scholarly journals An accessory wall teichoic acid glycosyltransferase protects Staphylococcus aureus from the lytic activity of Podoviridae

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Xuehua Li ◽  
David Gerlach ◽  
Xin Du ◽  
Jesper Larsen ◽  
Marc Stegger ◽  
...  
2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Noëlle Mistretta ◽  
Marina Brossaud ◽  
Fabienne Telles ◽  
Violette Sanchez ◽  
Philippe Talaga ◽  
...  

2015 ◽  
Vol 83 (11) ◽  
pp. 4247-4255 ◽  
Author(s):  
Jong-Ho Lee ◽  
Na-Hyang Kim ◽  
Volker Winstel ◽  
Kenji Kurokawa ◽  
Jesper Larsen ◽  
...  

ABSTRACTThe cell envelopes of many Gram-positive bacteria contain wall teichoic acids (WTAs).Staphylococcus aureusWTAs are composed of ribitol phosphate (RboP) or glycerol phosphate (GroP) backbones substituted withd-alanine andN-acetyl-d-glucosamine (GlcNAc) orN-acetyl-d-galactosamine (GalNAc). Two WTA glycosyltransferases, TarM and TarS, are responsible for modifying the RboP WTA with α-GlcNAc and β-GlcNAc, respectively. We recently reported that purified human serum anti-WTA IgG specifically recognizes β-GlcNAc of the staphylococcal RboP WTA and then facilitates complement C3 deposition and opsonophagocytosis ofS. aureuslaboratory strains. This prompted us to examine whether anti-WTA IgG can induce C3 deposition on a diverse set of clinicalS. aureusisolates. To this end, we compared anti-WTA IgG-mediated C3 deposition and opsonophagocytosis abilities using 13 different staphylococcal strains. Of note, the majority ofS. aureusstrains tested was recognized by anti-WTA IgG, resulting in C3 deposition and opsonophagocytosis. A minority of strains was not recognized by anti-WTA IgG, which correlated with either extensive capsule production or an alteration in the WTA glycosylation pattern. Our results demonstrate that the presence of WTAs with TarS-mediated glycosylation with β-GlcNAc in clinically isolatedS. aureusstrains is an important factor for induction of anti-WTA IgG-mediated C3 deposition and opsonophagocytosis.


2012 ◽  
Vol 67 (9) ◽  
pp. 2143-2151 ◽  
Author(s):  
T. Suzuki ◽  
J. Campbell ◽  
Y. Kim ◽  
J. G. Swoboda ◽  
E. Mylonakis ◽  
...  

2006 ◽  
Vol 75 (3) ◽  
pp. 1079-1088 ◽  
Author(s):  
Patrick H. Tu Quoc ◽  
Pierre Genevaux ◽  
Maria Pajunen ◽  
Harri Savilahti ◽  
Costa Georgopoulos ◽  
...  

ABSTRACT Staphylococcus aureus produces biofilm and this mode of colonization facilitates infections that are often difficult to treat and engender high morbidity and mortality. We have exploited bacteriophage Mu transposition methods to create an insertional mutant library in a highly biofilm-forming S. aureus clinical isolate. Our screen identified 38 insertions in 23 distinct genes together with one intergenic region that significantly reduced biofilm formation. Nineteen insertions were mapped in loci not previously known to affect biofilm in this organism. These include insertions in codY, srrA, mgrA, and fmtA, a putative DEAD-box helicase, two members of the zinc-metallo-β lactamase/β-CASP family, and a hypothetical protein with a GGDEF motif. Fifteen insertions occurred in the icaADBC operon, which produces intercellular adhesion antigen (PIA) and is important for biofilm formation in many strains of S. aureus and Staphylococcus epidermidis. Obtaining a high proportion of independent Em-Mu disruptions in icaADBC demonstrated both the importance of PIA for biofilm formation in this clinical strain and the strong validation of the screening procedure that concomitantly uncovered additional mutants. All non-ica mutants were further analyzed by immunoblotting and biochemical fractionation for perturbation of PIA and wall teichoic acid. PIA levels were diminished in the majority of non-ica insertional mutants. Three mutant strains were chosen and were functionally complemented for restored biofilm formation by transformation with plasmids carrying the cloned wild-type gene under the control of a xylose-inducible promoter. This is a comprehensive collection of biofilm-defective mutants that underscores the multifactorial genetic program underlying the establishment of biofilm in this insidious pathogen.


mBio ◽  
2015 ◽  
Vol 6 (4) ◽  
Author(s):  
Volker Winstel ◽  
Petra Kühner ◽  
Ferdinand Salomon ◽  
Jesper Larsen ◽  
Robert Skov ◽  
...  

ABSTRACT Nasal colonization by the human pathogen Staphylococcus aureus is a major risk factor for hospital- and community-acquired infections. A key factor required for nasal colonization is a cell surface-exposed zwitterionic glycopolymer, termed wall teichoic acid (WTA). However, the precise mechanisms that govern WTA-mediated nasal colonization have remained elusive. Here, we report that WTA GlcNAcylation is a pivotal requirement for WTA-dependent attachment of community-acquired methicillin-resistant S. aureus (MRSA) and emerging livestock-associated MRSA to human nasal epithelial cells, even under conditions simulating the nutrient composition and dynamic flow of nasal secretions. Depending on the S. aureus strain, WTA O-GlcNAcylation occurs in either α or β configuration, which have similar capacities to mediate attachment to human nasal epithelial cells, suggesting that many S. aureus strains maintain redundant pathways to ensure appropriate WTA glycosylation. Strikingly, a lack of WTA glycosylation significantly abrogated the ability of MRSA to colonize cotton rat nares in vivo. These results indicate that WTA glycosylation modulates S. aureus nasal colonization and may help to develop new strategies for eradicating S. aureus nasal colonization in the future. IMPORTANCE Nasal colonization by the major human pathogen Staphylococcus aureus is a risk factor for severe endogenous infections and contributes to the spread of this microbe in hospitals and the community. Here, we show that wall teichoic acid (WTA) O-GlcNAcylation is a key factor required for S. aureus nasal colonization. These data provide a mechanistic explanation for the capacity of WTA to modulate S. aureus nasal colonization and may stimulate research activities to establish valuable strategies to eradicate S. aureus nasal colonization in high-risk hospitalized patients and in the general community.


2009 ◽  
Vol 191 (13) ◽  
pp. 4482-4484 ◽  
Author(s):  
Thomas Kohler ◽  
Christopher Weidenmaier ◽  
Andreas Peschel

ABSTRACT Skin-colonizing gram-positive bacteria produce wall teichoic acids (WTAs) or related glycopolymers for unclear reasons. Using a WTA-deficient Staphylococcus aureus mutant, we demonstrated that WTA confers resistance to antimicrobial fatty acids from human sebaceous glands by preventing fatty acid binding. Thus, WTA is probably important for bacterial skin colonization.


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