Journal articles: 'Staphylococcus aureus Metabolism'

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Stingley, Robin L., Wen Zou, Thomas M. Heinze, Huizhong Chen, and Carl E. Cerniglia. "Metabolism of azo dyes by human skin microbiota." Journal of Medical Microbiology 59, no. 1 (January 1, 2010): 108–14. http://dx.doi.org/10.1099/jmm.0.012617-0.

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Reduction of Methyl Red (MR) and Orange II (Or II) by 26 human skin bacterial species was monitored by a rapid spectrophotometric assay. The analysis indicated that skin bacteria, representing the genera Staphylococcus, Corynebacterium, Micrococcus, Dermacoccus and Kocuria, were able to reduce MR by 74–100 % in 24 h, with only three species unable to reduce completely the dye in that time. Among the species tested, only Corynebacterium xerosis was unable to reduce Or II to any degree by 24 h, and only Staphylococcus delphini, Staphylococcus sciuri subsp. sciuri and Pseudomonas aeruginosa were able to reduce completely this dye within 24 h. MR reduction started with early-exponential growth in Staphylococcus aureus and Staphylococcus epidermidis, and around late-exponential/early-stationary growth in P. aeruginosa. Reduction of Or II, Ponceau S and Ponceau BS started during late-exponential/early-stationary growth for all three species. Using liquid chromatography/electrospray ionization mass spectrometry analyses, MR metabolites produced by Staph. aureus, Staph. epidermidis and P. aeruginosa were identified as N,N-dimethyl-p-phenylenediamine and 2-aminobenzoic acid. Searches of available genomic and proteomic data revealed that at least four of the staphylococci in this study, Staphylococcus haemolyticus, Staph. epidermidis, Staphylococcus cohnii and Staphylococcus saprophyticus, have hypothetical genes with 77, 76, 75 and 74 % sequence identity to azo1 encoding an azoreductase from Staph. aureus and hypothetical proteins with 82, 80, 72 and 74 % identity to Azo1, respectively. In addition, Staphylococcus capitis has a protein with 79 % identity to Azo1. Western analysis detected proteins similar to Azo1 in all the staphylococci tested, except Staph. delphini, Staph. sciuri subsp. sciuri and Staphylococcus auricularis. The data presented in this report will be useful in the risk assessment process for evaluation of public exposure to products containing these dyes.

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Reniere, Michelle L., Victor J. Torres, and Eric P. Skaar. "Intracellular metalloporphyrin metabolism in Staphylococcus aureus." BioMetals 20, no. 3-4 (March 27, 2007): 333–45. http://dx.doi.org/10.1007/s10534-006-9032-0.

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Massilamany, Chandirasegaran, Arunakumar Gangaplara, Donald Gardner, David Steffen, Greg Somerville, and Jay Reddy. "TCA cycle inactivation in Staphylococcus aureus alters nitric oxide production in RAW 264.7 cells (56.21)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 56.21. http://dx.doi.org/10.4049/jimmunol.186.supp.56.21.

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Abstract Inactivation of the Staphylococcus aureus tricarboxylic acid (TCA) cycle delays the resolution of cutaneous ulcers in a mouse soft tissue infection model. In the present study, we observed that cutaneous lesions in mice infected with wild-type or isogenic aconitase mutant S. aureus strains contained comparable inflammatory infiltrates, suggesting the delayed resolution was independent of the recruitment of immune cells. These observations led us to hypothesize that staphylococcal metabolism can modulate the host immune response. Using an in vitro model system involving RAW 264.7 cells, we observed that cells cultured with S. aureus aconitase mutant strains produced significantly lower amounts of nitric oxide (NO) and an inducible nitric oxide synthase as compared to those cells exposed to wild-type bacteria. Despite the decrease in NO synthesis, the expression of antigen-presentation and costimulatory molecules was similar in cells cultured with wild-type and those cultured with aconitase mutant bacteria. The data suggest that staphylococci can evade innate immune responses and potentially enhance their ability to survive in infected hosts by altering their metabolism. This may also explain the occurrence of TCA cycle mutants in clinical S. aureus isolates.

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Tan, Xin, Mathieu Coureuil, Alain Charbit, and Anne Jamet. "Multitasking Actors of Staphylococcus aureus Metabolism and Virulence." Trends in Microbiology 28, no. 1 (January 2020): 6–9. http://dx.doi.org/10.1016/j.tim.2019.10.013.

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Krasnoselskyi, Mykola V., Elena S. Pushkar, Larisa I. Simonova-Pushkar, and Mykhailo S. Myroshnychenko. "NITRIC OXIDE METABOLISM FEATURES UNDER CONDITIONS OF EXPERIMENTAL INFECTED RADIATION-INDUCED SKIN INJURIES DEVELOPMENT AND THEIR TREATMENT WITH PHOTODYNAMIC THERAPY." Wiadomości Lekarskie 73, no. 8 (2020): 1655–58. http://dx.doi.org/10.36740/wlek202008112.

