scholarly journals The Phosphoarginine Phosphatase PtpB from Staphylococcus aureus Is Involved in Bacterial Stress Adaptation during Infection

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 645
Author(s):  
Mohamed Ibrahem Elhawy ◽  
Sylvaine Huc-Brandt ◽  
Linda Pätzold ◽  
Laila Gannoun-Zaki ◽  
Ahmed Mohamed Mostafa Abdrabou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Treatment Strategies ◽  
Physiological Role ◽  
Aureus Strain ◽  
Stress Adaptation ◽  
Cellular Mechanisms ◽  
Host Interaction ◽  
Liver And Kidney

Staphylococcus aureus continues to be a public health threat, especially in hospital settings. Studies aimed at deciphering the molecular and cellular mechanisms that underlie pathogenesis, host adaptation, and virulence are required to develop effective treatment strategies. Numerous host-pathogen interactions were found to be dependent on phosphatases-mediated regulation. This study focused on the analysis of the role of the low-molecular weight phosphatase PtpB, in particular, during infection. Deletion of ptpB in S. aureus strain SA564 significantly reduced the capacity of the mutant to withstand intracellular killing by THP-1 macrophages. When injected into normoglycemic C57BL/6 mice, the SA564 ΔptpB mutant displayed markedly reduced bacterial loads in liver and kidney tissues in a murine S. aureus abscess model when compared to the wild type. We also observed that PtpB phosphatase-activity was sensitive to oxidative stress. Our quantitative transcript analyses revealed that PtpB affects the transcription of various genes involved in oxidative stress adaptation and infectivity. Thus, this study disclosed first insights into the physiological role of PtpB during host interaction allowing us to link phosphatase-dependent regulation to oxidative bacterial stress adaptation during infection.

scholarly journals Influence of Metal-Resistant Staphylococcus aureus Strain K1 on the Alleviation of Chromium Stress in Wheat

Agronomy ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1354 ◽  
Author(s):  
Fanrong Zeng ◽  
Munazza Zahoor ◽  
Muhammad Waseem ◽  
Alia Anayat ◽  
Muhammad Rizwan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Anthropogenic Activities ◽  
Toxic Metal ◽  
Triticum Aestivum L ◽  
Aureus Strain ◽  
Peat Moss ◽  
Cr Toxicity ◽  
Living Organisms

Chromium (Cr) is recognized as a toxic metal that has detrimental effects on living organisms; notably, it is discharged into soil by various industries as a result of anthropogenic activities. Microbe-assisted phytoremediation is one of the most emergent and environmentally friendly methods used for the detoxification of pollutants. In this study, the alleviative role of Staphylococcus aureus strain K1 was evaluated in wheat (Triticum aestivum L.) under Cr stress. For this, various Cr concentrations (0, 25, 50 and 100 mg·kg−1) with and without peat-moss-based bacterial inoculum were applied in the soil. Results depicted that Cr stress reduced the plants’ growth by causing oxidative stress in the absence of S. aureus K1 inoculation. However, the application of S. aureus K1 regulated the plants’ growth and antioxidant enzymatic activities by reducing oxidative stress and Cr toxicity through conversion of Cr6+ to Cr3+. The Cr6+ uptake by wheat was significantly reduced in the S. aureus K1 inoculated plants. It can be concluded that the application of S. aureus K1 could be an effective approach to alleviate the Cr toxicity in wheat and probably in other cereals grown under Cr stress.

scholarly journals Importance of Bacillithiol in the Oxidative Stress Response of Staphylococcus aureus

2013 ◽  
Vol 82 (1) ◽  
pp. 316-332 ◽  
Author(s):  
Ana C. Posada ◽  
Stacey L. Kolar ◽  
Renata G. Dusi ◽  
Patrice Francois ◽  
Alexandra A. Roberts ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Physiological Role ◽  
Content Type ◽  
Chromatography Analysis ◽  
Expression Of Genes ◽  
Fold Reduction ◽  
Fosfomycin Resistance ◽  
Microarray Analyses

