Role of OxyS of Mycobacterium tuberculosis in oxidative stress: overexpression confers increased sensitivity to organic hydroperoxides

2001 ◽  
Vol 3 (9) ◽  
pp. 713-721 ◽  
Author(s):  
Pilar Domenech ◽  
Nadine Honoré ◽  
Beate Heym ◽  
Stewart T. Cole
Keyword(s):  
Oxidative Stress ◽  
Mycobacterium Tuberculosis ◽  
Organic Hydroperoxides ◽  
Increased Sensitivity

scholarly journals Requirement of the mymA Operon for Appropriate Cell Wall Ultrastructure and Persistence of Mycobacterium tuberculosis in the Spleens of Guinea Pigs

2005 ◽  
Vol 187 (12) ◽  
pp. 4173-4186 ◽  
Author(s):  
Amit Singh ◽  
Radhika Gupta ◽  
R. A. Vishwakarma ◽  
P. R. Narayanan ◽  
C. N. Paramasivan ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Parental Strain ◽  
Guinea Pigs ◽  
Cell Envelope ◽  
Sodium Dodecyl ◽  
Phenotypic Traits ◽  
Antitubercular Drugs ◽  
Mycolic Acids ◽  
Increased Sensitivity

ABSTRACT We had recently reported that the mymA operon (Rv3083 to Rv3089) of Mycobacterium tuberculosis is regulated by AraC/XylS transcriptional regulator VirS (Rv3082c) and is important for the cell envelope of M. tuberculosis. In this study, we further show that a virS mutant (MtbΔvirS) and a mymA mutant (Mtbmym::hyg) of M. tuberculosis exhibit reduced contents and altered composition of mycolic acids along with the accumulation of saturated C24 and C26 fatty acids compared to the parental strain. These mutants were markedly more susceptible to major antitubercular drugs at acidic pH and also showed increased sensitivity to detergent (sodium dodecyl sulfate) and to acidic stress than the parental strain. We show that disruption of virS and mymA genes impairs the ability of M. tuberculosis to survive in activated macrophages, but not in resting macrophages, suggesting the importance of the mymA operon in protecting the bacterium against harsher conditions. Infection of guinea pigs with MtbΔvirS, Mtbmym::hyg, and the parental strain resulted in an ∼800-fold-reduced bacillary load of the mutant strains compared with the parental strain in spleens, but not in the lungs, of animals at 20 weeks postinfection. Phenotypic traits were fully complemented upon reintroduction of the virS gene into MtbΔvirS. These observations show the important role of the mymA operon in the pathogenesis of M. tuberculosis at later stages of the disease.

scholarly journals Regulation of Brucella abortusCatalase

2000 ◽  
Vol 68 (7) ◽  
pp. 3861-3866 ◽  
Author(s):  
Jeong-a Kim ◽  
Zengyu Sha ◽  
John E. Mayfield
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Pathogenic Bacteria ◽  
Sublethal Concentration ◽  
Subsequent Exposure ◽  
Catalase Peroxidase ◽  
Increased Sensitivity ◽  
Analysis Survival ◽  
Hostile Environments

ABSTRACT All aerobic organisms have mechanisms that protect against oxidative compounds. Catalase, peroxidase, superoxide dismutase, glutathione, and thioredoxin are widely distributed in many taxa and constitute elements of a nearly ubiquitous antioxidant metabolic strategy. Interestingly, the regulatory mechanisms that control these elements are rather different depending on the nature of the oxidative stress and the organism. Catalase is well documented to play an important role in protecting cells from oxidative stress. In particular, pathogenic bacteria seem to use this enzyme as a defensive tool against attack by the host. To investigate the significance of catalase in hostile environments, we made catalase deletion mutations in two different B. abortus strains and used two-dimensional gel analysis, survival tests, and adaptation experiments to explore the behavior and role of catalase under several oxidative stress conditions. These studies show that B. abortus strains that do not express catalase activity exhibit increased sensitivity to hydrogen peroxide. We also demonstrate that catalase expression is regulated in this species, and that preexposure to a sublethal concentration of hydrogen peroxide allows B. abortus to adapt so as to survive subsequent exposure to higher concentrations of hydrogen peroxide.

scholarly journals Impact of lgt mutation on lipoprotein biosynthesis and in vitro phenotypes of Streptococcus agalactiae

