O261 Role of the pentapeptidic proteins from Gram-positive bacteria as a possible source of Qnr-like quinolone resistance determinants

2007 ◽  
Vol 29 ◽  
pp. S52-S53
Author(s):  
J. Rodriguez-Martinez ◽  
C. Velasco ◽  
I. Garcia ◽  
M. Conejo ◽  
A. Pascual
Keyword(s):  
Quinolone Resistance ◽  
Gram Positive ◽  
Gram Positive Bacteria ◽  
Resistance Determinants

scholarly journals Role of gram‐positive bacteria in chronic pelvic pain syndrome (CPPS)

The Prostate ◽  
2018 ◽  
Vol 79 (2) ◽  
pp. 160-167 ◽  
Author(s):  
Stephen F. Murphy ◽  
Jonathan F. Anker ◽  
Daniel J. Mazur ◽  
Christel Hall ◽  
Anthony J. Schaeffer ◽  
...  
Keyword(s):  
Pelvic Pain ◽  
Chronic Pelvic Pain ◽  
Chronic Pelvic Pain Syndrome ◽  
Pain Syndrome ◽  
Pelvic Pain Syndrome ◽  
Gram Positive ◽  
Gram Positive Bacteria

scholarly journals Bitter Taste Receptor T2R14 Modulates Gram-Positive Bacterial Internalization and Survival in Gingival Epithelial Cells

2021 ◽  
Vol 22 (18) ◽  
pp. 9920
Author(s):  
Manoj Reddy Medapati ◽  
Anjali Yadav Bhagirath ◽  
Nisha Singh ◽  
Robert J. Schroth ◽  
Rajinder P. Bhullar ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bitter Taste ◽  
Taste Receptor ◽  
Gram Positive ◽  
Direct Role ◽  
Gram Positive Bacteria ◽  
Inhibition Of Growth ◽  
Gingival Epithelial Cells ◽  
Underlying Mechanisms

Bitter-taste receptors (T2Rs) have emerged as key players in host–pathogen interactions and important modulators of oral innate immunity. Previously, we reported that T2R14 is expressed in gingival epithelial cells (GECs) and interacts with competence stimulating peptides (CSPs) secreted by the cariogenic Streptococcus mutans. The underlying mechanisms of the innate immune responses and physiological effects of T2R14 on Gram-positive bacteria are not well characterized. In this study, we examined the role of T2R14 in internalization and growth inhibitory effects on Gram-positive bacteria, namely Staphylococcus aureus and S. mutans. We utilized CRISPR-Cas9 T2R14 knockdown (KD) GECs as the study model to address these key physiological mechanisms. Our data reveal that the internalization of S. aureus is significantly decreased, while the internalization of S. mutans remains unaffected upon knockdown of T2R14 in GECs. Surprisingly, GECs primed with S. mutans CSP-1 resulted in an inhibition of growth for S. aureus, but not for S. mutans. The GECs infected with S. aureus induced T2R14-dependent human β-defensin-2 (hBD-2) secretion; however, S. mutans–infected GECs did not induce hBD-2 secretion, but induced T2R14 dependent IL-8 secretion. Interestingly, our results show that T2R14 KD affects the cytoskeletal reorganization in GECs, thereby inhibiting S. aureus internalization. Our study highlights the distinct mechanisms and a direct role of T2R14 in influencing physiological responses to Gram-positive bacteria in the oral cavity.

scholarly journals The Recombination Genes addAB Are Not Restricted to Gram-Positive Bacteria: Genetic Analysis of the Recombination Initiation Enzymes RecF and AddAB in Rhizobium etli

2004 ◽  
Vol 186 (23) ◽  
pp. 7905-7913 ◽  
Author(s):  
Jacobo Zuñiga-Castillo ◽  
David Romero ◽  
Jaime M. Martínez-Salazar
Keyword(s):  
Recombination Frequency ◽  
Double Strand Breaks ◽  
Additive Effect ◽  
Gram Negative Bacteria ◽  
Rhizobium Etli ◽  
Gram Positive ◽  
Gram Negative ◽  
Strand Breaks ◽  
Gram Positive Bacteria