ABSTRACTInStaphylococcus aureus, the low-molecular-weight thiol called bacillithiol (BSH), together with cognateS-transferases, is believed to be the counterpart to the glutathione system of other organisms. To explore the physiological role of BSH inS. aureus, we constructed mutants with the deletion ofbshA(sa1291), which encodes the glycosyltransferase that catalyzes the first step of BSH biosynthesis, andfosB(sa2124), which encodes a BSH-S-transferase that confers fosfomycin resistance, in severalS. aureusstrains, including clinical isolates. Mutation offosBorbshAcaused a 16- to 60-fold reduction in fosfomycin resistance in theseS. aureusstrains. High-pressure liquid chromatography analysis, which quantified thiol extracts, revealed some variability in the amounts of BSH present acrossS. aureusstrains. Deletion offosBled to a decrease in BSH levels. ThefosBandbshAmutants of strain COL and a USA300 isolate, upon further characterization, were found to be sensitive to H2O2and exhibited decreased NADPH levels compared with those in the isogenic parents. Microarray analyses of COL and the isogenicbshAmutant revealed increased expression of genes involved in staphyloxanthin synthesis in thebshAmutant relative to that in COL under thiol stress conditions. However, thebshAmutant of COL demonstrated decreased survival compared to that of the parent in human whole-blood survival assays; likewise, the naturally BSH-deficient strain SH1000 survived less well than its BSH-producing isogenic counterpart. Thus, the survival ofS. aureusunder oxidative stress is facilitated by BSH, possibly via a FosB-mediated mechanism, independently of its capability to produce staphyloxanthin.

scholarly journals Role of Mitochondrial Cytochrome P450 2E1 in Healthy and Diseased Liver

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 288
Author(s):  
Julie Massart ◽  
Karima Begriche ◽  
Jessica H. Hartman ◽  
Bernard Fromenty
Keyword(s):  
Oxidative Stress ◽  
Cytochrome P450 ◽  
Liver Disease ◽  
Fatty Liver ◽  
Current Knowledge ◽  
Physiological Role ◽  
Experimental Investigations ◽  
Rat Liver Mitochondria ◽  
Cytochrome P450 2E1

Cytochrome P450 2E1 (CYP2E1) is pivotal in hepatotoxicity induced by alcohol abuse and different xenobiotics. In this setting, CYP2E1 generates reactive metabolites inducing oxidative stress, mitochondrial dysfunction and cell death. In addition, this enzyme appears to play a role in the progression of obesity-related fatty liver to nonalcoholic steatohepatitis. Indeed, increased CYP2E1 activity in nonalcoholic fatty liver disease (NAFLD) is deemed to induce reactive oxygen species overproduction, which in turn triggers oxidative stress, necroinflammation and fibrosis. In 1997, Avadhani’s group reported for the first time the presence of CYP2E1 in rat liver mitochondria, and subsequent investigations by other groups confirmed that mitochondrial CYP2E1 (mtCYP2E1) could be found in different experimental models. In this review, we first recall the main features of CYP2E1 including its role in the biotransformation of endogenous and exogenous molecules, the regulation of its expression and activity and its involvement in different liver diseases. Then, we present the current knowledge on the physiological role of mtCYP2E1, its contribution to xenobiotic biotransformation as well as the mechanism and regulation of CYP2E1 targeting to mitochondria. Finally, we discuss experimental investigations suggesting that mtCYP2E1 could have a role in alcohol-associated liver disease, xenobiotic-induced hepatotoxicity and NAFLD.

scholarly journals Contributions of the Response Regulators Ssk1p and Skn7p in the Pseudohyphal Development, Stress Adaptation, and Drug Sensitivity of the Opportunistic Yeast Candida lusitaniae

2008 ◽  
Vol 7 (6) ◽  
pp. 1071-1074 ◽  
Author(s):  
Gwenaël Ruprich-Robert ◽  
Florence Chapeland-Leclerc ◽  
Stéphanie Boisnard ◽  
Martine Florent ◽  
Gaël Bories ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Functional Analysis ◽  
Histidine Kinase ◽  
Drug Sensitivity ◽  
Stress Adaptation ◽  
Response Regulators ◽  
Candida Lusitaniae

ABSTRACT We recently characterized the histidine kinase receptor genes of Candida lusitaniae. For the present study, we have further investigated the role of SSK1 and SKN7, encoding response regulators. The results of functional analysis of mutants indicated that Ssk1p is involved in osmotolerance and pseudohyphal development, whereas Skn7p appears crucial for oxidative stress adaptation.

scholarly journals Staphylococcus aureus Infection Induced Oxidative Imbalance in Neutrophils: Possible Protective Role of Nanoconjugated Vancomycin

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Subhankari Prasad Chakraborty ◽  
Panchanan Pramanik ◽  
Somenath Roy
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Cell Damage ◽  
Treated Group ◽  
Protective Role ◽  
Control Group ◽  
Similar Dose ◽  
Cellular Components

