Click here to close
Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly.
We suggest using a current version of Chrome,
FireFox, or Safari.
Infect Immun
2008 May 01;765:2169-76. doi: 10.1128/IAI.01705-07.
Show Gene links
Show Anatomy links
Wall teichoic acid deficiency in Staphylococcus aureus confers selective resistance to mammalian group IIA phospholipase A(2) and human beta-defensin 3.
Koprivnjak T
,
Weidenmaier C
,
Peschel A
,
Weiss JP
.
???displayArticle.abstract???
Wall teichoic acids (WTAs) and membrane lipoteichoic acids (LTAs) are the major polyanionic polymers in the envelope of Staphylococcus aureus. WTAs in S. aureus play an important role in bacteriophage attachment and bacterial adherence to certain host cells, suggesting that WTAs are exposed on the cell surface and could also provide necessary binding sites for cationic antimicrobial peptides and proteins (CAMPs). Highly cationic mammalian group IIA phospholipase A(2) (gIIA PLA(2)) kills S. aureus at nanomolar concentrations by an action(s) that depends on initial electrostatic interactions, cell wall penetration, membrane phospholipid (PL) degradation, and activation of autolysins. A tagO mutant of S. aureus that lacks WTA is up to 100-fold more resistant to PL degradation and killing by gIIA PLA(2) and CAMP human beta-defensin 3 (HBD-3) but has the sensitivity of the wild type (wt) to other CAMPs, such as Magainin II amide, hNP1-3, LL-37, and lactoferrin. In contrast, there is little or no difference in either gIIA PLA(2) activity toward cell wall-depleted protoplasts of the wt and tagO strains of S. aureus or in binding of gIIA PLA(2) to wt and tagO strains. Scanning and transmission electron microscopy reveal increased surface protrusions in the S. aureus tagO mutant that might account for reduced activity of bound gIIA PLA(2) and HBD-3 toward the tagO mutant. In summary, the absence of WTA in S. aureus causes a selective increase in bacterial resistance to gIIA PLA(2) and HBD-3, the former apparently by reducing access and/or activity of bound antibacterial enzyme to the bacterial membrane.
BLIGH,
A rapid method of total lipid extraction and purification.
1959, Pubmed
BLIGH,
A rapid method of total lipid extraction and purification.
1959,
Pubmed
Beers,
The antibacterial properties of secreted phospholipases A2: a major physiological role for the group IIA enzyme that depends on the very high pI of the enzyme to allow penetration of the bacterial cell wall.
2002,
Pubmed
Bera,
Influence of wall teichoic acid on lysozyme resistance in Staphylococcus aureus.
2007,
Pubmed
Chatterjee,
Use of bacteriophage-resistant mutants to study the nature of the bacteriophage receptor site of Staphylococcus aureus.
1969,
Pubmed
Chatterjee,
Properties of a novel pleiotropic bacteriophage-resistant mutant of Staphylococcus aureus H.
1969,
Pubmed
Doyle,
Polyelectrolyte nature of bacterial teichoic acids.
1974,
Pubmed
Doyle,
Distribution of teichoic acid in the cell wall of Bacillus subtilis.
1975,
Pubmed
Dubrac,
New insights into the WalK/WalR (YycG/YycF) essential signal transduction pathway reveal a major role in controlling cell wall metabolism and biofilm formation in Staphylococcus aureus.
2007,
Pubmed
Elsbach,
Phagocytosis of bacteria and phospholipid degradation.
1988,
Pubmed
Fischer,
Lipoteichoic acid and lipids in the membrane of Staphylococcus aureus.
1994,
Pubmed
Foreman-Wykert,
Cell-wall determinants of the bactericidal action of group IIA phospholipase A2 against Gram-positive bacteria.
1999,
Pubmed
Foreman-Wykert,
Phospholipid synthesis by Staphylococcus aureus during (Sub)Lethal attack by mammalian 14-kilodalton group IIA phospholipase A2.
2000,
Pubmed
Ganz,
Defensins: antimicrobial peptides of innate immunity.
2003,
Pubmed
Gründling,
Synthesis of glycerol phosphate lipoteichoic acid in Staphylococcus aureus.
2007,
Pubmed
Howell,
Genes controlled by the essential YycG/YycF two-component system of Bacillus subtilis revealed through a novel hybrid regulator approach.
2003,
Pubmed
Inada,
Preferential distribution of group-II-like phospholipase A2 in mononuclear phagocytic cells in rat spleen and liver.
