scholarly journals Competitive adherence as a mechanism of bacterial interference

1983 ◽  
Vol 29 (6) ◽  
pp. 700-703 ◽  
Author(s):  
Debra Jan Bibel ◽  
Raza Aly ◽  
Charlene Bayles ◽  
Walter G. Strauss ◽  
Henry R. Shinefield ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Host Cell ◽  
Virulent Strain ◽  
Host Cells ◽  
Aureus Strain ◽  
Attachment Sites ◽  
Specific Attachment ◽  
Mucosal Cells ◽  
Bacterial Interference

To determine whether competition among bacteria for specific attachment sites on host cells can explain bacterial interference, Staphylococcus aureus strain 502A was tested in turn against two different nasal coryneforms, a strain of Pseudomonas aeruginosa, and a virulent strain of S. aureus, all in the presence of nasal mucosal cells. Particularly examined was the influence of sequence in which bacteria were presented to the nasal cells in comparison with initial mixtures and individual suspensions. Results paralleled those observed in clinical prophylaxis: the bacterium first to adhere to the epithelial cells was able, under uniform conditions, to interfere with the colonization of subsequently added bacteria. Secondary adherence was not eliminated but substantially reduced, and was probably related to steric blockage by the initial colonizer and its particular ability to dissociate from the host cell.

scholarly journals Intracellular Staphylococcus aureus employs the cysteine protease staphopain A to induce host cell death in epithelial cells

2020 ◽  
Author(s):  
Kathrin Stelzner ◽  
Tobias Hertlein ◽  
Aneta Sroka ◽  
Adriana Moldovan ◽  
Kerstin Paprotka ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Epithelial Cells ◽  
Host Cell ◽  
Cysteine Protease ◽  
Host Cells ◽  
Upper Respiratory Tract ◽  
Intracellular Replication ◽  
Tissue Destruction ◽  
Host Cell Death

AbstractStaphylococcus aureus is a major human pathogen, which can invade and survive in non-professional and professional phagocytes. Intracellularity is thought to contribute to pathogenicity and persistence of the bacterium. Upon internalization by epithelial cells, cytotoxic S. aureus strains can escape from the phagosome, replicate in the cytosol and induce host cell death. Here, we identified a staphylococcal cysteine protease to induce cell death by intracellular S. aureus after translocation into the host cell cytoplasm. We demonstrated that loss of staphopain A function leads to delayed onset of host cell death and prolonged intracellular replication of S. aureus in epithelial cells. Overexpression of staphopain A in a non-cytotoxic strain facilitated intracellular killing of the host cell even in the absence of detectable intracellular replication. Moreover, staphopain A contributed to efficient colonization of the lung in a mouse pneumonia model. Our study suggests that staphopain A is utilized by S. aureus to mediate escape from the host cell and thus contributes to tissue destruction and dissemination of infection.Author SummaryStaphylococcus aureus is a well-known antibiotic-resistant pathogen that emerges in hospital and community settings and can cause a variety of diseases ranging from skin abscesses to lung inflammation and blood poisoning. The bacterium asymptomatically colonizes the upper respiratory tract and skin of about one third of the human population and takes advantage of opportune conditions, like immunodeficiency or breached barriers, to cause infection. Although S. aureus is not regarded as a professional intracellular bacterium, it can be internalized by human cells and subsequently exit the host cells by induction of cell death, which is considered to cause tissue destruction and spread of infection. The bacterial virulence factors and underlying molecular mechanisms involved in the intracellular lifestyle of S. aureus remain largely unknown. We identified a bacterial cysteine protease to contribute to host cell death mediated by intracellular S. aureus. Staphopain A induced killing of the host cell after translocation of the pathogen into the cell cytosol, while bacterial proliferation was not required. Further, the protease enhanced survival of the pathogen during lung infection. These findings reveal a novel, intracellular role for the bacterial protease staphopain A.

