scholarly journals FATE OF NON-VIRULENT GROUP A STREPTOCOCCI PHAGOCYTIZED BY HUMAN AND MOUSE NEUTROPHILS

1957 ◽  
Vol 106 (6) ◽  
pp. 777-786 ◽  
Author(s):  
Armine T. Wilson ◽  
Grove G. Wiley ◽  
Pauline Bruno

The fate of non-virulent group A streptococci phagocytized in vitro has been investigated by destroying the phagocyte with electric current and observing whether the liberated cocci multiply. Human and mouse peripheral blood neutrophils quickly injure ingested cocci, the time required to produce 50 per cent non-survival of chains being 8 and 6¾ minutes, respectively.

1941 ◽  
Vol 73 (4) ◽  
pp. 493-506 ◽  
Author(s):  
George K. Hirst

1. Confirming the observations of other experimenters, it has been found that group A hemolytic streptococci produce a capsule containing a polysaccharide which is similar to, if not identical with, certain high molecular weight sugars found in the mammalian body. 2. Leech extract possesses a powerful enzyme capable of splitting one of the linkages in this polysaccharide and of decapsulating group A and group C hemolytic streptococci in vitro and in vivo. 3. Mice and guinea pigs can be protected from intraperitoneal infection with a virulent group C streptococcus by the intraperitoneal administration of leech extract. In contrast there is little protective action of leech extract in mice infected with group A hemolytic streptococci. 4. The protective effect of leech extract against streptococcal group C infection is probably due to the removal of the capsule in vivo. 5. The capsule of mouse virulent group C streptococci plays a major rôle in the virulence of that microorganism, while the capsule of certain mouse virulent group A streptococci plays little, if any, rôle in virulence, at least when the infection is intraperitoneal in the mouse.


2003 ◽  
Vol 47 (5) ◽  
pp. 1752-1755 ◽  
Author(s):  
Elizabeth A. Coyle ◽  
Raymond Cha ◽  
Michael J. Rybak

ABSTRACT An in vitro model was used to compare the effects of linezolid, clindamycin, and penicillin, alone and in combination, on streptococcal pyrogenic exotoxin A (SPE A) release against virulent group A streptococci (GAS). All regimens exhibited lower (P < 0.05) SPE A release at 1 h than those with penicillin alone. Linezolid and clindamycin, alone or in combination with penicillin, may optimize the treatment of GAS infections by reducing bacterial burden and exotoxin release.


Inflammation ◽  
1992 ◽  
Vol 16 (1) ◽  
pp. 21-30 ◽  
Author(s):  
D. M. Brown ◽  
G. M. Brown ◽  
W. Macnee ◽  
K. Donaldson

1952 ◽  
Vol 95 (1) ◽  
pp. 25-38 ◽  
Author(s):  
Armine T. Wilson ◽  
Herman Rosenblum

The measurement in vitro of lactenin, the antistreptococcal substance of milk, is affected by the size of the inoculum, the temperature of incubation, and the type of medium employed. Hemolytic streptococci belonging to the several serological groups vary in susceptibility to lactenin. All group A streptococci, regardless of type, are highly sensitive to it, and milk receiving a small inoculum sterilizes itself within 48 hours or less. By contrast, most strains of groups B, C, D, and E, although they may temporarily be inhibited, ultimately achieve full growth. Strains belonging to groups F, G, H, K, and L vary in sensitivity, some being fully inhibited and others achieving full growth. When streaked on the surface of milk-agar plates and examined at the end of 24 hours the streptococci fall into two classes: sensitive strains which do not produce visible colonies on the plate, and resistant strains which grow excellently. Very few strains show an intermediate degree of sensitivity. Human and goat milk contain an antistreptococcal principle which appears to be the same as the lactenin of cow milk, since streptococci which are inhibited by milk from one species are inhibited by milk from the others, and vice versa.


2002 ◽  
Vol 70 (4) ◽  
pp. 2166-2170 ◽  
Author(s):  
James B. Dale ◽  
Edna Y. Chiang ◽  
David L. Hasty ◽  
Harry S. Courtney

