scholarly journals Contribution of a ZIP‐family protein to manganese uptake and infective endocarditis virulence in Streptococcus sanguinis

2021 ◽  
Author(s):  
Tanya Puccio ◽  
Karina S. Kunka ◽  
Seon‐Sook An ◽  
Todd Kitten
Keyword(s):  
Infective Endocarditis ◽  
Streptococcus Sanguinis ◽  
Manganese Uptake ◽  
Zip Family ◽  
Family Protein

scholarly journals Contribution of metal transporters of the ABC, ZIP, and NRAMP families to manganese uptake and infective endocarditis virulence in Streptococcus sanguinis

2021 ◽  
Author(s):  
Tanya Puccio ◽  
Karina Kunka ◽  
Todd Kitten
Keyword(s):  
Infective Endocarditis ◽  
Iron Transport ◽  
Rabbit Model ◽  
Gene Encoding ◽  
Metal Transporters ◽  
Streptococcus Sanguinis ◽  
Manganese Uptake ◽  
Zip Family ◽  
Family Protein

Streptococcus sanguinis is an important cause of infective endocarditis. In strain SK36, the ABC-family manganese transporter, SsaACB, is essential for virulence. We have now identified a ZIP-family protein, TmpA, as a secondary manganese transporter. A tmpA mutant had no phenotype, but a ΔssaACB ΔtmpA mutant was far more attenuated for serum growth and somewhat more attenuated for virulence in a rabbit model than its ΔssaACB parent. The growth of both mutants was restored by supplemental manganese, but the ΔssaACB ΔtmpA mutant required twenty-fold more and accumulated less. Although ZIP-family proteins are known for zinc and iron transport, TmpA-mediated transport of either metal was minimal. In contrast to ssaACB and tmpA, which appear ubiquitous in S. sanguinis, a mntH gene encoding an NRAMP-family transporter has been identified in relatively few strains, including VMC66. As in SK36, deletion of ssaACB greatly diminished VMC66 endocarditis virulence and serum growth, and deletion of tmpA from this mutant diminished virulence further. Virulence was not significantly altered by deletion of mntH from either VMC66 or its ΔssaACB mutant. This and the accompanying paper together suggest that SsaACB is of primary importance for endocarditis virulence while secondary transporters TmpA and MntH contribute to growth under differing conditions.

scholarly journals Manganese transport by Streptococcus sanguinis in acidic conditions and its impact on growth in vitro and in vivo

2021 ◽  
Author(s):  
Tanya Puccio ◽  
Alexander C Schultz ◽  
Claudia A Lizarraga ◽  
Ashley S Bryant ◽  
David J Culp ◽  
...  
Keyword(s):  
Streptococcus Sanguinis ◽  
Manganese Uptake ◽  
Zip Family ◽  
Oral Environment ◽  
Colonization Model ◽  
Acidic Conditions ◽  
Oral Colonization ◽  
Manganese Transport

Streptococcus sanguinis is an oral commensal and an etiological agent of infective endocarditis. Previous studies have identified the SsaACB manganese transporter as essential for endocarditis virulence; however, the significance of SsaACB in the oral environment has never been examined. Here we report that a ΔssaACB mutant of strain SK36 exhibits reduced growth and manganese uptake under acidic conditions. Further studies revealed that these deficits resulted from the decreased activity of TmpA, shown in the accompanying paper to function as a ZIP-family manganese transporter. Transcriptomic analysis of fermentor-grown cultures of SK36 WT and ΔssaACB strains identified pH-dependent changes related to carbon catabolite repression in both strains, though their magnitude was generally greater in the mutant. In strain VMC66, which possesses a MntH transporter, loss of SsaACB did not significantly alter growth or cellular manganese levels under the same conditions. Interestingly, there were only modest differences between SK36 and its ΔssaACB mutant in competition with Streptococcus mutans in vitro and in a murine oral colonization model. Our results suggest that the heterogeneity of the oral environment may provide a rationale for the variety of manganese transporters found in S. sanguinis and point to strategies for enhancing the safety of oral probiotics.

scholarly journals Postcaesarean open-heart surgery for Streptococcus sanguinis infective endocarditis

2013 ◽  
Vol 2013 (nov14 1) ◽  
pp. bcr2013010103-bcr2013010103 ◽  
Author(s):  
K. Kongwattanakul ◽  
S. Tribuddharat ◽  
S. Prathanee ◽  
O. Pachirat
Keyword(s):  
Infective Endocarditis ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Open Heart ◽  
Streptococcus Sanguinis

scholarly journals Comprehensive Evaluation of Streptococcus sanguinis Cell Wall-Anchored Proteins in Early Infective Endocarditis