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The aim: To follow-up nitric oxide content values in rat serum at the development of Staphylococcus aureus infected radiation skin injuries and their photodynamic therapy. Materials and methods: Eighty WAG male rats were studied in an experiment. Four groups were identified for evaluation. Group 1 included unaffected intact rats (n=20). Group 2 involved rats (n=20) with a modeled radiation-induced ulcer of the skin. The rats (n=20) with a modeled radiation-induced skin ulcer followed by infecting with Staphylococcus aureus were referred to group 3. Group 4 included rats (n=20) with Staphylococcus aureus infected radiation skin ulcer exposed to photodynamic therapy. Rats of groups 1-4 were sampled for biochemical blood examination on days 7, 14, 21, 30 and 45. Total nitric oxide metabolites (nitrites and nitrates) were measured according to V.A. Metelskaya et al. method. Results: Infectious agent (Staphylococcus aureus) present in skin ulcer impairs nitric oxide metabolism in rat blood serum that manifested in decreased total nitric oxide metabolites content on day 7, followed by its increase within days 14 to 45. While photodynamic therapy exposed on the Staphylococcus aureus infected radiation skin ulcer, total nitric oxide metabolites in blood serum had increased by day 7, but days 14 to 45 level was compliant with physiological norm. Conclusions: Infecting radiation skin ulcers with Staphylococcus aureus causes impaired nitric oxide metabolism, while photodynamic therapy helps to normalize the metabolism of the above-mentioned chemical compound that can improve healing of radiation skin ulcers.

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Peng, Qi, Lu Guo, Yu Dong, Tingrui Bao, Huiyuan Wang, Tao Xu, Ying Zhang, and Jian Han. "PurN Is Involved in Antibiotic Tolerance and Virulence in Staphylococcus aureus." Antibiotics 11, no. 12 (November 25, 2022): 1702. http://dx.doi.org/10.3390/antibiotics11121702.

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Staphylococcus aureus can cause chronic infections which are closely related to persister formation. Purine metabolism is involved in S. aureus persister formation, and purN, encoding phosphoribosylglycinamide formyltransferase, is an important gene in the purine metabolism process. In this study, we generated a ΔpurN mutant of the S. aureus Newman strain and assessed its roles in antibiotic tolerance and virulence. The ΔpurN in the late exponential phase had a significant defect in persistence to antibiotics. Complementation of the ΔpurN restored its tolerance to different antibiotics. PurN significantly affected virulence gene expression, hemolytic ability, and biofilm formation in S. aureus. Moreover, the LD50 (3.28 × 1010 CFU/mL) of the ΔpurN for BALB/c mice was significantly higher than that of the parental strain (2.81 × 109 CFU/mL). Transcriptome analysis revealed that 58 genes that were involved in purine metabolism, alanine, aspartate, glutamate metabolism, and 2-oxocarboxylic acid metabolism, etc., were downregulated, while 24 genes involved in ABC transporter and transferase activity were upregulated in ΔpurN vs. parental strain. Protein-protein interaction network showed that there was a close relationship between PurN and GltB, and SaeRS. The study demonstrated that PurN participates in the formation of the late exponential phase S. aureus persisters via GltB and regulates its virulence by activating the SaeRS two-component system.

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Hammer, Neal D., and Eric P. Skaar. "The impact of metal sequestration on Staphylococcus aureus metabolism." Current Opinion in Microbiology 15, no. 1 (February 2012): 10–14. http://dx.doi.org/10.1016/j.mib.2011.11.004.

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Friedman, David B., Devin L. Stauff, Gleb Pishchany, Corbin W. Whitwell, Victor J. Torres, and Eric P. Skaar. "Staphylococcus aureus Redirects Central Metabolism to Increase Iron Availability." PLoS Pathogens 2, no. 8 (August 25, 2006): e87. http://dx.doi.org/10.1371/journal.ppat.0020087.

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Wong Fok Lung, Tania, and Alice Prince. "Consequences of Metabolic Interactions during Staphylococcus aureus Infection." Toxins 12, no. 9 (September 9, 2020): 581. http://dx.doi.org/10.3390/toxins12090581.

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Staphylococcus aureus is a metabolically flexible pathogen that causes infection in diverse settings. An array of virulence factors, including the secreted toxins, enables S. aureus to colonize different environmental niches and initiate infections by any of several discrete pathways. During these infections, both S. aureus and host cells compete with each other for nutrients and remodel their metabolism for survival. This metabolic interaction/crosstalk determines the outcome of the infection. The reprogramming of metabolic pathways in host immune cells not only generates adenosine triphosphate (ATP) to meet the cellular energy requirements during the infection process but also activates antimicrobial responses for eventual bacterial clearance, including cell death pathways. The selective pressure exerted by host immune cells leads to the emergence of bacterial mutants adapted for chronicity. These host-adapted mutants are often characterized by substantial changes in the expression of their own metabolic genes, or by mutations in genes involved in metabolism and biofilm formation. Host-adapted S. aureus can rewire or benefit from the metabolic activities of the immune cells via several mechanisms to cause persistent infection. In this review, we discuss how S. aureus activates host innate immune signaling, which results in an immune metabolic pressure that shapes S. aureus metabolic adaptation and determines the outcome of the infection.

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Riordan, James T., Arunachalam Muthaiyan, Wayne Van Voorhies, Christopher T. Price, James E. Graham, Brian J. Wilkinson, and John E. Gustafson. "Response of Staphylococcus aureus to Salicylate Challenge." Journal of Bacteriology 189, no. 1 (October 20, 2006): 220–27. http://dx.doi.org/10.1128/jb.01149-06.

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ABSTRACT Growth of Staphylococcus aureus with the nonsteroidal anti-inflammatory salicylate reduces susceptibility of the organism to multiple antimicrobials. Transcriptome analysis revealed that growth of S. aureus with salicylate leads to the induction of genes involved with gluconate and formate metabolism and represses genes required for gluconeogenesis and glycolysis. In addition, salicylate induction upregulates two antibiotic target genes and downregulates a multidrug efflux pump gene repressor (mgrA) and sarR, which represses a gene (sarA) important for intrinsic antimicrobial resistance. We hypothesize that these salicylate-induced alterations jointly represent a unique mechanism that allows S. aureus to resist antimicrobial stress and toxicity.