ABSTRACT Virtually all group A streptococci (GAS) produce streptolysin S (SLS), a cytolytic toxin that is responsible for the beta-hemolysis surrounding colonies of the organisms grown on blood agar. SLS is an important virulence determinant of GAS, and recent studies have identified a nine-gene locus that is responsible for synthesis and transport of the toxin. SLS is not immunogenic; thus, no neutralizing antibodies are evoked during the course of natural infection. In the present study, we show that a synthetic peptide containing amino acid residues 10 to 30 of the putative SLS (SagA) propeptide [SLS(10-30)] coupled to keyhole limpet hemocyanin evoked antibodies in rabbits that completely neutralized the hemolytic activity of the toxin in vitro. Inhibition of hemolysis was reversed by preincubation of the immune serum with soluble, unconjugated peptide, indicating the specificity of the antibodies. In addition, antibodies that were affinity purified over an SLS(10-30) peptide column completely inhibited SLS-mediated hemolysis. The SLS(10-30) antisera did not opsonize group A streptococci; however, when combined with type-specific M protein antisera, the SLS antibodies significantly enhanced phagocytosis mediated by M protein antibodies. Thus, we have shown for the first time that it is possible to raise neutralizing antibodies against one of the most potent bacterial cytolytic toxins known. Our data also provide convincing evidence that the sagA gene actually encodes the SLS peptide of GAS. The synthetic peptide may prove to be an important component of vaccines designed to prevent GAS infections.


2014 ◽  
Vol 202 (3) ◽  
pp. 536-542 ◽  
Author(s):  
Timothy J. Brazil ◽  
Padraic M. Dixon ◽  
Christopher Haslett ◽  
Joanna Murray ◽  
Bruce C. McGorum

2021 ◽  
Vol 8 ◽  
Author(s):  
Honghu Tang ◽  
Chunyu Tan ◽  
Xue Cao ◽  
Yi Liu ◽  
Hua Zhao ◽  
...  

Autophagy pathways play an important role in immunity and inflammation via pathogen clearance mechanisms mediated by immune cells, such as macrophages and neutrophils. In particular, autophagic activity is essential for the release of neutrophil extracellular traps (NETs), a distinct form of active neutrophil death. The current study set out to elucidate the mechanism of the NFIL3/REDD1/mTOR axis in neutrophil autophagy and NET formation during gout inflammation. Firstly, NFIL3 expression patterns were determined in the peripheral blood neutrophils of gout patients and monosodium urate (MSU)-treated neutrophils. Interactions between NFIL3 and REDD1 were identified. In addition, gain- or loss-of-function approaches were used to manipulate NFIL3 and REDD1 in both MSU-induced neutrophils and mice. The mechanism of NFIL3 in inflammation during gout was evaluated both in vivo and in vitro via measurement of cell autophagy, NET formation, MPO activity as well as levels of inflammatory factors. NFIL3 was highly-expressed in both peripheral blood neutrophils from gout patients and MSU-treated neutrophils. NFIL3 promoted the transcription of REDD1 by binding to its promoter. REDD1 augmented neutrophil autophagy and NET formation by inhibiting the mTOR pathway. In vivo experimental results further confirmed that silencing of NFIL3 reduced the inflammatory injury of acute gouty arthritis mice by inhibiting the neutrophil autophagy and NET formation, which was associated with down-regulation of REDD1 and activation of the mTOR pathway. Taken together, NFIL3 can aggravate the inflammatory reaction of gout by stimulating neutrophil autophagy and NET formation via REDD1/mTOR, highlighting NFIL3 as a potential therapeutic target for gout.


1992 ◽  
Vol 263 (5) ◽  
pp. H1492-H1498
Author(s):  
P. J. McKenna ◽  
D. L. Rosolia ◽  
Y. Ishihara ◽  
K. H. Albertine ◽  
N. C. Staub ◽  
...  

We have shown that infusion of zymosan-activated plasma (ZAP) in sheep causes acute lung injury and downregulates peripheral blood neutrophils in that elicited superoxide release is reduced for at least 24 h after the infusion. The present study was designed to test the following hypotheses: 1) peripheral blood neutrophils are representative of neutrophils marginated in the pulmonary circulation, 2) blood neutrophils are downregulated because neutrophils developing in bone marrow are similarly affected, and 3) downregulated neutrophils have a reduced capacity to produce tissue injury. In a series of experiments in 21 sheep, we showed that elicited superoxide release was similar in peripheral blood neutrophils and in marginated neutrophils washed out of the pulmonary vascular bed. Measurements of superoxide release from blood and bone marrow neutrophils collected 2-24 h after ZAP infusion revealed progressive downregulation with time and greater downregulation of superoxide release in bone marrow neutrophils compared with peripheral blood neutrophils. Finally, after downregulating peripheral blood neutrophils, subsequent infusion of ZAP in conscious sheep produced sequestration of neutrophils in the pulmonary circulation but failed to produce a sustained increase in lung lymph protein clearance. The results suggest that neutrophil downregulation, as measured in vitro, is expressed in vivo as reduced ability of neutrophils to produce tissue injury when challenged by an activating agent.


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