scholarly journals Reduced Innate Immune Response to a Staphylococcus aureus Small Colony Variant Compared to Its Wild-Type Parent Strain

2016 ◽  
Vol 6 ◽  
Author(s):  
Judy J. J. Ou ◽  
Amanda J. Drilling ◽  
Clare Cooksley ◽  
Ahmed Bassiouni ◽  
Stephen P. Kidd ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Response ◽  
Innate Immune Response ◽  
Parent Strain ◽  
Innate Immune ◽  
Wild Type ◽  
Small Colony Variant ◽  
Small Colony ◽  
Wild Type Parent

scholarly journals Genetic basis of host innate immune response in mastitis caused by Staphylococcus aureus

2012 ◽  
Vol 4 ◽  
pp. 405-409 ◽  
Author(s):  
Adrianna Pawlik ◽  
Grażyna Sender ◽  
Rafał Starzyński ◽  
Agnieszka Korwin-Kossakowska
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Response ◽  
Innate Immune Response ◽  
Genetic Basis ◽  
Innate Immune ◽  
Host Innate Immune Response

scholarly journals Enhanced production of exopolysaccharide matrix and biofilm by a menadione-auxotrophic Staphylococcus aureus small-colony variant

2010 ◽  
Vol 59 (5) ◽  
pp. 521-527 ◽  
Author(s):  
Rachna Singh ◽  
Pallab Ray ◽  
Anindita Das ◽  
Meera Sharma
Keyword(s):  
Staphylococcus Aureus ◽  
Tricarboxylic Acid Cycle ◽  
Surface Hydrophobicity ◽  
Tricarboxylic Acid ◽  
Polysaccharide Intercellular Adhesin ◽  
Wild Type ◽  
Small Colony Variant ◽  
Enhanced Production ◽  
Small Colony

The role of Staphylococcus aureus small-colony variants (SCVs) in the pathogenesis of biofilm-associated infections remains unclear. This study investigated the mechanism behind increased biofilm-forming potential of a menadione-auxotrophic Staphylococcus aureus SCV compared with the wild-type parental strain, as recently reported by our laboratory. SCVs displayed an autoaggregative phenotype, with a greater amount of polysaccharide intercellular adhesin (PIA), significantly reduced tricarboxylic acid cycle activity and a decreased susceptibility to aminoglycosides and cell-wall inhibitors compared with wild-type. The biofilms formed by the SCV were highly structured, consisting of large microcolonies separated by channels, and contained more biomass as well as significantly more PIA than wild-type biofilms. The surface hydrophobicity of the two phenotypes was similar. Thus, the autoaggregation and increased biofilm-forming capacity of menadione-auxotrophic Staphylococcus aureus SCVs in this study was related to the enhanced production of PIA in these variants.

scholarly journals A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection

10.3791/59015 ◽  
2019 ◽  
Author(s):  
Leif S. Anderson ◽  
Mack B. Reynolds ◽  
Kathryn R. Rivara ◽  
Lloyd S. Miller ◽  
Scott I. Simon
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Response ◽  
Mouse Model ◽  
Innate Immune Response ◽  
Innate Immune

scholarly journals Innate immunity mediator STING modulates nascent DNA metabolism at stalled forks in human cells

2021 ◽  
Author(s):  
Vy N. Nguyen ◽  
Salomé Brunon ◽  
Maria N. Pavlova ◽  
Pavlo Lazarchuk ◽  
Roya D. Sharifian ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Replication Forks ◽  
Wild Type ◽  
Feedback Connection ◽  
Pathway Activation ◽  
Foreign Dna ◽  
Sting Pathway

The cGAS/STING pathway, part of the innate immune response to foreign DNA, is known to be activated by cell's own DNA arising from the processing of the genome, including the excision of nascent DNA at arrested replication forks. We found STING activation to affect nascent DNA processing, suggesting a novel, unexpected feedback connection between the two events. Depletion of STING suppressed and re-expression of the protein in STING-deficient cells upregulated degradation of nascent DNA. Fork arrest was accompanied by the STING pathway activation, and a STING mutant that does not activate the pathway failed to upregulate nascent strand degradation. Consistent with this, cells expressing the STING mutant had a reduced level of RPA on parental and nascent DNA of arrested forks as well as a reduced CHK1 activation compared to the cells with wild type STING. Together our findings reveal a novel connection between replication stress and innate immunity.

scholarly journals Control of β-glucan exposure by the endo-1,3-glucanase Eng1 in Candida albicans modulates virulence

2020 ◽  
Author(s):  
Mengli Yang ◽  
Norma V. Solis ◽  
Michaela Marshall ◽  
Rachel Garleb ◽  
Tingting Zhou ◽  
...  
Keyword(s):  
Immune Response ◽  
Candida Albicans ◽  
Innate Immune Response ◽  
Type Strain ◽  
Wild Type Strain ◽  
Innate Immune ◽  
Yeast Cells ◽  
Parallel Mechanisms ◽  
Wild Type ◽  
Lectin Receptor