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Balibar, Carl J., Xiaoyu Shen, and Jianshi Tao. "The Mevalonate Pathway of Staphylococcus aureus." Journal of Bacteriology 191, no. 3 (November 21, 2008): 851–61. http://dx.doi.org/10.1128/jb.01357-08.

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ABSTRACT Isoprenoids are a class of ubiquitous organic molecules synthesized from the five-carbon starter unit isopentenyl pyrophosphate (IPP). Comprising more than 30,000 known natural products, isoprenoids serve various important biological functions in many organisms. In bacteria, undecaprenyl pyrophosphate is absolutely required for the formation of cell wall peptidoglycan and other cell surface structures, while ubiquinones and menaquinones, both containing an essential prenyl moiety, are key electron carriers in respiratory energy generation. There is scant knowledge on the nature and regulation of bacterial isoprenoid pathways. In order to explore the cellular responses to perturbations in the mevalonate pathway, responsible for producing the isoprenoid precursor IPP in many gram-positive bacteria and eukaryotes, we constructed three strains of Staphylococcus aureus in which each of the mevalonate pathway genes is regulated by an IPTG (isopropyl-β-d-thiogalactopyranoside)-inducible promoter. We used DNA microarrays to profile the transcriptional effects of downregulating the components of the mevalonate pathway in S. aureus and demonstrate that decreased expression of the mevalonate pathway leads to widespread downregulation of primary metabolism genes, an upregulation in virulence factors and cell wall biosynthetic determinants, and surprisingly little compensatory expression in other isoprenoid biosynthetic genes. We subsequently correlate these transcriptional changes with downstream metabolic consequences.

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Rajkarnikar, Arishma, Andrew Strankman, Shayla Duran, Derek Vargas, Alexandra A. Roberts, Kathryn Barretto, Heather Upton, Christopher J. Hamilton, and Mamta Rawat. "Analysis of mutants disrupted in bacillithiol metabolism in Staphylococcus aureus." Biochemical and Biophysical Research Communications 436, no. 2 (June 2013): 128–33. http://dx.doi.org/10.1016/j.bbrc.2013.04.027.

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Chang, Wook, David A. Small, Freshteh Toghrol, and William E. Bentley. "Global Transcriptome Analysis of Staphylococcus aureus Response to Hydrogen Peroxide." Journal of Bacteriology 188, no. 4 (February 15, 2006): 1648–59. http://dx.doi.org/10.1128/jb.188.4.1648-1659.2006.

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ABSTRACT Staphylococcus aureus responds with protective strategies against phagocyte-derived reactive oxidants to infect humans. Herein, we report the transcriptome analysis of the cellular response of S. aureus to hydrogen peroxide-induced oxidative stress. The data indicate that the oxidative response includes the induction of genes involved in virulence, DNA repair, and notably, anaerobic metabolism.

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Even, Sergine, Cathy Charlier, Sébastien Nouaille, Nouri L. Ben Zakour, Marina Cretenet, Fabien J. Cousin, Michel Gautier, Muriel Cocaign-Bousquet, Pascal Loubière, and Yves Le Loir. "Staphylococcus aureus Virulence Expression Is Impaired by Lactococcus lactis in Mixed Cultures." Applied and Environmental Microbiology 75, no. 13 (May 8, 2009): 4459–72. http://dx.doi.org/10.1128/aem.02388-08.

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ABSTRACT Staphylococcus aureus is responsible for numerous food poisonings due to the production of enterotoxins by strains contaminating foodstuffs, especially dairy products. Several parameters, including interaction with antagonistic flora such as Lactococcus lactis, a lactic acid bacterium widely used in the dairy industry, can modulate S. aureus proliferation and virulence expression. We developed a dedicated S. aureus microarray to investigate the effect of L. lactis on staphylococcal gene expression in mixed cultures. This microarray was used to establish the transcriptomic profile of S. aureus in mixed cultures with L. lactis in a chemically defined medium held at a constant pH (6.6). Under these conditions, L. lactis hardly affected S. aureus growth. The expression of most genes involved in the cellular machinery, carbohydrate and nitrogen metabolism, and stress responses was only slightly modulated: a short time lag in mixed compared to pure cultures was observed. Interestingly, the induction of several virulence factors and regulators, including the agr locus, sarA, and some enterotoxins, was strongly affected. This work clearly underlines the complexity of L. lactis antagonistic potential for S. aureus and yields promising leads for investigations into nonantibiotic biocontrol of this major pathogen.

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Tarrant, Emma, Gustavo P. Riboldi, Matthew R. McIlvin, Jack Stevenson, Anna Barwinska-Sendra, Louisa J. Stewart, Mak A. Saito, and Kevin J. Waldron. "Copper stress in Staphylococcus aureus leads to adaptive changes in central carbon metabolism." Metallomics 11, no. 1 (2019): 183–200. http://dx.doi.org/10.1039/c8mt00239h.

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Pathogenic Staphylococcus aureus respond to copper stress by altering central carbon metabolism in response to a specific inhibition of the glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase.