Microbiology ◽  
2009 ◽  
Vol 155 (5) ◽  
pp. 1451-1458 ◽  
Author(s):  
Beverley A. Bray ◽  
Iain C. Sutcliffe ◽  
Dean J. Harrington
Keyword(s):  
Oxidative Stress ◽  
Streptococcus Agalactiae ◽  
Molecular Basis ◽  
Cell Envelope ◽  
Host Cells ◽  
Human Endothelial Cells ◽  
Increased Sensitivity ◽  
Group B

Although Streptococcus agalactiae, the group B Streptococcus, is a leading cause of invasive neonatal disease worldwide the molecular basis of its virulence is still poorly understood. To investigate the role of lipoproteins in the physiology and interaction of this pathogen with host cells, we generated a mutant S. agalactiae strain (A909ΔLgt) deficient in the Lgt enzyme and thus unable to lipidate lipoprotein precursors (pro-lipoproteins). The loss of pro-lipoprotein lipidation did not affect the viability of S. agalactiae or its growth in several different media, including cation-depleted media. The processing of two well-characterized lipoproteins, but not a non-lipoprotein, was clearly shown to be aberrant in A909ΔLgt. The mutant strain was shown to be more sensitive to oxidative stress in vitro although the molecular basis of this increased sensitivity was not apparent. The inactivation of Lgt also resulted in changes to the bacterial cell envelope, as demonstrated by reduced retention of both the group B carbohydrate and the polysaccharide capsule and a statistically significant reduction (P=0.0079) in A909ΔLgt adherence to human endothelial cells of fetal origin. These data confirm that failure to process lipoproteins correctly has pleiotropic effects that may be of significance to S. agalactiae colonization and pathogenesis.

scholarly journals The Role of N-Acetyl Sistein in Pulmonary Tuberculosis

2020 ◽  
Vol 6 (1) ◽  
pp. 27
Author(s):  
Resti Yudhawati ◽  
Nitya Prasanta
Keyword(s):  
Oxidative Stress ◽  
Mycobacterium Tuberculosis ◽  
Pulmonary Tuberculosis ◽  
Respiratory Diseases ◽  
Antimicrobial Effect ◽  
Mycobacterium Tuberculosis Infection ◽  
Major Health Problem ◽  
Major Health ◽  
Mucolytic Agent

Pulmonary Tuberculosis is a chronic infection that caused by Mycobacterium tuberculosis (M.tb) infection and it is still the major health problem worldwide. Mycobacterium tuberculosis infection can induce oxidative stress. Some studies has proved that active TB patients have an association with excessive oxidative stress which causes glutathione (GSH) level decrease and free radicals increase. Glutathione (GSH) facilitates the control of M.TB intracellular bacterial growth in macrophages and has direct antimicrobial activity.  N-acetylcysteine (NAC) is thiol, a precursor of L-cysteine and glutathione synthesis (GSH) that has been used for decades as a mucolytic agent in the treatment of respiratory diseases. Some studies report beneficial role of NAC as immunomodulator, besides NAC also has anti-inflammatory and antimicrobial effect in TB management.

Role of neutrophils in the increased sensitivity to oxidative stress in diabetes

2000 ◽  
Vol 118 (4) ◽  
pp. A1128-A1129
Author(s):  
Steve Lawson ◽  
David T. Ward ◽  
Scott T. Rehrig ◽  
Sherry D. Fleming ◽  
Daniel Mulloy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Increased Sensitivity

scholarly journals Effect of Oxidative Stress on AhpC Activity and Virulence in katG Ser315 Thr Mycobacterium tuberculosis Mutant

2015 ◽  
Vol 16 (2) ◽  
pp. 100 ◽  
Author(s):  
Ning Rintiswati ◽  
Tri Wibawa ◽  
Widya Asmara ◽  
Hardyanto Soebono
Keyword(s):  
Oxidative Stress ◽  
Mycobacterium Tuberculosis ◽  
Stress Condition ◽  
Molecular Targets ◽  
Apoptosis Induction ◽  
Human Macrophages ◽  
Pcr Rflp ◽  
Mutant Strains ◽  
Experimental Subjects

