Cellular Mechanisms of Antibacterial Defense in Lymph Nodes

1959

Self Cite

Four strains of Group A streptococci, possessing different degrees of virulence for both mice and rats, were tested for susceptibility to phagocytosis on glass slides, in glass roller tubes, and on the surfaces of freshly excised tissues and moistened filter paper. All of the tests were performed in the absence of serum to exclude the possible presence of opsonins. Only under conditions which allowed surface phagocytosis to take place was there a correlation between virulence and susceptibility to phagocytosis. A similar relationship between virulence and surface phagocytosis was also demonstrable in vivo during the early stages of experimental streptococcal peritonitis. Systematic study of the evolution of the peritonitis revealed that its outcome was determined by the phagocytic reaction which occurred in the first few hours of the infection.

Section: Discussionsupporting

confidence: 82%

Studies on the Pathogenicity of Group a Streptococci

Foley

Smith

1959

Self Cite

“…The role of surface phagocytosis in antibacterial defense has been described in previous publications (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). Its destructive action upon certain common species of encapsulated bacteria in the absence of type-specific antibody has been confirmed by a number of investigators (14--17).…”

mentioning

confidence: 72%

“…The importance of such surfaces in determining whether or not fully encapsulated pneumococci are phagocyted in the absence of antibody has been conclusively demonstrated (1)(2)(3)(4)(5)(6)(7)(8)(9). Emphasis has been placed on the fact, however, that surface phagocytosis is of significance only in the destruction of encapsulated bacteria ~vhich are relatively resistant to phagocytosis (9,25).…”

Section: The Effect Of Parahydroxybenzoic Acid Upon the Phagocytosmentioning

confidence: 99%

Surface Phagocytosis

Smith

1958

Self Cite

Experiments recently reported (18) have been interpreted to indicate that surface phagocytosis plays no significant part in natural antipneumococcal defense. A repetition of these experiments has revealed: (a) that the cellular content of the leucocytic suspensions used in the phagocytic tests was of a different order of magnitude from that of the exudates which usually exist in infected tissues, (b) that the suspensions were too dilute to allow surface phagocytosis of pneumococci to occur, and (c) that the ratio of bacteria to leucocytes. was such that, when a sufficiently concentrated exudate was employed, the pneumococci injured the leucocytes and thus prevented phagocytosis from taking place. When conditions of the tests were suitably controlled, and conventional quantitative methods were employed to measure the end results of the phagocytic reaction, the essential observations relating to surface phagocytosis were fully confirmed. The significance of this non-antibody mechanism of defense in pneumococcal infections was thus further substantiated.

“…This observation is in keeping with the tentative hypothesis that the principal source of endogenous pyrogen in an acute granulocytic exudate is that fraction of the lencocytic population which has recently entered the site of infection. Once the infection has been brought under control, fresh leucocytes cease to enter the lesion (15), and as a result, it may be reasoned, the source of endogenous pyrogen becomes rapidly depleted. Such a theory provides a possible explanation for the presence of large numbers of morphologically intact leucocytes in pathologic lesions observed in patients who do not have fever at the time of death.…”

Section: Discussionmentioning

confidence: 99%

Studies on the Pathogenesis of Fever

King

1958

Self Cite

Evidence has been previously presented that an endogenous pyrogen is demonstrable in the circulation of rabbits with fever caused by the intravenous injection of typhoid vaccine (1, 2). The endogenous factor is readily differentiated from the pyrogenic component of the vaccine and reaches a maximum concentration well after the latter has been cleared from the blood stream. Its presence in the circulation is closely correlated with the fever. These observations have recently been confirmed in analogous studies made with dogs (3).The biological properties of the newly identified pyrogen were originally found to be identical with those of the heat-labile pyrogenic substance which is extractable from polymorphonuclear leucocytes (1, 2). Further evidence as to the identity of the two factors has subsequently been reported (4, 5). Because the endogenous factor makes its appearance in the blood stream shortly after the leucopenia which follows the injection of vaccine, the hypothesis has been advanced that the febrile response is caused by the action of endogenous pyrogen released from injured leucocytes (2).Although an endogenous pyrogen can be readily extracted from polymorphonuclear leucocytes (6--8), and a similar pyrogen can be demonstrated in the fluid portion of acute inflammatory exudates (8), doubt has arisen as to whether the pyrogen in the exudates is actually derived from the leucocytes. The doubt has been engendered primarily by two observations. First, a pyrogenic substance, with properties similar to those of leucocytic pyrogen, has been demon= strated in the fluid portion of acute infl~trnmatory exudates in agranulocytic rabbits, despite the virtual absence of polymorphonuclear leucocytes in the exudate (8). Secondly, rabbits and dogs made leucopenic with nitrogen mustard have been shown to exhibit the usual febrile response to bacterial pyrogens (9, lO).