2009 ◽  
Vol 77 (11) ◽  
pp. 4966-4975 ◽  
Author(s):  
Lauren Senty Turner ◽  
Taisei Kanamoto ◽  
Takeshi Unoki ◽  
Cindy L. Munro ◽  
Hui Wu ◽  
...  
Keyword(s):  
Cell Wall ◽  
Infective Endocarditis ◽  
Comprehensive Evaluation ◽  
Individual Cell ◽  
Rabbit Model ◽  
Surface Proteins ◽  
Initial Contact ◽  
Streptococcus Sanguinis ◽  
Fold Reduction ◽  
Life Threatening

ABSTRACT Streptococcus sanguinis is a member of the viridans group of streptococci and a leading cause of the life-threatening endovascular disease infective endocarditis. Initial contact with the cardiac infection site is likely mediated by S. sanguinis surface proteins. In an attempt to identify the proteins required for this crucial step in pathogenesis, we searched for surface-exposed, cell wall-anchored proteins encoded by S. sanguinis and then used a targeted signature-tagged mutagenesis (STM) approach to evaluate their contributions to virulence. Thirty-three predicted cell wall-anchored proteins were identified—a number much larger than those found in related species. The requirement of each cell wall-anchored protein for infective endocarditis was assessed in the rabbit model. It was found that no single cell wall-anchored protein was essential for the development of early infective endocarditis. STM screening was also employed for the evaluation of three predicted sortase transpeptidase enzymes, which mediate the cell surface presentation of cell wall-anchored proteins. The sortase A mutant exhibited a modest (∼2-fold) reduction in competitiveness, while the other two sortase mutants were indistinguishable from the parental strain. The combined results suggest that while cell wall-anchored proteins may play a role in S. sanguinis infective endocarditis, strategies designed to interfere with individual cell wall-anchored proteins or sortases would not be effective for disease prevention.

scholarly journals Association of Novel Streptococcus sanguinis Virulence Factors With Pathogenesis in a Native Valve Infective Endocarditis Model

2020 ◽  
Vol 11 ◽  
Author(s):  
Anthony M. Martini ◽  
Bridget S. Moricz ◽  
Allison K. Ripperger ◽  
Phuong M. Tran ◽  
Molly E. Sharp ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Virulence Factors ◽  
Native Valve ◽  
Streptococcus Sanguinis

scholarly journals Modulation of DNA binding properties of CCAAT/enhancer binding protein epsilon by heterodimer formation and interactions with NFkappaB pathway

Blood ◽  
2007 ◽  
Vol 109 (10) ◽  
pp. 4209-4219 ◽  
Author(s):  
Alexey M. Chumakov ◽  
Agnes Silla ◽  
Elizabeth A. Williamson ◽  
H. Phillip Koeffler
Keyword(s):  
Dna Binding ◽  
Myeloid Cell ◽  
Enhancer Binding Protein ◽  
Dna Binding Site ◽  
Zip Family ◽  
Family Protein ◽  
The Family ◽  
Dna Binding Properties

Abstract C/EBP epsilon is a transcription factor involved in myeloid cell differentiation. Along with C/EBP-α, -β, -γ, -δ, and -ζ, C/EBP-ϵ belongs to the family of CCAAT/enhancer binding proteins that are implicated in control of growth and differentiation of several cell lineages in inflammation and stress response. We have previously shown that C/EBP-ϵ preferentially binds DNA as a heterodimer with other C/EBP family members such as C/EBP-δ, CHOP (C/EBP-ζ), and the b-zip family protein ATF4. In this study, we define the consensus binding sites for C/EBP-ϵ dimers and C/EBP-ϵ–ATF4 heterodimers. We show that the activated NFkappaB pathway promotes interaction of the C/EBP-ϵ subunit with its cognate DNA binding site via interaction with RelA. RelA-C/EBP interaction is enhanced by phosphorylation of threonine at amino acid 75 and results in increased DNA binding compared with the wild-type nonphosphorylated C/EBP both in vitro and in vivo. We suggest that interaction of the activated NFkappaB pathway and C/EBP-ϵ may be important in selective activation of a subset of C/EBP-ϵ–responsive genes.

scholarly journals Identification of Streptococcus sanguinis Genes Required for Biofilm Formation and Examination of Their Role in Endocarditis Virulence