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Mellergaard, Maiken, Rikke Illum Høgh, Astrid Lund, Blanca Irene Aldana, Romain Guérillot, Sofie Hedlund Møller, Ashleigh S. Hayes, et al. "Staphylococcus aureus induces cell-surface expression of immune stimulatory NKG2D ligands on human monocytes." Journal of Biological Chemistry 295, no. 33 (June 30, 2020): 11803–21. http://dx.doi.org/10.1074/jbc.ra120.012673.

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Staphylococcus aureus is among the leading causes of bacterial infections worldwide. The pathogenicity and establishment of S. aureus infections are tightly linked to its ability to modulate host immunity. Persistent infections are often associated with mutant staphylococcal strains that have decreased susceptibility to antibiotics; however, little is known about how these mutations influence bacterial interaction with the host immune system. Here, we discovered that clinical S. aureus isolates activate human monocytes, leading to cell-surface expression of immune stimulatory natural killer group 2D (NKG2D) ligands on the monocytes. We found that expression of the NKG2D ligand ULBP2 (UL16-binding protein 2) is associated with bacterial degradability and phagolysosomal activity. Moreover, S. aureus–induced ULBP2 expression was linked to altered host cell metabolism, including increased cytoplasmic (iso)citrate levels, reduced glycolytic flux, and functional mitochondrial activity. Interestingly, we found that the ability of S. aureus to induce ULBP2 and proinflammatory cytokines in human monocytes depends on a functional ClpP protease in S. aureus. These findings indicate that S. aureus activates ULBP2 in human monocytes through immunometabolic mechanisms and reveal that clpP inactivation may function as a potential immune evasion mechanism. Our results provide critical insight into the interplay between the host immune system and S. aureus that has evolved under the dual selective pressure of host immune responses and antibiotic treatment. Our discovery of an immune stimulatory pathway consisting of human monocyte-based defense against S. aureus suggests that targeting the NKG2D pathway holds potential for managing persistent staphylococcal infections.

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Reiß, Swantje, Jan Pané-Farré, Stephan Fuchs, Patrice François, Manuel Liebeke, Jacques Schrenzel, Ulrike Lindequist, et al. "Global Analysis of the Staphylococcus aureus Response to Mupirocin." Antimicrobial Agents and Chemotherapy 56, no. 2 (November 21, 2011): 787–804. http://dx.doi.org/10.1128/aac.05363-11.

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ABSTRACTIn the present study, we analyzed the response ofS. aureusto mupirocin, the drug of choice for nasal decolonization. Mupirocin selectively inhibits the bacterial isoleucyl-tRNA synthetase (IleRS), leading to the accumulation of uncharged isoleucyl-tRNA and eventually the synthesis of (p)ppGpp. The alarmone (p)ppGpp induces the stringent response, an important global transcriptional and translational control mechanism that allows bacteria to adapt to nutritional deprivation. To identify proteins with an altered synthesis pattern in response to mupirocin treatment, we used the highly sensitive 2-dimensional gel electrophoresis technique in combination with mass spectrometry. The results were complemented by DNA microarray, Northern blot, and metabolome analyses. Whereas expression of genes involved in nucleotide biosynthesis, DNA metabolism, energy metabolism, and translation was significantly downregulated, expression of isoleucyl-tRNA synthetase, the branched-chain amino acid pathway, and genes with functions in oxidative-stress resistance (ahpCandkatA) and putative roles in stress protection (theyvyDhomologueSACOL0815andSACOL1759andSACOL2131) and transport processes was increased. A comparison of the regulated genes to known regulons suggests the involvement of the global regulators CodY and SigB in shaping the response ofS. aureusto mupirocin. Of particular interest was the induced transcription of genes encoding virulence-associated regulators (i.e.,arlRS,saeRS,sarA,sarR,sarS, andsigB), as well as genes directly involved in the virulence ofS. aureus(i.e.,fnbA,epiE,epiG, andseb).

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Baba, Tadashi, Kyoko Kuwahara-Arai, Ikuo Uchiyama, Fumihiko Takeuchi, Teruyo Ito, and Keiichi Hiramatsu. "Complete Genome Sequence of Macrococcus caseolyticus Strain JSCS5402, Reflecting the Ancestral Genome of the Human-Pathogenic Staphylococci." Journal of Bacteriology 191, no. 4 (December 12, 2008): 1180–90. http://dx.doi.org/10.1128/jb.01058-08.

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ABSTRACT We isolated the methicillin-resistant Macrococcus caseolyticus strain JCSC5402 from animal meat in a supermarket and determined its whole-genome nucleotide sequence. This is the first report on the genome analysis of a macrococcal species that is evolutionarily closely related to the human pathogens Staphylococcus aureus and Bacillus anthracis. The essential biological pathways of M. caseolyticus are similar to those of staphylococci. However, the species has a small chromosome (2.1 MB) and lacks many sugar and amino acid metabolism pathways and a plethora of virulence genes that are present in S. aureus. On the other hand, M. caseolyticus possesses a series of oxidative phosphorylation machineries that are closely related to those in the family Bacillaceae. We also discovered a probable primordial form of a Macrococcus methicillin resistance gene complex, mecIRAm , on one of the eight plasmids harbored by the M. caseolyticus strain. This is the first finding of a plasmid-encoding methicillin resistance gene. Macrococcus is considered to reflect the genome of ancestral bacteria before the speciation of staphylococcal species and may be closely associated with the origin of the methicillin resistance gene complex of the notorious human pathogen methicillin-resistant S. aureus.

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Choueiry, Fouad, Rui Xu, and Jiangjiang Zhu. "Adaptive Metabolism of Staphylococcus aureus Revealed by Untargeted Metabolomics." Journal of Proteome Research 21, no. 2 (January 19, 2022): 470–81. http://dx.doi.org/10.1021/acs.jproteome.1c00797.

