The physiology of teichoic acid deficient staphylococci

1973 ◽  
Vol 19 (11) ◽  
pp. 1393-1399 ◽  
Author(s):  
Li-Tse Ou ◽  
A. N. Chatterjee ◽  
F. E. Young ◽  
R. E. Marquis

Cell walls isolated from a teichoic acid deficient mutant (52A5) of Staphylococcus aureus strain H were found to have lower capacities to bind cations than did walls of the parent strain. Both types of walls had higher binding affinities for Mg2+ and Ca2+ than for K+ and Na+. The reduced number of phosphate groups in 52A5 walls was reflected in a higher apparent pKa of 4.3 for displacement of Mg2+ (or Ca2+) during acid titration with HCl. The comparable pKa value for displacement of bound Mg2+ from parent-strain walls was 3.7. The reduced capacity of 52A5 walls to bind cations was not reflected in any significant increase in sensitivity to the growth inhibitory actions of ethylenediaminetetraacetate, low pH, or high NaCl concentrations. However, the 52A5 strain was somewhat more sensitive to the inhibitory effects of high pH. Also, mutant walls were found to be structurally more compact than walls of the parent strain, presumably because of less extensive electrostatic repulsion within the wall matrix.

1962 ◽  
Vol 116 (2) ◽  
pp. 229-245 ◽  
Author(s):  
Stephen I. Morse

The cell walls of an 80/81 strain of Staphylococcus aureus (NYH-6) contain alanine, glycine, glutamic acid, lysine, muramic acid, glucosamine, and ribitol phosphate. 94 per cent of the phosphorus and 41 per cent of the glucosamine are removed by extraction of the cell walls with hot 5 per cent TCA, but significant amounts of the other constituents are not extracted by this procedure. The residue after hot TCA extraction (mucopeptide) is susceptible to lysozyme whereas the intact cell walls are resistant. Staphylococcus aureus cell walls are agglutinated by S. aureus antisera. Agglutination of the cell walls of one S. aureus strain is inhibited by absorption of antisera with cell walls of other S. aureus strains but not by absorption with S. albus cell walls. The ribitol teichoic acid can be isolated from cold TCA extracts of the cell walls. This compound consists almost entirely of ribitol phosphate and glucosamine. The isolated teichoic acid of strain NYH-6 is readily fixed to tanned sheep erythrocytes and these sensitized cells are agglutinated by S. aureus antisera. Cold TCA extracts of cell walls of other strains of S. aureus inhibit hemagglutination whereas extracts of S. albus walls do not. Studies on the inhibition of both hemagglutination and precipitation indicate that the antigenic determinant of S. aureus NYH-6 teichoic acid is ß-N-acetylglucosamine.


1963 ◽  
Vol 117 (6) ◽  
pp. 925-935 ◽  
Author(s):  
William G. Juergens ◽  
Arnold R. Sanderson ◽  
Jack L. Strominger

Antisera, prepared against formalin-killed cells of Staphylococcus aureus, strain Copenhagen, agglutinated the cell walls of this strain. The agglutination was inhibited by the teichoic acid from the cell wall of this strain, by any degradation product of this teichoic acid which contained the α-acetylglucosaminyl-ribitol unit, by α-phenyl-acetylglucosaminide, and by N-acetylglucosamine, but not by a large number of other haptens related to the cell wall. In quantitative experiments, however, only 40 to 50 per cent of antibody adsorption to cell wall could be inhibited by teichoic acid or by N-acetylglucosamine. The α-acetylglucosaminyl-ribitol unit in the teichoic acid is, therefore, an important immunological determinant in the cell wall of this strain, although other immunological specificities may also exist. The cell walls were also agglutinated by heterologous antisera prepared against streptococcal Group A carbohydrate or against horse serum azophenyl-ß-acetylglucosaminide. The heterologous agglutination, however, was specific for the ß-acetylglucosaminyl-ribitol units in the teichoic acid.