ABSTRACT Single-strand gaps (SSGs) and double-strand breaks (DSBs) are the major initiation sites for recombination. In bacteria, the SSGs are repaired by RecFOR, while the DSBs are processed by RecBCD in gram-negative bacteria and AddAB in gram-positive bacteria. Unexpectedly, instead of recBCD genes, the addAB genes were found in members of the α-proteobacteria group (gram negative). Taking Rhizobium etli as a model, the role of recF and addAB genes in homologous recombination and repair of damaged DNA was evaluated. Inactivation of either recF or addA provoked strong sensitivity to UV radiation and mitomycin C, while an additive effect was observed in the recF-addA mutant. The DSBs generated by nalidixic acid caused low viability only in the addA mutant. The recombination frequency of large and small plasmids was reduced in the recF mutant (24- and 36-fold, respectively), whereas a slight decrease (threefold) in the addA mutant was observed. Moreover, an additive effect (47- and 90-fold, respectively) was observed in the double mutant, but it was not as dramatic as that in a recA mutant. Interestingly, the frequency of deletion and Campbell-type recombination was slightly affected in either single or double mutants. These results suggest that another pathway exists that allows plasmid and Campbell-type recombination in the absence of recF and addA genes.

scholarly journals Mutations of the Listeria monocytogenes PeptidoglycanN-Deacetylase andO-Acetylase Result in Enhanced Lysozyme Sensitivity, Bacteriolysis, and Hyperinduction of Innate Immune Pathways

2011 ◽  
Vol 79 (9) ◽  
pp. 3596-3606 ◽  
Author(s):  
Chris S. Rae ◽  
Aimee Geissler ◽  
Paul C. Adamson ◽  
Daniel A. Portnoy
Keyword(s):  
Listeria Monocytogenes ◽  
Transcriptional Responses ◽  
Gram Positive ◽  
Content Type ◽  
Growth Defects ◽  
Gram Positive Bacteria ◽  
Host Cell Death

ABSTRACTListeria monocytogenesis a Gram-positive intracellular pathogen that is naturally resistant to lysozyme. Recently, it was shown that peptidoglycan modification by N-deacetylation or O-acetylation confers resistance to lysozyme in various Gram-positive bacteria, includingL. monocytogenes.L. monocytogenespeptidoglycan is deacetylated by the action ofN-acetylglucosamine deacetylase (Pgd) and acetylated byO-acetylmuramic acid transferase (Oat). We characterized Pgd−, Oat−, and double mutants to determine the specific role ofL. monocytogenespeptidoglycan acetylation in conferring lysozyme sensitivity during infection of macrophages and mice. Pgd−and Pgd−Oat−double mutants were attenuated approximately 2 and 3.5 logs, respectively,in vivo. In bone-marrow derived macrophages, the mutants demonstrated intracellular growth defects and increased induction of cytokine transcriptional responses that emanated from a phagosome and the cytosol. Lysozyme-sensitive mutants underwent bacteriolysis in the macrophage cytosol, resulting in AIM2-dependent pyroptosis. Each of thein vitrophenotypes was rescued upon infection of LysM−macrophages. The addition of extracellular lysozyme to LysM−macrophages restored cytokine induction, host cell death, andL. monocytogenesgrowth inhibition. This surprising observation suggests that extracellular lysozyme can access the macrophage cytosol and act on intracellular lysozyme-sensitive bacteria.

scholarly journals Mechanism of persistence of indigenous bifidobacteria under the impact of acetate in the human colon biotope

2021 ◽  
Vol 98 (3) ◽  
pp. 276-282
Author(s):  
O. V. Bukharin ◽  
S. V. Andryuschenko ◽  
N. B. Perunova ◽  
E. V. Ivanova
Keyword(s):  
Acetic Acid ◽  
Ammonium Acetate ◽  
Growth Parameters ◽  
Bifidobacterium Longum ◽  
Human Colon ◽  
Bifidobacterium Bifidum ◽  
Gram Positive ◽  
Gram Positive Bacteria ◽  
The Impact