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Weiss, Andy, Renee M. Fleeman, and Lindsey N. Shaw. "Exposing the Unique Connection between Metabolism and Virulence in Staphylococcus aureus." Cell Chemical Biology 23, no. 11 (November 2016): 1317–19. http://dx.doi.org/10.1016/j.chembiol.2016.11.003.

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Pätzold, Linda, Anne-Christine Brausch, Evelyn-Laura Bielefeld, Lisa Zimmer, Greg A. Somerville, Markus Bischoff, and Rosmarie Gaupp. "Impact of the Histidine-Containing Phosphocarrier Protein HPr on Carbon Metabolism and Virulence in Staphylococcus aureus." Microorganisms 9, no. 3 (February 24, 2021): 466. http://dx.doi.org/10.3390/microorganisms9030466.

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Carbon catabolite repression (CCR) is a common mechanism pathogenic bacteria use to link central metabolism with virulence factor synthesis. In gram-positive bacteria, catabolite control protein A (CcpA) and the histidine-containing phosphocarrier protein HPr (encoded by ptsH) are the predominant mediators of CCR. In addition to modulating CcpA activity, HPr is essential for glucose import via the phosphotransferase system. While the regulatory functions of CcpA in Staphylococcus aureus are largely known, little is known about the function of HPr in CCR and infectivity. To address this knowledge gap, ptsH mutants were created in S. aureus that either lack the open reading frame or harbor a ptsH variant carrying a thymidine to guanosine mutation at position 136, and the effects of these mutations on growth and metabolism were assessed. Inactivation of ptsH altered bacterial physiology and decreased the ability of S. aureus to form a biofilm and cause infections in mice. These data demonstrate that HPr affects central metabolism and virulence in S. aureus independent of its influence on CcpA regulation.

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Nouaille, Sébastien, Sergine Even, Cathy Charlier, Yves Le Loir, Muriel Cocaign-Bousquet, and Pascal Loubière. "Transcriptomic Response of Lactococcus lactis in Mixed Culture with Staphylococcus aureus." Applied and Environmental Microbiology 75, no. 13 (May 8, 2009): 4473–82. http://dx.doi.org/10.1128/aem.02653-08.

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ABSTRACT The mechanisms of interaction between Lactococcus lactis and the food pathogen Staphylococcus aureus are of crucial importance, as one major role of lactic acid bacteria (LAB) in fermented foods is to inhibit undesirable and pathogenic flora. It was never questioned if the presence of a pathogen can actively modify the gene expression patterns of LAB in a shared environment. In this study, transcriptome and biochemical analyses were combined to assess the dynamic response of L. lactis in a mixed culture with S. aureus. The presence of S. aureus hardly affected the growth of L. lactis but dramatically modified its gene expression profile. The main effect was related to earlier carbon limitation and a concomitantly lower growth rate in the mixed culture due to the consumption of glucose by both species. More specific responses involved diverse cellular functions. Genes associated with amino acid metabolism, ion transport, oxygen response, menaquinone metabolism, and cell surface and phage expression were differentially expressed in the mixed culture. This study led to new insights into possible mechanisms of interaction between L. lactis and S. aureus. Moreover, new and unexpected effects of L. lactis on the virulence of S. aureus were discovered, as described elsewhere (S. Even, C. Charlier, S. Nouaille, N. L. Ben Zakour, M. Cretenet, F. J. Cousin, M. Gautier, M. Cocaign-Bousquet, P. Loubière, and Y. Le Loir, Appl. Environ. Microbiol. 75:4459-4472, 2009).

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Sieradzki, Krzysztof, and Alexander Tomasz. "Gradual Alterations in Cell Wall Structure and Metabolism in Vancomycin-Resistant Mutants ofStaphylococcus aureus." Journal of Bacteriology 181, no. 24 (December 15, 1999): 7566–70. http://dx.doi.org/10.1128/jb.181.24.7566-7570.1999.

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ABSTRACT In five vancomycin-resistant laboratory step mutants selected from the highly and homogeneously methicillin-resistant Staphylococcus aureus strain COL (MIC of methicillin, 800 μg/ml; MIC of vancomycin, 1.5 μg/ml), the gradually increasing levels of resistance to vancomycin were accompanied by parallel decreases in the levels of methicillin resistance and abnormalities in cell wall metabolism. The latter included a gradual reduction in the proportion of highly cross-linked muropeptide species in peptidoglycan, down-regulation of the production of penicillin-binding protein 2A (PBP2A) and PBP4, and hypersensitivity to β-lactam antibiotics each with a relatively selective affinity for the various staphylococcal PBPs; the PBP2-specific inhibitor ceftizoxime was particularly effective.

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Pouget, Cassandra, Claude-Alexandre Gustave, Christelle Ngba-Essebe, Frédéric Laurent, Emmanuel Lemichez, Anne Tristan, Albert Sotto, Catherine Dunyach-Rémy, and Jean-Philippe Lavigne. "Adaptation of Staphylococcus aureus in a Medium Mimicking a Diabetic Foot Environment." Toxins 13, no. 3 (March 22, 2021): 230. http://dx.doi.org/10.3390/toxins13030230.