scholarly journals The Impact of Apple Variety and the Production Methods on the Antibacterial Activity of Vinegar Samples

Molecules ◽  
2021 ◽  
Vol 26 (18) ◽  
pp. 5437
Author(s):  
Mohammed Kara ◽  
Amine Assouguem ◽  
Omkulthom Mohamed Al kamaly ◽  
Safaâ Benmessaoud ◽  
Hamada Imtara ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Antibacterial Activity ◽  
Aureus Strain ◽  
Klebsiella Pneumonia ◽  
Apple Variety ◽  
Production Methods ◽  
Golden Delicious

Apple vinegar is a natural product widely used in food and traditional medicine as it contains many bioactive compounds. The apple variety and production methods are two factors that play a major role in determining the quality of vinegar. Therefore, this study aims to determine the quality of apple vinegar samples from different varieties (Red Delicious, Gala, Golden Delicious, and Starking Delicious) prepared by three methods using small apple pieces, apple juice, and crushed apple, through determining the physicochemical properties and antibacterial activity of these samples. The antibacterial activity was studied against five pathogenic bacteria: Staphylococcus aureus, Klebsiella pneumonia, Escherichia coli (ATB: 57), Escherichia coli (ATB: 97), and Pseudomonas aeruginosa, using two methods, disk diffusion and microdilution, for determining the minimum inhibitory concentrations and the minimum bactericidal concentrations. The results of this study showed that the lowest pH value was 3.6 for Stark Delicious, obtained by liquid fermentation, and the highest acetic acid values were 4.7 and 4% for the vinegar of Red Delicious and Golden Delicious, prepared by solid fermentation, respectively. The results of the antibacterial activity showed considerable activity of apple vinegar on the tested strains. Generally, the Staphylococcus aureus strain appears less sensitive and Pseudomonas aeruginosa seems to be very sensitive against all samples, while the other strains have distinct sensitivities depending on the variety studied and the method used. A higher antibacterial activity was found in vinegar obtained by the apple pieces method and the Red Delicious variety, with a low MIC and MBC recorded, at 1.95 and 3.90 µL/mL, respectively. This study has shown that the choice of both apple variety and production method is therefore an essential step in determining and aiming for the desired quality of apple vinegar.

scholarly journals Truncation of Fibronectin-Binding Proteins in Staphylococcus aureus Strain Newman Leads to Deficient Adherence and Host Cell Invasion Due to Loss of the Cell Wall Anchor Function

2004 ◽  
Vol 72 (12) ◽  
pp. 7155-7163 ◽  
Author(s):  
Matthias Grundmeier ◽  
Muzaffar Hussain ◽  
Petra Becker ◽  
Christine Heilmann ◽  
Georg Peters ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Host Cell ◽  
Cell Invasion ◽  
Binding Proteins ◽  
Stop Codon ◽  
Aureus Strain ◽  
Host Cell Invasion ◽  
Fibronectin Receptor ◽  
Fibronectin Binding

ABSTRACT Staphylococcus aureus fibronectin-binding proteins (FnBPs) play a critical role in S. aureus pathogenesis. FnBPs mediate adhesion to fibronectin and invasion of mammalian cells, including epithelial, endothelial, and fibroblastic cells, by fibronectin bridging to the host cell fibronectin receptor integrin (α5)β1. Strain Newman is a laboratory strain frequently used for genetic, functional, and in vivo studies. However, despite pronounced production of FnBPs, strain Newman is only weakly adherent to immobilized Fn and weakly invasive. We examined whether these effects are due to a structural difference of FnBPs. Here, we show that both fnbA Newman and fnbB Newman contain a centrally located point mutation resulting in a stop codon. This leads to a truncation of both FnBPs at the end of the C domain at identical positions. Most likely, the stop codon occurred first in fnbB Newman and was subsequently transferred to fnbA Newman by replacement of the entire region encompassing the C, D, and W domains with the respective sequence of fnbB Newman. Using heterologous expression in Staphylococcus carnosus, we found that truncated FnBPs were completely secreted into the culture medium and not anchored to the cell wall, since they lack the sortase motif (LPETG). Consequently, this led to a loss of FnBP-dependent functions, such as strong adhesion to immobilized fibronectin, binding of fibrinogen, and host cell invasion. This mutation may explain some of the earlier reported conflicting data with strain Newman. Thus, care should be taken when drawing negative conclusions about the role of FnBPs as a virulence factor in a given model.