Aim. To determine the role of the acetate in the persistence of indigenous bifidobacteria in the colon biotope through the lysozyme resistance in model conditions of the acetylation–deacetylation of peptidoglycan.Materials and methods. The study was performed on 16 strains of the two indigenous bifidobacteria speсies: Bifidobacterium bifidum и Bifidobacterium longum subsp. longum. Bifidobacteria was cultivated in the 0.6% O2 and 9% CO2 atmosphere at the temperature 37ºС in CO2 incubator for 48 hours. The production of the acetate by the bifidobacteria was determined by gas chromatography. The effect of the acetate on the lysozyme resistance of non-indigenous gram-positive bacteria was determined on the Listeria monocytogenes ICIS-280 model strain by the cultivation in LB-Lennox broth with ammonium acetate added in the concentration range matching the concentrations produced by the studied bifidobacteria, in lysozyme serial dilutions at final concentrations 5 μg/ml to 40 μg/ml within 24 hours.Results. It was found that the acetate release of Bifidobacterium longum subsp. longum was on average two times higher that of Bifidobacterium bifidum (27.0 and 14.7 mmol/liter, respectively) and was quite consistent with the concentrations of acetic acid determined in the intestinal contents (up to 50 mmol/liter). Cultivation of bifidobacteria in a medium with lysozyme, ammonium acetate and their combination did not have a significant impact on their growth parameters at the maximum used concentrations of these substances. In the test strain, the addition of ammonium acetate in the range created by bifidobacteria caused a decrease in the minimum inhibitory concentration of lysozyme by more than two times — from 40 μg/ml to less than 20 μg/ml. In the control medium without lysozyme, no inhibition of the growth of the indicator culture was observed up to the maximum concentrations of ammonium acetate.Conclusion. The mechanism of persistence (survival) of indigenous bifidobacteria in the human intestinal biotope has been identified, which is associated with the production of acetic acid at a level that selectively suppresses lysozyme resistance of non-indigenous gram-positive microbiota viareversible deacetylation of peptidoglycan. This allows indigenous bifidobacteria to maintain a stable dominant position in the biotope.

Antimicrobial-Resistant Gram-Positive Bacteria in PD Peritonitis and the Newer Antibiotics Used to Treat Them

2005 ◽  
Vol 25 (4) ◽  
pp. 313-319 ◽  
Author(s):  
William Salzer
Keyword(s):  
Methicillin Resistant Staphylococcus Aureus ◽  
Natural Habitat ◽  
Gram Positive ◽  
Gram Positive Bacteria ◽  
The Past ◽  
Vancomycin Resistant Enterococci ◽  
Resistant Strains ◽  
Vancomycin Resistant ◽  
Novel Antibiotics

The incidence of resistant gram-positive bacteria in nosocomial and, more recently, community-acquired infections is increasing. Staphylococci, because of their natural habitat on the skin, have always been the leading cause of peritonitis in patients receiving peritoneal dialysis (PD). These organisms have demonstrated a remarkable ability to develop resistance to antibiotics, first with penicillin, then antistaphylococcal penicillins (methicillin-resistant Staphylococcus aureus), and more recently, strains expressing resistance to vancomycin (vancomycin-intermediate and vancomycin-resistant S. aureus) have emerged. Enterococci are normal inhabitants of the gastrointestinal tract and occasionally cause PD peritonitis. In the past 15 years, vancomycin-resistant enterococci have emerged as significant pathogens in many areas. In the past 5 years, novel antibiotics that have activity on gram-positive bacteria, including vancomycin-resistant strains, have become available. The problem of resistant gram-positive bacteria in PD peritonitis, their therapy, and the role of these newer agents, quinupristin/dalfopristin, linezolid, and daptomycin, are reviewed.

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