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Staphylococcus aureus is the most prevalent pathogen isolated from diabetic foot infections (DFIs). The purpose of this study was to evaluate its behavior in an in vitro model mimicking the conditions encountered in DFI. Four clinical S. aureus strains were cultivated for 16 weeks in a specific environment based on the wound-like medium biofilm model. The adaptation of isolates was evaluated as follows: by Caenorhabditis elegans model (to evaluate virulence); by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) (to evaluate expression of the main virulence genes); and by Biofilm Ring test® (to assess the biofilm formation). After 16 weeks, the four S. aureus had adapted their metabolism, with the development of small colony variants and the loss of β-hemolysin expression. The in vivo nematode model suggested a decrease of virulence, confirmed by qRT-PCRs, showing a significant decrease of expression of the main staphylococcal virulence genes tested, notably the toxin-encoding genes. An increased expression of genes involved in adhesion and biofilm was noted. Our data based on an in vitro model confirm the impact of environment on the adaptation switch of S. aureus to prolonged stress environmental conditions. These results contribute to explore and characterize the virulence of S. aureus in chronic wounds.

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Lamichhane-Khadka, Reena, Santosh Dulal, Jesus A. Cuaron, Richard Pfeltz, Sushim Kumar Gupta, Brian J. Wilkinson, and John E. Gustafson. "Apt (Adenine Phosphoribosyltransferase) Mutation in Laboratory-Selected Vancomycin-Intermediate Staphylococcus aureus." Antibiotics 10, no. 5 (May 14, 2021): 583. http://dx.doi.org/10.3390/antibiotics10050583.

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Comparative genomic sequencing of laboratory-derived vancomycin-intermediate Staphylococcusaureus (VISA) (MM66-3 and MM66-4) revealed unique mutations in both MM66-3 (in apt and ssaA6), and MM66-4 (in apt and walK), compared to hetero-VISA parent strain MM66. Transcriptional profiling revealed that both MM66 VISA shared 79 upregulated genes and eight downregulated genes. Of these, 30.4% of the upregulated genes were associated with the cell envelope, whereas 75% of the downregulated genes were associated with virulence. In concordance with mutations and transcriptome alterations, both VISA strains demonstrated reduced autolysis, reduced growth in the presence of salt and reduced virulence factor activity. In addition to mutations in genes linked to cell wall metabolism (ssaA6 and walK), the same mutation in apt which encodes adenine phosphoribosyltransferase, was confirmed in both MM66 VISA. Apt plays a role in both adenine metabolism and accumulation and both MM66 VISA grew better than MM66 in the presence of adenine or 2-fluoroadenine indicating a reduction in the accumulation of these growth inhibiting compounds in the VISA strains. MM66 apt mutants isolated via 2-fluoroadenine selection also demonstrated reduced susceptibility to the cell wall lytic dye Congo red and vancomycin. Finding that apt mutations contribute to reduced vancomycin susceptibility once again suggests a role for altered purine metabolism in a VISA mechanism.

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Qazi, S. N. A., S. E. Harrison, T. Self, P. Williams, and P. J. Hill. "Real-Time Monitoring of Intracellular Staphylococcus aureus Replication." Journal of Bacteriology 186, no. 4 (February 15, 2004): 1065–77. http://dx.doi.org/10.1128/jb.186.4.1065-1077.2004.

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ABSTRACT A high-throughput system to rapidly assess the intracellular replication of Staphylococcus aureus has been developed utilizing S. aureus transformed with a dual gfp-luxABCDE reporter operon under the control of a growth-dependent promoter. Replication of tagged bacteria internalized into bovine mammary epithelial cells (MAC-T) could be measured by monitoring fluorescence and bioluminescence from the reporter operon following removal of extracellular bacteria from the plates. Bacterial replication inside cells was confirmed by a novel ex vivo time-lapse confocal microscopic method. This assay of bacterial replication was used to evaluate the efficacy of antibiotics which are commonly used to treat staphylococcal infections. Not all antibiotics tested were able to prevent intracellular replication of S. aureus and some were ineffective at preventing replication of intracellular bacteria at concentrations above the MIC determined for bacteria in broth culture. Comparison of the fluorescence and bioluminescence signals from the bacteria enabled effects on protein synthesis and metabolism to be discriminated and gave information on the entry of compounds into the eukaryotic cell, even if bacterial replication was not prevented. Elevated resistance of S. aureus to antibiotics inside host cells increases the likelihood of selecting S. aureus strains which are resistant to commonly used antimicrobial agents within the intracellular niche. The approach presented directly assesses intracellular efficacy of antibiotics and provides an evidence-based approach to antibiotic selection for prescribing physicians and medical microbiologists.

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Richter, Katharina, Freija Van den Driessche, and Tom Coenye. "Innovative approaches to treat Staphylococcus aureus biofilm-related infections." Essays in Biochemistry 61, no. 1 (February 28, 2017): 61–70. http://dx.doi.org/10.1042/ebc20160056.

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Many bacterial infections in humans and animals are caused by bacteria residing in biofilms, complex communities of attached organisms embedded in an extracellular matrix. One of the key properties of microorganisms residing in a biofilm is decreased susceptibility towards antimicrobial agents. This decreased susceptibility, together with conventional mechanisms leading to antimicrobial resistance, makes biofilm-related infections increasingly difficult to treat and alternative antibiofilm strategies are urgently required. In this review, we present three such strategies to combat biofilm-related infections with the important human pathogen Staphylococcus aureus: (i) targeting the bacterial communication system with quorum sensing (QS) inhibitors, (ii) a ‘Trojan Horse’ strategy to disturb iron metabolism by using gallium-based therapeutics and (iii) the use of ‘non-antibiotics’ with antibiofilm activity identified through screening of repurposing libraries.

