Leucocidal agents of hæmolytic streptococci

Bernheimer, Alan W.; Schwartz, Lois L.

doi:10.1002/path.1700790105

Cited by 21 publications

(11 citation statements)

References 12 publications

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“…II, for instance). This apparent variation in leucocyte susceptibility to streptolysin toxicity was also noted in a previous study (3), and is unexplained.…”

Section: Resultssupporting

confidence: 79%

Motion Picture Study of the Toxic Action of Streptolysins on Leucocytes

Hirsch

Bernheimer

Weissmann

1963

The Journal of Experimental Medicine

106

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The preceding communication presents evidence that streptolysins bring about release of hydrolytic enzymes from lysosomes isolated from various tissues (1). This finding, considered along with previous reports establishing the lysosomal nature of leucocytic granules (2) and the leucocidal action of streptolysins (3), led to speculation that these bacterial products might disrupt granules in intact white cells, releasing autolytic enzymes to digest other leucocyte structures and result eventually in cell death. Such a sequence of events, if supported by experimental observations, would be in keeping with de Duve's (4) concise and colorful designation of lysosomes as "suicide bags."This communication presents cinemicrophotographic studies done to elucidate detailed morphologic aspects of streptolysin toxicity on rabbit polymorphonuclear leucocytes and macrophages. MethodsThe streptolysin O preparation was the same as that designated preparation A in the preceding paper (1). The streptolysin S used was a lyophilized product described previously (5). Streptolysins were dissolved in phosphate-buffered saline and centrifuged at high speed to remove any particles which might otherwise confuse observations on degranulation. Streptolysin O was activated by addition of 3.5 mm cysteine.Rabbit granulocytes were obtained from peritoneal exudates as described previously (2).Rabbit alveolar macrophages, collected by a modification of the technique of Myrvik et al.(6), were kindly supplied by Dr. Zanvil Cohn. Leucocytes were washed twice in saline by centrifuging at 250 g for 5 minutes at room temperature, and were then suspended in Hanks' solution containing 10 per cent rabbit serum at a cell concentration of approximately 20,000 per mms. Small drops of the white cell suspension and of appropriate dilutions of streptolysin solution (or, for control, Hanks' with or without cysteine but no streptolysin) were mixed and made *

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“…II, for instance). This apparent variation in leucocyte susceptibility to streptolysin toxicity was also noted in a previous study (3), and is unexplained.…”

Section: Resultssupporting

confidence: 79%

Motion Picture Study of the Toxic Action of Streptolysins on Leucocytes

Hirsch

Bernheimer

Weissmann

1963

The Journal of Experimental Medicine

106

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“…The possible involvement of immune mediators in the observed inhibition of human neutrophils was considered and excluded by the following studies. White blood cells from humans with humoral or cellular immune deficiencies responded in a manner similar to normal human cells; supernatant solutions from SO-treated human white blood cells did not contain a chemotactic suppressor; preincubation of SO with cholesterol (an inhibitor of SO hemolytic activity) caused loss of the chemotactic suppressive effect of the toxin on human leukocytes; and leukocytes from rabbits preimmunized with SO remained refractory to chemotactic suppression.Streptolysin 0 (SO), the oxygen-labile hemolysin of beta-hemolytic streptococci, is capable of degranulating and lysing white blood cells (WBC) (1,2,4) when the cells are treated with high doses of the toxin. Andersen and Van Epps (1) have shown that treatment of human WBC with low doses of SO, which were incapable of lysing the WBC or of causing any observable morphological changes, resulted in suppression of neutrophilic chemotaxis and mobility.…”

mentioning

confidence: 99%

“…Streptolysin 0 (SO), the oxygen-labile hemolysin of beta-hemolytic streptococci, is capable of degranulating and lysing white blood cells (WBC) (1,2,4) when the cells are treated with high doses of the toxin. Andersen and Van Epps (1) have shown that treatment of human WBC with low doses of SO, which were incapable of lysing the WBC or of causing any observable morphological changes, resulted in suppression of neutrophilic chemotaxis and mobility.…”

mentioning

confidence: 99%

Streptolysin O Inhibition of Neutrophil Chemotaxis and Mobility: Nonimmune Phenomenon with Species Specificity