AbstractCandida albicans is a major cause of invasive candidiasis, which has a high mortality rate. The hyphal form of C. albicans is virulent and activates the host innate immune response, while the yeast form is hypovirulent and less immunogenic. The innate immune response is critical for host defense, but overactivation can cause tissue damage and sepsis. The innate immune response can be triggered when the C-type lectin receptor Dectin-1 recognizes β-glucans, which is protected by the outer mannan layer of the cell wall on C. albicans. Here, we demonstrate that there is low level of Dectin-1 binding at the septum of yeast cells, but high level of Dectin-1 binding over the entire surface of hyphae. We find that β-glucan masking in yeast is controlled by two highly expressed yeast proteins, the endo-1,3-β-glucanase Eng1 and the Yeast Wall Protein Ywp1. An eng1 deletion mutant shows enhanced Dectin-1 binding at the septa, while an eng1 ywp1 double mutant, but not an ywp1 single mutant, shows strong overall Dectin-1 binding. Thus, Eng1-mediated β-glucan trimming and Ywp1-mediated β-glucan masking are two parallel mechanisms utilized by C. albicans yeast to minimize recognition by Dectin-1. In the model of disseminated candidiasis, mice infected with the eng1 deletion mutant showed delayed mortality with an increased renal immune response in males compared to mice infected with the wild-type strain, but earlier mortality with a higher renal immune response in females. Using the eng1 mutant that is specifically defective in β-glucan masking in yeast, this study demonstrates that the level of β-glucan exposure is important for modulating the balance between immune protection and immunopathogenesis.Abstract ImportanceCandida albicans is a major opportunistic fungal pathogen of humans. Systemic Candidiasis has high mortality rates. C. albicans is also a constituent of the human microbiome and found in gastrointestinal and genitourinary tracts of most healthy individuals. C. albicans is able to switch reversibly between yeast and hyphae in response to environmental cues. The hyphal form is virulent, while the yeast form is hypovirulent and less immunogenic. This study demonstrates that β-glucan exposure in yeast is protected by two highly expressed yeast proteins, the endo-1,3-β-glucanase Eng1 and the Yeast Wall Protein Ywp1. Eng1-mediated β-glucan trimming and Ywp1-mediated β-glucan masking are two parallel mechanisms utilized by C. albicans yeast to minimize recognition by the host C-type lectin receptor Dectin-1. The eng1 mutant triggers a higher immune response and leads to earlier mortality compared to the wild-type strain. Thus, β-glucan masking in yeast keeps yeast cells less immunogenic and hypovirulent.

scholarly journals Staphylococcus aureus Biofilm-Conditioned Medium Impairs Macrophage-Mediated Antibiofilm Immune Response by Upregulating KLF2 Expression

2019 ◽  
Vol 87 (4) ◽  
Author(s):  
Talib Alboslemy ◽  
Bing Yu ◽  
Tara Rogers ◽  
Min-Ho Kim
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Response ◽  
Conditioned Medium ◽  
Innate Immune Response ◽  
Immune Defense ◽  
Innate Immune ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Content Type ◽  
Cell Functions

ABSTRACT Staphylococcus aureus infections associated with the formation of biofilms on medical implants or host tissue play a critical role in the persistence of chronic infections. One critical mechanism of biofilm infection that leads to persistent infection lies in the capacity of biofilms to evade the macrophage-mediated innate immune response. It is now increasingly apparent that microorganisms exploit the negative regulatory mechanisms of the pattern recognition receptor (PRR)-mediated inflammatory response to subvert host cell functions by using various virulence factors. However, the detailed molecular mechanism, along with the identity of a target molecule, underlying the evasion of the macrophage-mediated innate immune response against S. aureus infection associated with biofilm formation remains to be elucidated. Here, using an in vitro culture model of murine macrophage-like RAW 264.7 cells, we demonstrate that S. aureus biofilm-conditioned medium significantly attenuated the capacity for macrophage bactericidal and proinflammatory responses. Importantly, the responses were associated with attenuated activation of NF-κB and increased expression of Kruppel-like factor 2 (KLF2) in RAW 264.7 cells. Small interfering RNA (siRNA)-mediated silencing of KLF2 in RAW 264.7 cells could restore the activation of NF-κB toward the bactericidal activity and generation of proinflammatory cytokines in the presence of S. aureus biofilm-conditioned medium. Collectively, our results suggest that factors secreted from S. aureus biofilms might exploit the KLF2-dependent negative regulatory mechanism to subvert macrophage-mediated innate immune defense against S. aureus biofilms.

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