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Zhang, Bingyan, Jiayi Xu, Xiaoqi He, Yigang Tong, and Huiying Ren. "Interactions between Jumbo Phage SA1 and Staphylococcus: A Global Transcriptomic Analysis." Microorganisms 10, no. 8 (August 7, 2022): 1590. http://dx.doi.org/10.3390/microorganisms10081590.

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Staphylococcus aureus (S. aureus) is an important zoonotic pathogen that poses a serious health concern to humans and cattle worldwide. Although it has been proven that lytic phages may successfully kill S. aureus, the interaction between the host and the phage has yet to be thoroughly investigated, which will likely limit the clinical application of phage. Here, RNA sequencing (RNA-seq) was used to examine the transcriptomics of jumbo phage SA1 and Staphylococcus JTB1-3 during a high multiplicity of infection (MOI) and RT-qPCR was used to confirm the results. The RNA-seq analysis revealed that phage SA1 took over the transcriptional resources of the host cells and that the genes were categorized as early, middle, and late, based on the expression levels during infection. A minor portion of the resources of the host was employed to enable phage replication after infection because only 35.73% (997/2790) of the host genes were identified as differentially expressed genes (DEGs). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses showed that the phage infection mainly affected the nucleotide metabolism, protein metabolism, and energy-related metabolism of the host. Moreover, the expression of the host genes involved in anti-phage systems, virulence, and drug resistance significantly changed during infection. This research gives a fresh understanding of the relationship between jumbo phages and their Gram-positive bacteria hosts and provides a reference for studying phage treatment and antibiotics.

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Turner, Mark S., Raquel Lo, and Philip M. Giffard. "Inhibition of Staphylococcus aureus Growth on Tellurite-Containing Media by Lactobacillus reuteri Is Dependent on CyuC and Thiol Production." Applied and Environmental Microbiology 73, no. 3 (December 1, 2006): 1005–9. http://dx.doi.org/10.1128/aem.02100-06.

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ABSTRACT Lactobacillus reuteri inhibits Staphylococcus aureus growth on Baird-Parker agar. This activity required the presence of tellurite and was not shared with other lactic acid bacteria or an L. reuteri mutant defective in cystine metabolism. Secreted products generated from L. reuteri cystine metabolism and thiols were shown to augment tellurite toxicity.

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Frank, Matthew W., Sarah G. Whaley, and Charles O. Rock. "Branched-chain amino acid metabolism controls membrane phospholipid structure in Staphylococcus aureus." Journal of Biological Chemistry 297, no. 5 (November 2021): 101255. http://dx.doi.org/10.1016/j.jbc.2021.101255.

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Patel, Jimmy S., Javiera Norambuena, Hassan Al-Tameemi, Yong-Mo Ahn, Alexander L. Perryman, Xin Wang, Samer S. Daher, et al. "Bayesian Modeling and Intrabacterial Drug Metabolism Applied to Drug-Resistant Staphylococcus aureus." ACS Infectious Diseases 7, no. 8 (August 3, 2021): 2508–21. http://dx.doi.org/10.1021/acsinfecdis.1c00265.

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Lu, K., B. Pedersen, R. La Rosa, H. Krogh-Johansen, B. Conlon, and M. Muhlebach. "503 Bacterial characteristics and metabolism of persistent methicillin-resistant Staphylococcus aureus infection." Journal of Cystic Fibrosis 21 (October 2022): S284. http://dx.doi.org/10.1016/s1569-1993(22)01193-6.

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Henze, U., T. Sidow, J. Wecke, H. Labischinski, and B. Berger-Bächi. "Influence of femB on methicillin resistance and peptidoglycan metabolism in Staphylococcus aureus." Journal of Bacteriology 175, no. 6 (1993): 1612–20. http://dx.doi.org/10.1128/jb.175.6.1612-1620.1993.

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Ledala, N., B. Zhang, J. Seravalli, R. Powers, and G. A. Somerville. "Influence of Iron and Aeration on Staphylococcus aureus Growth, Metabolism, and Transcription." Journal of Bacteriology 196, no. 12 (April 4, 2014): 2178–89. http://dx.doi.org/10.1128/jb.01475-14.

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An, Jeongshin, Hyungju Kwon, Woosung Lim, and Byung-In Moon. "Staphylococcus aureus-Derived Extracellular Vesicles Enhance the Efficacy of Endocrine Therapy in Breast Cancer Cells." Journal of Clinical Medicine 11, no. 7 (April 5, 2022): 2030. http://dx.doi.org/10.3390/jcm11072030.

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The microbiome involved in the human estrogen metabolism is known as the estrobolome. This study aimed to show that the estrobolome can be used in breast cancer treatment. We first analyzed the blood microbiome composition of healthy controls and patients with breast cancer. In particular, we investigated the bacteria producing β−glucuronidase and/or β−galactosidase, which are involved in estrogen metabolism in the human body. Staphylococcus species were more abundant in healthy controls than in breast cancer patients and therefore were selected for further analyses. The effect of Staphylococcus aureus on endocrine therapy was analyzed by a combination treatment with tamoxifen. Analysis of the microbiome of blood samples showed that species producing β−glucuronidase were more abundant in breast cancer patients than in healthy controls. Further experiments confirmed that the efficacy of tamoxifen increased when administered in conjugation with the extracellular vesicles (EVs) of S. aureus. Based on our results, we deduced that S. aureus EVs could potentially be used as adjuvants for breast cancer treatment in the future.

