidase alters the platelet membrane resulting in its rapid and permanent removal by the reticuloendothelial system.

Sialic acid in cardiovascular diseases

“…Platelet sialic acid has been shown to have the following functions: (i) It is responsible for the surface negative charge of the platelets which play an important role both in platelet adhesion and aggregation (57)(58)(59)(60). An alteration in platelet sialic acid content results in altered electrophoretic mobility (61-64) (ii) platelet sialic acid is responsible for the life span of platelets as platelets depleted of sialic acid are rapidly cleared from circulation (65). Platelets from Bernard-Soulier patients which are deficient in glycoprotein I and sialic acid have a shortened survival time (66).…”

Mechanism of Thrombocytopenia Induced in Mice by Anti-Platelet Serum

“…In addition, nonimmunologic ma terials can cause thrombocytopenia in vivo. For example, neuraminidase can cause thrombocytopenia in rats [2] by alteration of the platelet membrane resulting in the platelets' rapid and permanent removal from the circulation. However, neuraminidase failed to induce in vitro aggregation of platelets in dicating that neuraminidase action is quite different from the action of anti platelet sera as observed in the present work.…”

The trans -Sialidase from Trypanosoma cruzi Induces Thrombocytopenia during Acute Chagas' Disease by Reducing the Platelet Sialic Acid Contents

“…It is known that even a small decrease in the sialic acid contents of platelet and red cell surfaces results in a reduction in the life span (35), and in vitro treatment of platelets with neuraminidase induces accelerated clearance from the blood (23). In addition, injection of neuraminidases into mammals also reduces the half-life of the platelets (10,19). More importantly, cell surface sialylation is physiologically decreased in several human diseases, resulting in faster removal of platelets from the blood (1,11,17,28).…”