Evidence has been presented that the introduction of large numbers of bacteria into the blood stream causes a widespread intravascular reaction, characterized by the sticking of leucocytes to the endothelium of capillaries, arterioles, and venules. The adherent granulocytes promptly become motile and thus potentially phagocytic. This intravascular leucocytic response affords a rapid and efficient mobilization of a vast number of active phagocytes within the blood stream. In some of the smaller vessels of both the systemic and pulmonary circulation the reaction is accompanied by the deposition of what appears to be intravascular fibrin.

Direct observation by the rabbit ear chamber technique has revealed that leucocytes thus mobilized in small peripheral vessels are capable of phagocyting fully encapsulated Friedländer’s bacilli in the absence of antibody. Ingestion of the encapsulated blood-borne bacteria results from surface phagocytosis and occurs primarily in those vessels in which the flow of blood is either slowed or has temporarily stopped altogether. Leucocytes can be seen to phagocyte the organisms by first trapping them against the walls of the vessels or against adjacent leucocytes. Bacteria caught in the interstices of the intravascular "fibrin" may likewise be immobilized and readily phagocyted. Thus granulocytes, without the aid of opsonins, are able to ingest and destroy encapsulated blood-borne bacteria by the same mechanisms that operate in extravascular tissues.

It is concluded from these studies that intravascular surface phagocytosis by polymorphonuclear leucocytes supplements the well known phagocytic activities of the reticulo-endothelial cells and therefore serves as an important defense of the host in acute infections caused by encapsulated bacteria and complicated by bacteriemia.

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