scholarly journals Transcriptional Induction of the Pseudomonas aeruginosa Type III Secretion System by Low Ca2+ and Host Cell Contact Proceeds through Two Distinct Signaling Pathways

2006 ◽  
Vol 74 (6) ◽  
pp. 3334-3341 ◽  
Author(s):  
Nandini Dasgupta ◽  
Alix Ashare ◽  
Gary W. Hunninghake ◽  
Timothy L. Yahr
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Host Cell ◽  
Type Iii Secretion ◽  
Mammalian Cells ◽  
Type Iii Secretion System ◽  
Growth Conditions ◽  
Secretion System ◽  
Host Cells ◽  
Dependent Manner ◽  
Type Iii

ABSTRACT The opportunistic pathogen Pseudomonas aeruginosa utilizes a type III secretion system (T3SS) to intoxicate eukaryotic host cells. Transcription of the T3SS is induced under calcium-limited growth conditions or following intimate contact of P. aeruginosa with host cells. In the present study, we demonstrate that expression of the T3SS is controlled by two distinct regulatory mechanisms and that these mechanisms are differentially activated in a host cell-dependent manner. The first mechanism is dependent upon ExsC, a regulatory protein that couples transcription of the T3SS to the activity of the type III secretion machinery. ExsC is essential for induction of the T3SS under low-calcium-growth conditions and for T3SS-dependent cytotoxicity towards social amoebae, insect cells, and erythrocytes. The second regulatory mechanism functions independently of ExsC and is sufficient to elicit T3SS-dependent cytotoxicity towards certain types of mammalian cells. Although this second pathway (ExsC independent) is sufficient, an exsC mutant demonstrates a lag in the induction of cytotoxicity towards Chinese hamster ovary cells and is attenuated for virulence in a mouse pneumonia model. We propose that the ExsC-dependent pathway is required for full cytotoxicity towards all host cell types tested whereas the ExsC-independent pathway may represent an adaptation that allows P. aeruginosa to increase expression of the T3SS in response to specific types of mammalian cells.

scholarly journals Genome Sequence of Staphylococcus aureus Strain Newman and Comparative Analysis of Staphylococcal Genomes: Polymorphism and Evolution of Two Major Pathogenicity Islands

2007 ◽  
Vol 190 (1) ◽  
pp. 300-310 ◽  
Author(s):  
Tadashi Baba ◽  
Taeok Bae ◽  
Olaf Schneewind ◽  
Fumihiko Takeuchi ◽  
Keiichi Hiramatsu
Keyword(s):  
Staphylococcus Aureus ◽  
Genome Sequence ◽  
Virulent Strain ◽  
Phylogenetic Analyses ◽  
Human Infection ◽  
Aureus Strain ◽  
Pathogenicity Islands ◽  
Sequence Information ◽  
Polymorphism Analysis ◽  
Evolutionary Pathway