Staphylococcus aureus infection causes oxidative stress in neutrophils. The immune cells use reactive oxygen species (ROS) for carrying out their normal functions while an excess amount of ROS can attack cellular components that lead to cell damage. The present study was aimed to test the protective role of nanoconjugated vancomycin against vancomycin-sensitive Staphylococcus aureus (VSSA) and vancomycin-resistant Staphylococcus aureus (VRSA) infection induced oxidative stress in neutrophils. VSSA- and VRSA-infection were developed in Swiss mice by intraperitoneal injection of 5×106 CFU/mL bacterial solutions. Nanoconjugated vancomycin was treated to VSSA- and VRSA-infected mice at its effective dose for 10 days. Vancomycin was treated to VSSA and VRSA infected mice at similar dose, respectively, for 10 days. The result reveals that in vivo VSSA and VRSA infection significantly increases the level of lipid peroxidation, protein oxidation, oxidized glutathione level, and nitrite generation and decreases the level of reduced glutathione, antioxidant enzyme status, and glutathione-dependent enzymes as compared to control group; which were increased or decreased significantly near to normal in nanoconjugated vancomycin-treated group. These finding suggests the potential use and beneficial protective role of nanoconjugated vancomycin against VSSA and VRSA infection induced oxidative imbalance in neutrophils.

Oxidative stress as a common pathway to chronic tubulointerstitial injury in kidney allografts

2007 ◽  
Vol 293 (2) ◽  
pp. F445-F455 ◽  
Author(s):  
Arjang Djamali
Keyword(s):  
Oxidative Stress ◽  
Interstitial Fibrosis ◽  
Treatment Strategies ◽  
Specific Treatment ◽  
Common Mechanism ◽  
Placebo Control ◽  
Tubulointerstitial Injury ◽  
Tubular Atrophy ◽  
Mesenchymal Transition

A major challenge for kidney transplantation is to dissect out the identifiable causes of chronic allograft tubulointerstitial fibrosis and to develop cause-specific treatment strategies. There has been a recent interest in the role of oxidative stress (OS) as a mediator of injury in chronic allograft tubular atrophy (TA) and interstitial fibrosis (IF). A review of the literature and data from my laboratory studying chronic allograft TA/IF in rat, rhesus monkey, and human kidneys suggests that OS is increased in graft-infiltrating macrophages, activated myofibroblasts, interstitium, and areas of tubular injury. Chronic allograft OS may be induced by inflammation, abnormal tissue oxygenation, immunosuppressant drugs, and comorbid clinical conditions including diabetes, hypertension, proteinuria, anemia, and dyslipidemia. Moreover, OS-induced chronic TA/IF is associated with signaling pathways including inflammation, apoptosis, hypoxia, and epithelial-to-mesenchymal transition. Most of these injury pathways participate in a self-perpetuating cycle with OS. In conclusion, evidence suggests that OS is a common mechanism of injury in chronic allograft TA/IF. However, most available data demonstrate a correlation and no causal relationship. Furthermore, the extent to which TA/IF is dependent on OS is unknown. These questions may be answered by prospective randomized placebo-control trials examining the role of select antioxidants in the prevention of chronic allograft TA/IF.

Multiple methionine sulfoxide reductase genes in Staphylococcus aureus: expression of activity and roles in tolerance of oxidative stress

Microbiology ◽  
2003 ◽  
Vol 149 (10) ◽  
pp. 2739-2747 ◽  
Author(s):  
Vineet K. Singh ◽  
Jackob Moskovitz
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Stress Response ◽  
Double Mutant ◽  
Mutational Analysis ◽  
Physiological Role ◽  
Methionine Sulfoxide ◽  
Oxidative Stress Response ◽  
Methionine Sulfoxide Reductase ◽  
Activity Data