2008 ◽  
Vol 76 (6) ◽  
pp. 2551-2559 ◽  
Author(s):  
Xiuchun Ge ◽  
Todd Kitten ◽  
Zhenming Chen ◽  
Sehmi P. Lee ◽  
Cindy L. Munro ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Dental Plaque ◽  
Biofilm Formation ◽  
Bacterial Colonization ◽  
Abundant Species ◽  
Oral Biofilm ◽  
Streptococcus Sanguinis ◽  
Streptococcal Species

ABSTRACT Streptococcus sanguinis is one of the pioneers in the bacterial colonization of teeth and is one of the most abundant species in the oral biofilm called dental plaque. S. sanguinis is also the most common viridans group streptococcal species implicated in infective endocarditis. To investigate the association of biofilm and endocarditis, we established a biofilm assay and examined biofilm formation with a signature-tagged mutagenesis library of S. sanguinis. Four genes that have not previously been associated with biofilm formation in any other bacterium, purB, purL, thrB, and pyrE, were putatively identified as contributing to in vitro biofilm formation in S. sanguinis. By examining 800 mutants for attenuation in the rabbit endocarditis model and for reduction in biofilm formation in vitro, we found some mutants that were both biofilm defective and attenuated for endocarditis. However, we also identified mutants with only reduced biofilm formation or with only attenuation in the endocarditis model. This result indicates that the ability to form biofilms in vitro is not associated with endocarditis virulence in vivo in S. sanguinis.

scholarly journals Similar genomic patterns of clinical infective endocarditis and oral isolates of Streptococcus sanguinis and Streptococcus gordonii

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Katrine Højholt Iversen ◽  
Louise Hesselbjerg Rasmussen ◽  
Kosai Al-Nakeeb ◽  
Jose Juan Almagro Armenteros ◽  
Christian Salgård Jensen ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Streptococcus Gordonii ◽  
Streptococcus Sanguinis ◽  
Genomic Patterns

scholarly journals Radial Mycotic Aneurysm Complicated with Infective Endocarditis Caused by Streptococcus sanguinis

2013 ◽  
Vol 52 (20) ◽  
pp. 2361-2365 ◽  
Author(s):  
Masako Kadowaki ◽  
Mika Hashimoto ◽  
Mai Nakashima ◽  
Mitsuhiro Fukata ◽  
Keita Odashiro ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Mycotic Aneurysm ◽  
Streptococcus Sanguinis

scholarly journals Identification of Virulence Determinants for Endocarditis in Streptococcus sanguinis by Signature-Tagged Mutagenesis

2005 ◽  
Vol 73 (9) ◽  
pp. 6064-6074 ◽  
Author(s):  
Sehmi Paik ◽  
Lauren Senty ◽  
Sankar Das ◽  
Jody C. Noe ◽  
Cindy L. Munro ◽  
...  
Keyword(s):  
Infective Endocarditis ◽  
Virulence Factors ◽  
Ribonucleotide Reductase ◽  
Large Scale ◽  
Broth Culture ◽  
Strictly Anaerobic ◽  
Anaerobic Conditions ◽  
Streptococcus Sanguinis ◽  
Competitive Index ◽  
Homoserine Kinase

ABSTRACT Streptococcus sanguinis is a gram-positive, facultative anaerobe and a normal inhabitant of the human oral cavity. It is also one of the most common agents of infective endocarditis, a serious endovascular infection. To identify virulence factors for infective endocarditis, signature-tagged mutagenesis (STM) was applied to the SK36 strain of S. sanguinis, whose genome is being sequenced. STM allows the large-scale creation, in vivo screening, and recovery of a series of mutants with altered virulence. Screening of 800 mutants by STM identified 38 putative avirulent and 5 putative hypervirulent mutants. Subsequent molecular analysis of a subset of these mutants identified genes encoding undecaprenol kinase, homoserine kinase, anaerobic ribonucleotide reductase, adenylosuccinate lyase, and a hypothetical protein. Virulence reductions ranging from 2-to 150-fold were confirmed by competitive index assays. One putatively hypervirulent strain with a transposon insertion in an intergenic region was identified, though increased virulence was not confirmed in competitive index assays. All mutants grew comparably to SK36 in aerobic broth culture except for the homoserine kinase mutant. Growth of this mutant was restored by the addition of threonine to the medium. Mutants containing an insertion or in-frame deletion in the anaerobic ribonucleotide reductase gene failed to grow under strictly anaerobic conditions. The results suggest that housekeeping functions such as cell wall synthesis, amino acid and nucleic acid synthesis, and the ability to survive under anaerobic conditions are important virulence factors in S. sanguinis endocarditis.

Sign in / Sign up

Export Citation Format

Share Document