1991,
Pubmed
Iordanescu,
Two restriction and modification systems in Staphylococcus aureus NCTC8325.
1976,
Pubmed
Kobayashi,
Regulation of the neutrophil-mediated inflammatory response to infection.
2003,
Pubmed
Koduri,
Action of human group IIa secreted phospholipase A2 on cell membranes. Vesicle but not heparinoid binding determines rate of fatty acid release by exogenously added enzyme.
1998,
Pubmed
Koduri,
Bactericidal properties of human and murine groups I, II, V, X, and XII secreted phospholipases A(2).
2002,
Pubmed
Kokai-Kun,
Lysostaphin as a treatment for systemic Staphylococcus aureus infection in a mouse model.
2007,
Pubmed
Koprivnjak,
Role of charge properties of bacterial envelope in bactericidal action of human group IIA phospholipase A2 against Staphylococcus aureus.
2002,
Pubmed
Kramer,
Structure and properties of a human non-pancreatic phospholipase A2.
1989,
Pubmed
Kusuma,
Comparison of four methods for determining lysostaphin susceptibility of various strains of Staphylococcus aureus.
2005,
Pubmed
Laine,
Protection by group II phospholipase A2 against Staphylococcus aureus.
1999,
Pubmed
Laine,
Resistance of transgenic mice expressing human group II phospholipase A2 to Escherichia coli infection.
2000,
Pubmed
Lekstrom-Himes,
Immunodeficiency diseases caused by defects in phagocytes.
2000,
Pubmed
Lowy,
Staphylococcus aureus infections.
1998,
Pubmed
Neuhaus,
A continuum of anionic charge: structures and functions of D-alanyl-teichoic acids in gram-positive bacteria.
2003,
Pubmed
Nevalainen,
Synovial-type (group II) phospholipase A2 human seminal plasma.
1993,
Pubmed
Nevalainen,
Secretion of group 2 phospholipase A2 by lacrimal glands.
1994,
Pubmed
Nevalainen,
Roles of secretory phospholipases A(2) in inflammatory diseases and trauma.
2000,
Pubmed
Peacock,
What determines nasal carriage of Staphylococcus aureus?
2001,
Pubmed
Peschel,
Inactivation of the dlt operon in Staphylococcus aureus confers sensitivity to defensins, protegrins, and other antimicrobial peptides.
1999,
Pubmed
Qu,
Secretory phospholipase A2 is the principal bactericide for staphylococci and other gram-positive bacteria in human tears.
1998,
Pubmed
Schaloske,
The phospholipase A2 superfamily and its group numbering system.
2006,
Pubmed
Schibli,
The solution structures of the human beta-defensins lead to a better understanding of the potent bactericidal activity of HBD3 against Staphylococcus aureus.
2002,
Pubmed
Takayama,
Detection of 14-kDa group II phospholipase A2 in human seminal plasma.
1991,
Pubmed
Umeda,
Location of peptidoglycan and teichoic acid on the cell wall surface of Staphylococcus aureus as determined by immunoelectron microscopy.
1992,
Pubmed
Walsh,
Improved pharmacokinetics and reduced antibody reactivity of lysostaphin conjugated to polyethylene glycol.
2003,
Pubmed
Weidenmaier,
Role of teichoic acids in Staphylococcus aureus nasal colonization, a major risk factor in nosocomial infections.
2004,
Pubmed
Weidenmaier,
Lack of wall teichoic acids in Staphylococcus aureus leads to reduced interactions with endothelial cells and to attenuated virulence in a rabbit model of endocarditis.
2005,
Pubmed
Weinrauch,
The potent anti-Staphylococcus aureus activity of a sterile rabbit inflammatory fluid is due to a 14-kD phospholipase A2.
1996,
Pubmed
Weinrauch,
Mobilization of potent plasma bactericidal activity during systemic bacterial challenge. Role of group IIA phospholipase A2.
1998,
Pubmed
Weiss,
Structural determinants of the action against Escherichia coli of a human inflammatory fluid phospholipase A2 in concert with polymorphonuclear leukocytes.
1994,
Pubmed
Zhao,
RL-37, an alpha-helical antimicrobial peptide of the rhesus monkey.
2001,
Pubmed
von Eiff,
Nasal carriage as a source of Staphylococcus aureus bacteremia. Study Group.
2001,
Pubmed
