scholarly journals Analysis of genes encoding two unique type IIa immunoglobulin G-binding proteins expressed by a single group A streptococcal isolate.

1994 ◽  
Vol 62 (4) ◽  
pp. 1336-1347 ◽  
Author(s):  
M D Boyle ◽  
J Hawlitzky ◽  
R Raeder ◽  
A Podbielski
ImmunoMethods ◽  
1993 ◽  
Vol 2 (1) ◽  
pp. 55-64 ◽  
Author(s):  
A. Podbielski ◽  
A. Kaufhold ◽  
P.P. Cleary

2000 ◽  
Vol 38 (1) ◽  
pp. 389-392
Author(s):  
Alison M. Goodfellow ◽  
Megan Hibble ◽  
Susanne R. Talay ◽  
Bernd Kreikemeyer ◽  
Bart J. Currie ◽  
...  

ABSTRACT Fibronectin binding proteins play an important role in the adherence and invasion of group A streptococci (GAS). Genotypically distinct GAS isolates were screened for the presence and expression of two streptococcal fibronectin binding protein genes, sfbI and sfbII . Of the tested strains, 64 and 36% were shown to harbor and express the sfbI and sfbII genes, respectively. All sfbII -positive strains tested were also positive for sfbI , but only 28% of the sfbII -negative strains were positive for sfbI . High levels of immunoglobulin G antibodies to both SfbI and SfbII were found in sera from 80 subjects with defined streptococcal infections.


2021 ◽  
Vol 22 (13) ◽  
pp. 6748
Author(s):  
Heling Wang ◽  
Sofie Lautrup ◽  
Domenica Caponio ◽  
Jianying Zhang ◽  
Evandro F. Fang

DNA repair ensures genomic stability to achieve healthy ageing, including cognitive maintenance. Mutations on genes encoding key DNA repair proteins can lead to diseases with accelerated ageing phenotypes. Some of these diseases are xeroderma pigmentosum group A (XPA, caused by mutation of XPA), Cockayne syndrome group A and group B (CSA, CSB, and are caused by mutations of CSA and CSB, respectively), ataxia-telangiectasia (A-T, caused by mutation of ATM), and Werner syndrome (WS, with most cases caused by mutations in WRN). Except for WS, a common trait of the aforementioned progerias is neurodegeneration. Evidence from studies using animal models and patient tissues suggests that the associated DNA repair deficiencies lead to depletion of cellular nicotinamide adenine dinucleotide (NAD+), resulting in impaired mitophagy, accumulation of damaged mitochondria, metabolic derailment, energy deprivation, and finally leading to neuronal dysfunction and loss. Intriguingly, these features are also observed in Alzheimer’s disease (AD), the most common type of dementia affecting more than 50 million individuals worldwide. Further studies on the mechanisms of the DNA repair deficient premature ageing diseases will help to unveil the mystery of ageing and may provide novel therapeutic strategies for AD.


2007 ◽  
Vol 75 (6) ◽  
pp. 2981-2990 ◽  
Author(s):  
Samuel A. Shelburne ◽  
Nnaja Okorafor ◽  
Izabela Sitkiewicz ◽  
Paul Sumby ◽  
David Keith ◽  
...  

ABSTRACT Group A Streptococcus (GAS) genes that encode proteins putatively involved in polysaccharide utilization show growth phase-dependent expression in human saliva. We sought to determine whether the putative polysaccharide transcriptional regulator MalR influences the expression of such genes and whether MalR helps GAS infect the oropharynx. Analysis of 32 strains of 17 distinct M protein serotypes revealed that MalR is highly conserved across GAS strains. malR transcripts were detectable in patients with GAS pharyngitis, and the levels increased significantly during growth in human saliva compared to the levels during growth in glucose-containing or nutrient-rich media. To determine if MalR influenced the expression of polysaccharide utilization genes, we compared the transcript levels of eight genes encoding putative polysaccharide utilization proteins in the parental serotype M1 strain MGAS5005 and its ΔmalR isogenic mutant derivative. The transcript levels of all eight genes were significantly increased in the ΔmalR strain compared to the parental strain, especially during growth in human saliva. Following experimental infection, the ΔmalR strain persistently colonized the oropharynx in significantly fewer mice than the parental strain colonized, and the numbers of ΔmalR strain CFU recovered were significantly lower than the numbers of the parental strain CFU recovered. These data led us to conclude that MalR influences the expression of genes putatively involved in polysaccharide utilization and that MalR contributes to the persistence of GAS in the oropharynx.


ImmunoMethods ◽  
1993 ◽  
Vol 2 (1) ◽  
pp. 41-53 ◽  
Author(s):  
Michael D.P. Boyle ◽  
Roberta Raeder

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Pontus Hedberg ◽  
Madle Sirel ◽  
Kirsten Moll ◽  
Mpungu Steven Kiwuwa ◽  
Petter Höglund ◽  
...  

Abstract Background The histo-blood group ABO system has been associated with adverse outcomes in COVID-19, thromboembolic diseases and Plasmodium falciparum malaria. An integral part of the severe malaria pathogenesis is rosetting, the adherence of parasite infected red blood cells (RBCs) to uninfected RBCs. Rosetting is influenced by the host’s ABO blood group (Bg) and rosettes formed in BgA have previously been shown to be more resilient to disruption by heparin and shield the parasite derived surface antigens from antibodies. However, data on rosetting in weak BgA subgroups is scarce and based on investigations of relatively few donors. Methods An improved high-throughput flow cytometric assay was employed to investigate rosetting characteristics in an extensive panel of RBC donor samples of all four major ABO Bgs, as well as low BgA expressing samples. Results All non-O Bgs shield the parasite surface antigens from strain-specific antibodies towards P. falciparum erythrocyte membrane protein 1 (PfEMP1). A positive correlation between A-antigen levels on RBCs and rosette tightness was observed, protecting the rosettes from heparin- and antibody-mediated disruption. Conclusions These results provide new insights into how the ABO Bg system affects the disease outcome and cautions against interpreting the results from the heterogeneous BgA phenotype as a single group in epidemiological and experimental studies. Graphical Abstract


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