1999 ◽  
Vol 43 (9) ◽  
pp. 2314-2316 ◽  
Author(s):  
Arnold H. Horwitz ◽  
Robert E. Williams ◽  
Pei-Syan Liu ◽  
Rossana Nadell

ABSTRACT Bactericidal/permeability-increasing protein (BPI) inhibited growth of cell wall-deficient Acholeplasma laidlawii and L forms of certain strains of Staphylococcus aureus andStreptococcus pyogenes. However, the same strains ofS. aureus and S. pyogenes with intact cell walls were not susceptible to the growth-inhibitory effects of BPI.


1998 ◽  
Vol 180 (8) ◽  
pp. 2093-2101 ◽  
Author(s):  
Janet Yother ◽  
Klaus Leopold ◽  
Johanna White ◽  
Werner Fischer

A mutant (JY2190) of Streptococcus pneumoniae Rx1 which had acquired the ability to grow in the absence of choline and analogs was isolated. Lipoteichoic acid (LTA) and wall teichoic acid (TA) isolated from the mutant were free of phosphocholine and other phosphorylated amino alcohols. Both polymers showed an unaltered chain structure and, in the case of LTA, an unchanged glycolipid anchor. The cell wall composition was also not altered except that, due to the lack of phosphocholine, the phosphate content of cell walls was half that of the parent strain. Isolated cell walls of the mutant were resistant to hydrolysis by pneumococcal autolysin (N-acetylmuramyl-l-alanine amidase) but were cleaved by the muramidases CPL and cellosyl. The lack of active autolysin in the mutant cells became apparent by impaired cell separation at the end of cell division and by resistance against stationary-phase and penicillin-induced lysis. As a result of the absence of choline in the LTA, pneumococcal surface protein A (PspA) was no longer retained on the cytoplasmic membrane. During growth in the presence of choline, which was incorporated as phosphocholine into LTA and TA, the mutant cells separated normally, did not release PspA, and became penicillin sensitive. However, even under these conditions, they did not lyse in the stationary phase, and they showed poor reactivity with antibody to phosphocholine and an increased release of C-polysaccharide from the cell. In contrast to ethanolamine-grown parent cells (A. Tomasz, Proc. Natl. Acad. Sci. USA 59:86–93, 1968), the choline-free mutant cells retained the capability to undergo genetic transformation but, compared to Rx1, with lower frequency and at an earlier stage of growth. The properties of the mutant could be transferred to the parent strain by DNA of the mutant.


Pharmaceutics ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 758
Author(s):  
Hirofumi Yamakawa ◽  
Shuichi Setoguchi ◽  
Shotaro Goto ◽  
Daisuke Watase ◽  
Kazuki Terada ◽  
...  

The first-choice drug for acute promyelocytic leukemia (APL), all-trans retinoic acid (ATRA), frequently causes drug-resistance and some adverse effects. Thus, an effective and safe agent for ATRA-resistant APL is needed. Menaquinone-4 (MK-4, vitamin K2(20)), used for osteoporosis treatment, does not have serious adverse effects. It has been reported that MK-4 has growth-inhibitory effects on HL60 cells by inducing apoptosis via the activation of Bcl-2 antagonist killer 1 (BAK). However, the effect of MK-4 on ATRA-resistant APL has not been reported. Here, we show that ester derivatives of menahydroquinone-4 (MKH; a reduced form of MK-4), MKH 1,4-bis-N,N-dimethylglycinate (MKH-DMG) and MKH 1,4-bis-hemi-succinate (MKH-SUC), exerted strong growth-inhibitory effects even on ATRA-resistant HL60 (HL-60R) cells compared with ATRA and MK-4. MKH delivery after MKH-SUC treatment was higher than that after MK-4 treatment, and the results indicated apoptosis induced by BAK activation. In contrast, for MKH-DMG, reconversion to MKH was slow and apoptosis was not observed. We suggest that the ester forms, including monoesters of MKH-DMG, exhibit another mechanism independent of apoptosis. In conclusion, the MKH derivatives (MKH-SUC and MKH-DMG) inhibited not only HL60 cells but also HL-60R cells, indicating a potential to overcome ATRA resistance.