Staphylococcus aureus contains three genes encoding MsrA-specific methionine sulfoxide reductase (Msr) activity (msrA1, msrA2 and msrA3) and an additional gene that encodes MsrB-specific Msr activity. Data presented here suggest that MsrA1 is the major contributor of the MsrA activity in S. aureus. In mutational analysis, while the total Msr activity in msrA2 mutant was comparable to that of the parent, Msr activity was significantly up-regulated in the msrA1 or msrA1 msrA2 double mutant. Assessment of substrate specificity together with increased reactivity of the cell-free protein extracts of the msrA1 mutants to anti-MsrB polyclonal antibodies in Western analysis provided evidence that increased Msr activity was due to elevated synthesis of MsrB in the MsrA1 mutants. Previously, it was reported that oxacillin treatment of S. aureus cells led to induced synthesis of MsrA1 and a mutation in msrA1 increased the susceptibility of the organism to H2O2. A mutation in the msrA2 gene, however, was not significant for the bacterial oxidative stress response. In complementation assays, while the msrA2 gene was unable to complement the msrA1 msrA2 double mutant for H2O2 resistance, the same gene restored H2O2 tolerance in the double mutant when placed under the control of the msrA1 promoter. However, msrA1 which was able to complement the oxidative stress response in msrA1 mutants could not restore the tolerance of the msrA1 msrA2 mutants to H2O2 when placed under the control of the msrA2 promoter. Additionally, although the oxacillin minimum inhibitory concentration of the msrA1 mutant was comparable to that of the wild-type parent, in shaking liquid culture, the msrA1 mutant responded more efficiently to sublethal doses of oxacillin. The data suggest complex regulation of Msr proteins and a more significant physiological role for msrA1/msrB in S. aureus.

scholarly journals The Role of Na/K-ATPase Signaling in Oxidative Stress Related to Aging: Implications in Obesity and Cardiovascular Disease

2018 ◽  
Vol 19 (7) ◽  
pp. 2139 ◽  
Author(s):  
David Bartlett ◽  
Richard Miller ◽  
Scott Thiesfeldt ◽  
Hari Lakhani ◽  
Joseph Shapiro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Patient Outcomes ◽  
Molecular Mechanisms ◽  
Treatment Options ◽  
Cellular Mechanisms ◽  
General Decline ◽  
Pumping Function ◽  
Improve Patient

Aging has been associated with a series of pathophysiological processes causing general decline in the overall health of the afflicted population. The cumulative line of evidence suggests an important role of oxidative stress in the development and progression of the aging process and metabolic abnormalities, exacerbating adipocyte dysfunction, cardiovascular diseases, and associated complications at the same time. In recent years, robust have established the implication of Na/K-ATPase signaling in causing oxidative stress and alterations in cellular mechanisms, in addition to its distinct pumping function. Understanding the underlying molecular mechanisms and exploring the possible sources of pro-oxidants may allow for developing therapeutic targets in these processes and formulate novel intervention strategies for patients susceptible to aging and associated complications, such as obesity and cardiovascular disease. The attenuation of oxidative stress with targeted treatment options can improve patient outcomes and significantly reduce economic burden.

scholarly journals Internalization ofStaphylococcus aureusin Lymphocytes Induces Oxidative Stress and DNA Fragmentation: Possible Ameliorative Role of Nanoconjugated Vancomycin

2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
Subhankari Prasad Chakraborty ◽  
Santanu Kar Mahapatra ◽  
Sumanta Kumar Sahu ◽  
Sabyasachi Das ◽  
Satyajit Tripathy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Immune Cell ◽  
Bloodstream Infections ◽  
Treated Group ◽  
Control Group ◽  
Similar Dose ◽  
Effective Doses

Staphylococcus aureusis the most frequently isolated pathogen causing bloodstream infections, skin and soft tissue infections and pneumonia. Lymphocyte is an important immune cell. The aim of the present paper was to test the ameliorative role of nanoconjugated vancomycin against Vancomycin-sensitiveStaphylococcus aureus(VSSA) and vancomycin-resistantStaphylococcus aureus(VRSA) infection-induced oxidative stress in lymphocytes. VSSA and VRSA infections were developed in Swiss mice by intraperitoneal injection of  CFU/mL bacterial solutions. Nanoconjugated vancomycin was adminstrated to VSSA- and VRSA-infected mice at its effective dose for 10 days. Vancomycin was adminstrated to VSSA- and VRSA-infected mice at a similar dose, respectively, for 10 days. Vancomycin and nanoconjugated vancomycin were adminstrated to normal mice at their effective doses for 10 days. The result of this study reveals that in vivo VSSA and VRSA infection significantly increases the level of lipid peroxidation, protein oxidation, oxidized glutathione level, nitrite generation, nitrite release, and DNA damage and decreases the level of reduced glutathione, antioxidant enzyme status, and glutathione-dependent enzymes as compared to control group, which were increased or decreased significantly near to normal in nanoconjugated vancomycin-treated group. These findings suggest the potential use and beneficial role of nanoconjugated vancomycin against VSSA and VRSA infection-induced oxidative stress in lymphocytes.

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