scholarly journals Demonstration of opsonic activity and in vivo protection against group B streptococci type III by Streptococcus pneumoniae type 14 antisera.

1978 ◽  
Vol 148 (3) ◽  
pp. 776-786 ◽  
Author(s):  
G W Fischer ◽  
G H Lowell ◽  
M H Crumrine ◽  
J W Bass

The present studies demonstrate that antisera directed against Streptococcus pneumoniae type 14 is opsonic for group B streptococci type III in a neutrophile-mediated bactericidal assay. Specificity was demonstrated by the observations that group B streptococci type III and S. pneumoniae type 14 adsorbed the opsonic activity of anti-S. pneumoniae type 14 antisera. Group B streptococci strain 090R (devoid of type antigens) and S. pneumoniae type 3, did not remove the opsonic activity of anti-S. pneumoniae type 14 serum. In vivo studies using a suckling rat model of neonatal group B streptococcal type III sepsis demonstrated that antisera directed against S. pneumoniae type 14 was highly protective.

2021 ◽  
pp. 1-20
Author(s):  
Sophie McKenna ◽  
Kristin Krohn Huse ◽  
Sean Giblin ◽  
Max Pearson ◽  
Mohammed Said Majid Al Shibar ◽  
...  

Bacteria possess the ability to evolve varied and ingenious strategies to outwit the host immune system, instigating an evolutionary arms race. Proteases are amongst the many weapons employed by bacteria, which specifically cleave and neutralize key signalling molecules required for a coordinated immune response. In this article, we focus on a family of S8 subtilisin-like serine proteases expressed as cell-envelope proteases (CEPs) by group A and group B streptococci. Two of these proteases known as <i>Streptococcus pyogenes</i> CEP (SpyCEP) and C5a peptidase cleave the chemokine CXCL8 and the complement fragment C5a, respectively. Both CXCL8 and C5a are potent neutrophil-recruiting chemokines, and by neutralizing their activity, streptococci evade a key defence mechanism of innate immunity. We review the mechanisms by which CXCL8 and C5a recruit neutrophils and the characterization of SpyCEP and C5a peptidase, including both in vitro and in vivo studies. Recently described structural insights into the function of this CEP family are also discussed. We conclude by examining the progress of prototypic vaccines incorporating SpyCEP and C5a peptidase in their preparation. Since streptococci-producing SpyCEP and C5a peptidase are responsible for a considerable global disease burden, targeting these proteases by vaccination strategies or by small-molecule antagonists should provide protection from and promote the resolution of streptococcal infections.


1999 ◽  
Vol 86 (1) ◽  
pp. 61-65 ◽  
Author(s):  
Richard M. Whitehurst ◽  
Rachel Laskey ◽  
Ronald N. Goldberg ◽  
Donald Herbert ◽  
Cornelius Van Breemen

To study whether a sepsis-induced increase in des-Arg9-bradykinin (des-Arg9-BK) and bradykinin (BK) B1-receptor activity participates in the observed increase in pulmonary vascular resistance in neonatal group B streptococcal sepsis (GBS), isometric force bioassays of pulmonary artery (PA) rings were studied, after 4-h exposure to either Krebs or GBS, by using the following protocols: 1) BK dose-response curve, 2) vascular response to BK with N G-nitro-l-arginine methyl ester (l-NAME), and 3) response to des-Arg9-BK (BK metabolite and B1 agonist). PA rings exposed to BK resulted in contraction in the GBS group and a decrease in resting tension in the Control group ( P = 0.034) at a concentration of 10−5 M. GBS-treated PA rings contracted more to des-Arg9-BK than did Controls ( P < 0.001). BK (10−6 M) relaxed preconstricted PA rings incubated in GBS less than BK relaxed Controls ( P < 0.001), and preincubation withl-NAME decreased relaxation in both. These results suggest that GBS decreased endothelium-dependent BK relaxation and increased contractile response to des-Arg9-BK. We speculate that this occurs secondary to upregulation of B1 receptors reflected by B1-agonist-mediated PA contraction.


PEDIATRICS ◽  
1978 ◽  
Vol 62 (4) ◽  
pp. 620-621
Author(s):  
Gerald W. Fischer ◽  
James W. Bass ◽  
George H. Lowell ◽  
Martin H. Crumrine

The article by Bortolussi et al. on pneumococcal septicemia and meningitis in the neonat (Pediatrics 60:352, September 1977) was of great interest to us, since we have been analyzing the effect of antibody directed against Streptococcus pneumoniae on group B Streptococcus type III. We have recently shown (unpublished data) that antibody directed against S. pneumoniae type 14 precipitates the hot hydrochloric acid-extracted polysaccharide antigen of group B Streptococcus type III. Further studies have shown that this antibody is opsonic for group B Streptococcus type III in an in vitro bactericidal assay and protective in a suckling rat model of group B Streptococcus type III sepsis.1


Author(s):  
Carlos Edmundo Rodrigues FONTES ◽  
Ana Paula de ABREU ◽  
Aretuza Zaupa GASPARIM

ABSTRACT Background: Researches on Chagas disease still use several animals and rats, due to size and susceptibility were preferred by many authors. Aim: To develop an experimental model of megacolon in rats inoculated with the strain Y of Trypanosoma cruzi. Methods: Thirty male Wistar rats were distributed in three groups inoculated with different inoculants: Group A: 600000, Group B: 1000000 and Group C: 1500000 blood trypomastigotes of T. cruzi. Animals were sedated intramuscularly at zero inoculation time (T0) and 60 days after inoculation (T60), to perform the barium enema in order to evaluate the dilatation of the different segments of colon in a comparative study of the measurements obtained, using a digital caliper. Evidence of infection was performed by blood smear collected from the animal’s tail 18 days after inoculation with observation of blood forms. Results: Comparing the intestinal diameter of the inoculated animals with 60,0000 trypomastigotes in the T0 of infection with T60 days after the inoculation, significant dilatation was observed between the proximal, medial and distal segments (p<0.01), indicating the establishment of the megacolon model. In addition, comparing intestinal diameter between the different segments, with in the T0 of infection and the T60 after inoculation, significant alterations were observed (p<0.05). Conclusion: The proposed model was possible for in vivo studies of alterations due to infection by T. cruzi and functional alterations of the colon. In addition, the changes manifested in the colon are not directly proportional to the size of the inoculum, but to the time of infection that the animals were submitted, since the animals inoculated with 60,0000 blood forms were the ones which presented the most significant alterations.


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