1971 ◽  
Vol 20 (3) ◽  
pp. 442-450 ◽  
Author(s):  
Jean Heijenoort ◽  
Daniele Menjon ◽  
Bernard Flouret ◽  
Jekisiel Szulmajster ◽  
Jean Laporte ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yuting Meng ◽  
Xixi Qian ◽  
Li Zhao ◽  
Nan Li ◽  
Shengjie Wu ◽  
...  

Abstract Background The third-generation epithelial growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have shown significant therapeutic effects on patients with non-small cell lung carcinoma (NSCLC) who carry active EGFR mutations, as well as those who have developed acquired resistance to the first-generation of EGFR-TKIs due to the T790M mutation. However, most patients develop drug resistance after 8–10 months of treatment. Currently, the mechanism has not been well clarified, and new therapeutic strategies are urgently needed. Methods Osimertinib resistant cell lines were established by culturing sensitive cells in chronically increasing doses of osimertinib. The anticancer effect of reagents was examined both in vitro and in vivo using the sulforhodamine B assay and a xenograft mouse model. The molecular signals were detected by western blotting. The combination effect was analyzed using CompuSyn software. Results We found that bromodomain and extra-terminal proteins (BETs) were upregulated in osimertinib resistant (H1975-OR) cells compared with those in the paired parental cells (H1975-P), and that knockdown of BETs significantly inhibited the growth of H1975-OR cells. The BET inhibitor JQ1 also exhibited stronger growth-inhibitory effects on H1975-OR cells and a greater expression of BETs and the downstream effector c-Myc than were observed in H1975-P cells. The histone deacetylase (HDAC) inhibitor trichostatin A (TSA) showed stronger growth suppression in H1975-OR cells than in H1975-P cells, but vorinostat, another HDAC inhibitor, showed equal inhibitory efficacy in both cell types. Consistently, downregulation of BET and c-Myc expression was greater with TSA than with vorinostat. TSA restrained the growth of H1975-OR and H1975-P xenograft tumors. The combination of TSA and JQ1 showed synergistic growth-inhibitory effects in parallel with decreased BET and c-Myc expression in both H1975-OR and H1975-P cells and in xenograft nude mouse models. BETs were not upregulated in osimertinib resistant HCC827 cells compared with parental cells, while TSA and vorinostat exhibited equal inhibitory effects on both cell types. Conclusion Upregulation of BETs contributed to the osimertinib resistance of H1975 cells. TSA downregulated BET expression and enhanced the growth inhibitory effect of JQ1 both in vitro and in vivo. Our findings provided new strategies for the treatment of osimertinib resistance.


2002 ◽  
Vol 726 ◽  
Author(s):  
Yongsoon Shin ◽  
Jun Liu ◽  
Li-Qiong Wang ◽  
Jeong Ho Chang ◽  
William D. Samuels ◽  
...  

AbstractWe here report the synthesis of ordered ceramic materials with hierarchy produced by an in-situ mineralization of ordered wood cellular structures with surfactant-templated sol-gel at different pH. At low pH, a silicic acid is coated onto inner surface of wood cellular structure and it penetrates into pores left, where degraded lignin and hemicellulose are leached out, to form a positive replica, while at high pH the precipitating silica particles due to fast condensation clog the cells and pit structures to form a negative replica of wood. The calcined monoliths produced in different pHs contain ordered wood cellular structures, multi-layered cell walls, pits, vessels well-preserved with positive or negative contrasts, respectively. The surfactant-templated mineralization produces ordered hexagonal nanopores with 20Å in the cell walls after calcination.


Sign in / Sign up

Export Citation Format

Share Document