1. Evidence has been presented in previous publications that the phagocytosis of pneumococci in the pneumonic lung during chemotherapy is due neither to specific opsonins nor to capsular injury (1, 2). The present studies have shown that the phagocytosis taking place in the lung is independent of any sort of intermediary factor and results from a direct action of the phagocytic cells upon the pneumococci.

2. Phagocytosis in the absence of antibody has been demonstrated not only in the lungs of living rats but in formalin-fixed lungs, on the surfaces of a variety of tissues (both freshly removed from the animal and previously "killed" with heat), and on the surfaces of such inert materials as moistened filter paper, cloth, and fiber glass. On the other hand, smooth materials such as glass, cellophane, albumin, and paraffin have failed to support the phagocytic reaction. This latter observation indicates that the physical character of the surface to which the leucocytes have access constitutes a determining factor in the non-antibody mechanism of phagocytosis.

3. Further experiments have defined the relationship of "surface phagocytosis" to that induced by specific opsonins. The non-antibody mechanism was found to operate only upon surfaces of suitable physical properties, whereas opsonins enabled phagocytes floating freely in a fluid medium to engulf the fully encapsulated organisms.

4. Direct visualization of the surface phenomenon in the lung revealed that leucocytes phagocyte the virulent organisms in the absence of antibody only after having trapped them against the alveolar walls. Once the encapsulated pneumococci have been ingested, they can be seen to undergo digestion within a few hours.

The discovery of the phenomenon of surface phagocytosis affords clarification of previously unanswered problems concerning the mechanism of recovery in pneumococcal pneumonia.

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