ABSTRACT Strains of Staphylococcus aureus, an important human pathogen, display up to 20% variability in their genome sequence, and most sequence information is available for human clinical isolates that have not been subjected to genetic analysis of virulence attributes. S. aureus strain Newman, which was also isolated from a human infection, displays robust virulence properties in animal models of disease and has already been extensively analyzed for its molecular traits of staphylococcal pathogenesis. We report here the complete genome sequence of S. aureus Newman, which carries four integrated prophages, as well as two large pathogenicity islands. In agreement with the view that S. aureus Newman prophages contribute important properties to pathogenesis, fewer virulence factors are found outside of the prophages than for the highly virulent strain MW2. The absence of drug resistance genes reflects the general antibiotic-susceptible phenotype of S. aureus Newman. Phylogenetic analyses reveal clonal relationships between the staphylococcal strains Newman, COL, NCTC8325, and USA300 and a greater evolutionary distance to strains MRSA252, MW2, MSSA476, N315, Mu50, JH1, JH9, and RF122. However, polymorphism analysis of two large pathogenicity islands distributed among these strains shows that the two islands were acquired independently from the evolutionary pathway of the chromosomal backbones of staphylococcal genomes. Prophages and pathogenicity islands play central roles in S. aureus virulence and evolution.

scholarly journals Nonprofessional Phagocytic Cell Receptors Involved inStaphylococcus aureusInternalization

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Nayeli Alva-Murillo ◽  
Joel Edmundo López-Meza ◽  
Alejandra Ochoa-Zarzosa
Keyword(s):  
Staphylococcus Aureus ◽  
Host Cell ◽  
Soft Tissues ◽  
Scavenger Receptor ◽  
Host Cells ◽  
Phagocytic Cell ◽  
Phagocytic Cells ◽  
Cell Receptors ◽  
Life Threatening ◽  
Bacterial Effectors

Staphylococcus aureusis a successful human and animal pathogen. The majority of infections caused by this pathogen are life threatening, primarily becauseS. aureushas developed multiple evasion strategies, possesses intracellular persistence for long periods, and targets the skin and soft tissues. Therefore, it is very important to understand the mechanisms employed byS. aureusto colonize and proliferate in these cells. The aim of this review is to describe the recent discoveries concerning the host receptors of nonprofessional phagocytes involved inS. aureusinternalization. Most of the knowledge related to the interaction ofS. aureuswith its host cells has been described in professional phagocytic cells such as macrophages. Here, we showed that in nonprofessional phagocytes theα5β1 integrin host receptor, chaperons, and the scavenger receptor CD36 are the main receptors employed duringS. aureusinternalization. The characterization and identification of new bacterial effectors and the host cell receptors involved will undoubtedly lead to new discoveries with beneficial purposes.

scholarly journals Excreted Cytoplasmic Proteins Contribute to Pathogenicity in Staphylococcus aureus

2016 ◽  
Vol 84 (6) ◽  
pp. 1672-1681 ◽  
Author(s):  
Patrick Ebner ◽  
Janina Rinker ◽  
Minh Thu Nguyen ◽  
Peter Popella ◽  
Mulugeta Nega ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Host Cell ◽  
Host Cells ◽  
Infection Model ◽  
Bacterial Cells ◽  
Host Matrix ◽  
Content Type ◽  
Cell Internalization ◽  
Cytoplasmic Proteins ◽  
The Impact

Excretion of cytoplasmic proteins in pro- and eukaryotes, also referred to as “nonclassical protein export,” is a well-known phenomenon. However, comparatively little is known about the role of the excreted proteins in relation to pathogenicity. Here, the impact of two excreted glycolytic enzymes, aldolase (FbaA) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), on pathogenicity was investigated inStaphylococcus aureus. Both enzymes bound to certain host matrix proteins and enhanced adherence of the bacterial cells to host cells but caused a decrease in host cell invasion. FbaA and GAPDH also bound to the cell surfaces of staphylococcal cells by interaction with the major autolysin, Atl, that is involved in host cell internalization. Surprisingly, FbaA showed high cytotoxicity to both MonoMac 6 (MM6) and HaCaT cells, while GAPDH was cytotoxic only for MM6 cells. Finally, the contribution of external FbaA and GAPDH toS. aureuspathogenicity was confirmed in an insect infection model.

scholarly journals WIPI-1 Positive Autophagosome-Like Vesicles Entrap PathogenicStaphylococcus aureusfor Lysosomal Degradation

