Teichoic Acid of a Stabilized L-Form of<i>Streptococcus pyogenes</i>

Slabyj, Bohdan M.; Panos, Charles

doi:10.1128/jb.114.3.934-942.1973

Cited by 41 publications

(49 citation statements)

References 35 publications

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“…However, when the peptidoglycan is lost through the action of lysozyme or under the treatment with penicillin and other cell wall inhibitors, LTA is exposed in its full length on the surface of the protoplast or L-form variant. Moreover, L forms of group A streptococci have been found to be no longer able to incorporate alanine into LTA (6), so that the LTA of the L form is lacking alanine ester in contrast to the LTA of bacterial-phase cells (29,34). It is of interest in this context that L variants of S. aureus and S. faecalis have been reported to activate complement via the alternative pathway, which resulted in death of these cells (31).…”

Section: Discussionmentioning

confidence: 99%

Interaction of purified lipoteichoic acid with the classical complement pathway

Loos¹,

Clas²,

Fischer³

1986

Infect Immun

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Glycerophosphate-containing lipoteichoic acids (LTAs) interact with the first component of the classical complement pathway (C1). This resulted in the activation of the classical complement pathway in serum, shown by the consumption of Cl, C2, and C4. The dose-dependent interaction of LTAs with purified Cl and Clq was dependent on the negative charges of the phosphate groups of LTA. It was reduced by charge compensation through D-alanine ester substituents and by sterical hindrance through di-and trihexosyl residues linked to position 2 of the glycerol moieties. The charge density of LTA may also play a role: poly(digalactosylglycerophosphate) LTAs, in which the phosphate groups are in a greater distance from each other, were less effective, and the loss of micellar organization by deacylation of LTA drastically reduced the complement activation capacity. 595 on July 31, 2020 by guest http://iai.asm.org/ Downloaded from

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Section: Discussionmentioning

confidence: 99%

Interaction of purified lipoteichoic acid with the classical complement pathway

Loos¹,

Clas²,

Fischer³

1986

Infect Immun

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“…Although it was shown that addition of salt to peptidoglycan synthetase reaction mixtures inhibited the streptococcal enzyme severely at concentrations of salt similar to that employed in the b-form growth medium, it does not follow that this difference between the two growth media is directly responsible for the inability of the L-form to synthesize peptidoglycan because the parent streptococcus synthesizes a cell wall when grown in L-form medium (24). Also, this L-form is still unable to synthesize a rigid cell wall when adapted to grow in physiologically isotonic media (C. Panos and 0.…”

Section: Temperature (C)mentioning

confidence: 99%

Defective synthesis of lipid intermediates for peptidoglycan formation in a stabilized L-form of Streptococcus pyogenes

Reusch¹,

Panos²

1976

J Bacteriol

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Membrane preparations obtained from a stabilized L-form of Streptococcus pyogenes are incapable of synthesizing peptidoglycan from uridine-5'-diphospho-N-acetyl-muramyl-LAla-i-iso-Glu-L-bys-D-Ala-D-Ala and uridine-5'-diphospho-N-acetyl-D-glucosamine, in contrast with similar preparations from the parental streptococcus. Furthermore, 50-fold higher levels of lipid intermediates which serve as membrane-bound substrates for peptidoglycan synthesis are synthesized in reaction mixtures containing streptococcal membranes than with similar preparations from the L-form. These observations suggest that the inability of this stabilized L-form to form a cell wall in vivo lies, at least in part, in its failure to synthesize significant quantities of the lipid substrates for peptidoglycan synthesis.The pathway by which peptidoglycan is synthesized from uridine-5'-diphospho-N-acetyl-Dmuramyl-L-Ala-D-iso -Glu-L-Lys-D-Ala-D-Ala (UMPPMp) and uridine-5'-diphospho-N-acetyl-D-glucosamine (UDP-GlcNAc) is established. These reactions are catalyzed by membranebound enzymes. In the first step (Fig. 1), phospho-N-acetyl-muramyl-peptapeptide, from UMPPMp, is transferred reversibly from uridine-5'-monophosphate (UMP) to endogenous undecaprenol phosphate (C55OP) by phospho-N-acetyl-i>muramyl-pentapeptide translocase (12). In the second step, incorporation ofN-acetyli-glucosamine from UDP-GlcNAc into undecaprenyl pyrophosphoryl-N-acetyl-D-muramyl-L-300 on August 1, 2020 by guest

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“…Therefore, L-form cytotoxicity appears to be equally as effective for cultured mouse glomeruli and human cell monolayers. Bar, 1 1>m. an earlier study that had documented the lack of any apparent difference in the destructive ability of the LTA isolated from either the L-form or its parental S. pyogenes for human kidney monolayers in tissue culture despite differences in the length and composition of this amphiphile from these two organisms (13,14). Finally, and as opposed to an earlier study with cultured human cell monolayers (1), glomerular destruction did not increase when the concentration of LTA was increased.…”

Section: Discussionmentioning

confidence: 61%

Morphological changes and pathology of mouse glomeruli infected with a streptococcal L-form or exposed to lipoteichoic acid

Tomlinson¹,

Leon²,

Panos³

1983

Infect Immun

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The morphology and pathology of cultured mouse glomeruli were examined at the cellular and subcellular levels after infection with a physiological isotonic Lform of Streptococcus pyogenes type 12 or exposure to streptococcal lipoteichoic acid. These changes, as viewed by light microscopy, were identical regardless of the method used to induce glomerular cytotoxicity. They were characterized by an initial reduction in the outgrowth of cells, some cellular granulation, and later, destruction of the confluent monolayer. Once initiated, cytotoxicity could not be reversed by refeedings, and complete glomerular destruction resulted after 2 weeks. Electron microscope studies revealed that the basement membrane of intact glomeruli exposed to streptococcal lipoteichoic acid had become greatly thickened (twoto fourfold) and electron dense. Our recent biochemical findings have shown that streptococcal lipoteichoic acid increases the amount of collagen formed and retained by mouse fibroblasts in tissue culture as well as causing a reduction in the hydroxylation of proline in both intracellular and secreted collagenous material (Leon and Panos, Infect. Immun. 40:785-794, 1983). These results, together with the present findings, suggest that the thickening of the glomerular basement membrane may be due to defective collagen biosynthesis as a result of streptococcal lipoteichoic acid. The use of cultured glomeruli as a model system for studying the earliest basement membrane alterations in the absence of an immune response as a result of streptococcal lipoteichoic acid is suggested.

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Teichoic Acid of a Stabilized L-Form ofStreptococcus pyogenes

Cited by 41 publications

References 35 publications

Interaction of purified lipoteichoic acid with the classical complement pathway

Interaction of purified lipoteichoic acid with the classical complement pathway

Defective synthesis of lipid intermediates for peptidoglycan formation in a stabilized L-form of Streptococcus pyogenes

Morphological changes and pathology of mouse glomeruli infected with a streptococcal L-form or exposed to lipoteichoic acid

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