Epps

Andersen

1974

Infect Immun

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The effects of streptolysin 0 (SO) (1 to 4 hemolytic units) on the mobility of neutrophilic leukocytes from humans, baboons, sheep, and rabbits were compared. After SO treatment, chemotaxis and random mobility of human neutrophils were markedly suppressed, baboon and sheep neutrophils were partially suppressed, and rabbit neutrophils were unaffected and demonstrated normal chemotaxis and mobility. The amounts of SO used in the mobility studies caused no leukocyte lysis or trypan blue uptake by human, baboon, or sheep cells, and minimal lysis or trypan blue uptake by rabbit cells. The possible involvement of immune mediators in the observed inhibition of human neutrophils was considered and excluded by the following studies. White blood cells from humans with humoral or cellular immune deficiencies responded in a manner similar to normal human cells; supernatant solutions from SO-treated human white blood cells did not contain a chemotactic suppressor; preincubation of SO with cholesterol (an inhibitor of SO hemolytic activity) caused loss of the chemotactic suppressive effect of the toxin on human leukocytes; and leukocytes from rabbits preimmunized with SO remained refractory to chemotactic suppression.Streptolysin 0 (SO), the oxygen-labile hemolysin of beta-hemolytic streptococci, is capable of degranulating and lysing white blood cells (WBC) (1,2,4) when the cells are treated with high doses of the toxin. Andersen and Van Epps (1) have shown that treatment of human WBC with low doses of SO, which were incapable of lysing the WBC or of causing any observable morphological changes, resulted in suppression of neutrophilic chemotaxis and mobility. The present study is the result of further investigations of this effect and demonstrates species specificity and the absence of immune mediators as effectors in SO chemotactic suppression.MATERIALS AND METHODS Preparation of leuk6eytes. WBC preparations were obtained from the peripheral blood of humans, baboons, sheep, and rabbits. Coagulation was prevented by heparin (10 U/ml), except in the rabbit, where the excessive amounts of heparin needed to prevent coagulation were avoided by glass bead defibrination. Defibrination of human blood with glass beads gave results similar to those where heparin was used. Red blood cells (RBC) were then sedimented for 30 min with Plasmagel (Roger Bellon Laboratories, Neuilly, France; 1 ml per 5 cm3) or with a one-third volume of pigskin gelatin (United Chemical and Organic Products, Calumet City, Ill.). In the rabbit and the sheep, pigskin gelatin proved to be a more efficient means of erythrocyte sedimentation. The supernatant solutions containing a high percentage of WBC were then decanted and centrifuged at 1,500 rpm (270 x g) for 10 min. The cells were washed twice with Hanks balanced salt solution (HBSS) and adjusted to the white cell count needed in each experiment. The human cell preparations contained approximately 65% polymorphonuclear leukocytes, 34% mononuclear cells, and a red cell-to-white cell ratio of approximately 1.4 ...

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“…The hemolytic and cytotoxic properties of streptococcal filtrates have been shown to be associated with two extracellular hemolytic substances: streptolysin 0 and streptolysin S (3,5,11,14,18,19,21,26,28,30). Whereas streptolysin 0 is an immunogenic, SH-dependent protein (18,19,28), streptolysin S is nonimmunogenic and is considered to be a complex between nonspecific carrier molecules (ribonucleic acid [RNA], albumin, alpha-lipoprotein, Tween, Triton, trypan blue, etc.)…”

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confidence: 99%

Oxygen-Stable Hemolysins of Group A Streptococci VIII. Leukotoxic and Antiphagocytic Effects of Streptolysins S and O

1972

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Streptolysin S exists in a cell-bound form and as an extracellular complex between a nonspecific carrier (serum, serum albumin, ribonucleic acid [RNA], Triton, Tween) and a hemolytic moiety (probably a peptide) synthesized by streptococci. Although all the forms of streptolysin S, at 100 hemolytic units, killed mouse leukocyte monolayers, the time needed to kill 100% of the cells varied with the different streptolysin S preparations. Whereas 30 min was sufficient for the cell-bound hemolysin to kill all of the cells, 60 and 180 min were required when RNA streptolysin S and serum streptolysin S, respectively, were employed. Addition of 10% mouse serum to RNA streptolysin S or to cell-bound hemolysin delayed the killing of the leukocytes. The delayed killing observed with serum and albumin hemolysins is probably due to competition for the hemolytic moiety between the carrier molecules and target sites (phospholipids) upon the leukocyte membrane. Serum streptolysin S must

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Leucocidal agents of hæmolytic streptococci

Cited by 21 publications

References 12 publications

Motion Picture Study of the Toxic Action of Streptolysins on Leucocytes

Motion Picture Study of the Toxic Action of Streptolysins on Leucocytes

Streptolysin O Inhibition of Neutrophil Chemotaxis and Mobility: Nonimmune Phenomenon with Species Specificity

Oxygen-Stable Hemolysins of Group A Streptococci VIII. Leukotoxic and Antiphagocytic Effects of Streptolysins S and O

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