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Mario Mauthe ◽  
Wenqi Yu ◽  
Oleg Krut ◽  
Martin Krönke ◽  
Friedrich Götz ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Staphylococcus Aureus ◽  
Cell Division ◽  
Membrane Protein ◽  
Host Cell ◽  
Effector Function ◽  
Host Cells ◽  
Lysosomal Degradation ◽  
Content Analyses ◽  
Confocal And Electron Microscopy

Invading pathogens provoke the autophagic machinery and, in a process termed xenophagy, the host cell survives because autophagy is employed as a safeguard for pathogens that escaped phagosomes. However, some pathogens can manipulate the autophagic pathway and replicate within the niche of generated autophagosome-like vesicles. By automated fluorescence-based high content analyses, we demonstrate thatStaphylococcus aureusstrains (USA300, HG001, SA113) stimulate autophagy and become entrapped in intracellular PtdIns(3)P-enriched vesicles that are decorated with human WIPI-1, an essential PtdIns(3)P effector of canonical autophagy and membrane protein of both phagophores and autophagosomes. Further,agr-positiveS. aureus(USA300, HG001) strains were more efficiently entrapped in WIPI-1 positive autophagosome-like vesicles when compared toagr-negative cells (SA113). By confocal and electron microscopy we provide evidence that single- and multiple-Staphylococci entrapped undergo cell division. Moreover, the number of WIPI-1 positive autophagosome-like vesicles entrapping Staphylococci significantly increased upon (i) lysosomal inhibition by bafilomycin A1and (ii) blocking PIKfyve-mediated PtdIns(3,5)P2generation by YM201636. In summary, our results provide evidence that the PtdIns(3)P effector function of WIPI-1 is utilized during xenophagy ofStaphylococcus aureus. We suggest that invadingS. aureuscells become entrapped in autophagosome-like WIPI-1 positive vesicles targeted for lysosomal degradation in nonprofessional host cells.

scholarly journals Post-invasion events after infection with Staphylococcus aureus are strongly dependent on both the host cell type and the infecting S. aureus strain

2016 ◽  
Vol 22 (9) ◽  
pp. 799-809 ◽  
Author(s):  
M. Strobel ◽  
H. Pförtner ◽  
L. Tuchscherr ◽  
U. Völker ◽  
F. Schmidt ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Host Cell ◽  
Aureus Strain ◽  
Cell Type

Ceramide in bacterial infections and cystic fibrosis

2008 ◽  
Vol 389 (11) ◽  
Author(s):  
Heike Grassmé ◽  
Katrin Anne Becker ◽  
Yang Zhang ◽  
Erich Gulbins
Keyword(s):  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Bacterial Infections ◽  
De Novo ◽  
Acid Sphingomyelinase ◽  
Temporal Organization ◽  
Host Cells ◽  
Host Responses ◽  
Mammalian Host ◽  
Membrane Domains

AbstractCeramide is formed by the activity of sphingomyelinases, by degradation of complex sphingolipids, reverse ceramidase activity orde novosynthesized. The formation of ceramide within biological membranes results in the formation of large ceramide-enriched membrane domains. These domains serve the spatial and temporal organization of receptors and signaling molecules. The acid sphingomyelinase-ceramide system plays an important role in the infection of mammalian host cells with bacterial pathogens such asNeisseria gonorrhoeae,Escherichia coli,Staphylococcus aureus,Listeria monocytogenes,Salmonella typhimuriumandPseudomonas aeruginosa. Ceramide and ceramide-enriched membrane platforms are also involved in the induction of apoptosis in infected cells, such as in epithelial and endothelial cells after infection withPseudomonas aeruginosaandStaphylococcus aureus, respectively. Finally, ceramide-enriched membrane platforms are critical regulators of the release of pro-inflammatory cytokines upon infection. The diverse functions of ceramide in bacterial infections suggest that ceramide and ceramide-enriched membrane domains are key players in host responses to many pathogens and thus are potential novel targets to treat infections.

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