Mycobacterium tuberculosis strains resistance to INH is mainly caused by the alteration in several genesencoding the molecular targets. Mutation of katG at codon 315 especially Ser315Thr are responsible forINH resistance in a large proportion of TB cases. The aim of this study is to evaluate the influence of stressoxidative on AhpC activity of katG Ser315Thr of M.tuberculosis, and to find out the relation of AhpC and thevirulence of this mutant. The study design was laboratoric experimental, subjects of study were M.tuberculosisINH resistance strains, and the treatment were serial dose of H2O2. Eighty five M.tuberculosis INH resistantclinical strain were screened for mutation of katGSer315Thr by PCR/RFLP and characterized on the basis ofphenotypic properties (catalase activity and AhpC activity). AhpC activity of katG Ser315Thr M.tuberculosisstrains in response to oxidative stress condition was evaluated by culturing the strains on liquid culturemedium containing 1mM H2O2.To ascertain role of AhpC in the virulence of katGSer315Thr mutant strains, themutants were infected into human macrophages culture, and several indicator of virulence were observed (i.e:replication competence, and apoptosis induction on human macrophages). The results showed that katG Ser315Thr were identified in 23 (27,05%) of 85 INH resistance strains, all mutant strains had decrease of catalaseactivity. AhpC activity of katG Ser315Thr of M.tuberculosis increased significantly with increase of hydrogenperoxide dose. In addition , it has been shown that increased AhpC activity related to replication ability ofmutant, and reduction of apoptosis macrophages induction significantly. We conclude that the productionof AhpC of katG Ser315Thr M.tuberculosis induced by oxidative stress. There was a role of AhpC in virulenceof the M.tuberculosis katG Ser315Thr strains by replication capability and macrophages apoptosis.

Reactive cold plasma particles generate oxidative stress in yeast but do not trigger apoptosis

2018 ◽  
Vol 64 (6) ◽  
pp. 367-375
Author(s):  
Peter Polčic ◽  
Lucia Pakosová ◽  
Petra Chovančíková ◽  
Zdenko Machala
Keyword(s):  
Oxidative Stress ◽  
Cold Plasma ◽  
Cell Killing ◽  
Yeast Cells ◽  
Cell Physiology ◽  
Apoptotic Pathway ◽  
Yeast Saccharomyces Cerevisiae ◽  
Increased Sensitivity ◽  
Genetic Mutants

Interactions of living cells with cold plasma of electrical discharges affect cell physiology, often resulting in the loss of viability. However, the mechanisms involved in cell killing are poorly understood, and dissection of cellular pathways or structures affected by plasma using simple eukaryotic models is needed. Using selected genetic mutants of yeast (Saccharomyces cerevisiae), we investigated the role of oxidative stress and yeast apoptosis in plasma-induced cell killing. Increased sensitivity of yeast strains deficient in superoxide dismutases indicated that reactive oxygen species generated in the plasma are among the most prominent factors involved in killing of yeast cells. In mutant strains with a deletion of the key components of yeast apoptotic pathway, the sensitivity of cells towards the plasma treatment remained unaffected. Yeast apoptosis, thus, does not appear to play a significant role in plasma-induced cell killing of yeast.

scholarly journals Transcriptional Regulation of furAand katG upon Oxidative Stress inMycobacterium smegmatis

2001 ◽  
Vol 183 (23) ◽  
pp. 6801-6806 ◽  
Author(s):  
Anna Milano ◽  
Francesca Forti ◽  
Claudia Sala ◽  
Giovanna Riccardi ◽  
Daniela Ghisotti
Keyword(s):  
Oxidative Stress ◽  
Mycobacterium Tuberculosis ◽  
Transcriptional Regulation ◽  
Reverse Transcriptase ◽  
Reporter Gene ◽  
Mycobacterium Smegmatis ◽  
Northern Blotting ◽  
Terminal Part ◽  
Transcription Pattern

ABSTRACT The DNA region upstream of katG inMycobacterium smegmatis was cloned and sequenced. ThefurA gene, highly homologous to Mycobacterium tuberculosis furA, mapped in this region. ThefurA-katG organization appears to be conserved among several mycobacteria. The transcription pattern of furAand katG in M. smegmatisupon oxidative stress was analyzed by Northern blotting and primer extension. Although transcription of both furA andkatG was induced upon oxidative stress, transcripts covering both genes could not be identified either by Northern blotting or by reverse transcriptase PCR. Specific transcripts and 5′ ends were identified for furA and katG, respectively. By cloning M. smegmatis andM. tuberculosis DNA regions upstream of a reporter gene, we demonstrated the presence of two promoters,pfurA, located immediately upstream of thefurA gene, and pkatG, located within the terminal part of the furA coding sequence. Transcription from pfurA was induced upon oxidative stress. A 23-bp sequence overlapping the pfurA −35 region is highly conserved among mycobacteria and streptomycetes and might be involved in controlling pfurA activity. Transcription from a cloned pkatG, lacking the upstream pfurAregion, was not induced upon oxidative stress, suggesting acis-acting regulatory role of this region.

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