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Pohl, Konstanze, Patrice Francois, Ludwig Stenz, Frank Schlink, Tobias Geiger, Silvia Herbert, Christiane Goerke, Jacques Schrenzel, and Christiane Wolz. "CodY in Staphylococcus aureus: a Regulatory Link between Metabolism and Virulence Gene Expression." Journal of Bacteriology 191, no. 9 (February 27, 2009): 2953–63. http://dx.doi.org/10.1128/jb.01492-08.

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ABSTRACT The repressor CodY is reported to inhibit metabolic genes mainly involved in nitrogen metabolism. We analyzed codY mutants from three unrelated Staphylococcus aureus strains (Newman, UAMS-1, and RN1HG). The mutants grew more slowly than their parent strains in a chemically defined medium. However, only codY mutants were able to grow in medium lacking threonine. An excess of isoleucine resulted in growth inhibition in the wild type but not in the codY mutants, indicating that isoleucine plays a role in CodY-dependent repression. Prototypic CodY-repressed genes including the virulence regulator agr are repressed after up-shift with isoleucine. The CodY-dependent repression of agr is consistent with the concomitant influence of CodY on typical agr-regulated genes such as cap, spa, fnbA, and coa. However, some of these virulence genes (e.g., cap, fnbA, and spa) were also regulated by CodY in an agr-negative background. Microarray analysis revealed that the large majority of CodY-repressed genes were involved in amino acid metabolism; CodY-activated genes were mainly involved in nucleotide metabolism or virulence. In summary, CodY in S. aureus not only acts as a repressor for genes involved in nitrogen metabolism but also contributes to virulence gene regulation by supporting as well as substituting for agr function.

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Jenkins, Carrie L., and Heather D. Bean. "Dependence of the Staphylococcal Volatilome Composition on Microbial Nutrition." Metabolites 10, no. 9 (August 27, 2020): 347. http://dx.doi.org/10.3390/metabo10090347.

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In vitro cultivation of staphylococci is fundamental to both clinical and research microbiology, but few studies, to-date, have investigated how the differences in rich media can influence the volatilome of cultivated bacteria. The objective of this study was to determine the influence of rich media composition on the chemical characteristics of the volatilomes of Staphylococcus aureus and Staphylococcus epidermidis. S. aureus (ATCC 12600) and S. epidermidis (ATCC 12228) were cultured in triplicate in four rich complex media (brain heart infusion (BHI), lysogeny broth (LB), Mueller Hinton broth (MHB), and tryptic soy broth (TSB)), and the volatile metabolites produced by each culture were analyzed using headspace solid-phase microextraction combined with comprehensive two-dimensional gas chromatography—time-of-flight mass spectrometry (HS-SPME-GC×GC-TOFMS). When comparing the chemical compositions of the staph volatilomes by the presence versus absence of volatiles produced in each medium, we observed few differences. However, when the relative abundances of volatiles were included in the analyses, we observed that culturing staph in media containing free glucose (BHI and TSB) resulted in volatilomes dominated by acids and esters (67%). The low-glucose media (LB and MHB) produced ketones in greatest relative abundances, but the volatilome compositions in these two media were highly dissimilar. We conclude that the staphylococcal volatilome is strongly influenced by the nutritional composition of the growth medium, especially the availability of free glucose, which is much more evident when the relative abundances of the volatiles are analyzed, compared to the presence versus absence.

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Grosser, Melinda R., Andy Weiss, Lindsey N. Shaw, and Anthony R. Richardson. "Regulatory Requirements for Staphylococcus aureus Nitric Oxide Resistance." Journal of Bacteriology 198, no. 15 (May 16, 2016): 2043–55. http://dx.doi.org/10.1128/jb.00229-16.

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ABSTRACTThe ability ofStaphylococcus aureusto resist host innate immunity augments the severity and pervasiveness of its pathogenesis. Nitric oxide (NO˙) is an innate immune radical that is critical for the efficient clearance of a wide range of microbial pathogens. Exposure of microbes to NO˙ typically results in growth inhibition and induction of stress regulons.S. aureus, however, induces a metabolic state in response to NO˙ that allows for continued replication and precludes stress regulon induction. The regulatory factors mediating this distinctive response remain largely undefined. Here, we employ a targeted transposon screen and transcriptomics to identify and characterize five regulons essential for NO˙ resistance inS. aureus: three virulence regulons not formerly associated with NO˙ resistance, SarA, CodY, and Rot, as well as two regulons with established roles, Fur and SrrAB. We provide new insights into the contributions of Fur and SrrAB during NO˙ stress and show that theS. aureusΔsarAmutant, the most sensitive of the newly identified mutants, exhibits metabolic dysfunction and widespread transcriptional dysregulation following NO˙ exposure. Altogether, our results broadly characterize the regulatory requirements for NO˙ resistance inS. aureusand suggest an intriguing overlap between the regulation of NO˙ resistance and virulence in this well-adapted human pathogen.IMPORTANCEThe prolific human pathogenStaphylococcus aureusis uniquely capable of resisting the antimicrobial radical nitric oxide (NO˙), a crucial component of the innate immune response. However, a complete understanding of howS. aureusregulates an effective response to NO˙ is lacking. Here, we implicate three central virulence regulators, SarA, CodY, and Rot, as major players in theS. aureusNO˙ response. Additionally, we elaborate on the contribution of two regulators, SrrAB and Fur, already known to play a crucial role inS. aureusNO˙ resistance. Our study sheds light on a unique facet ofS. aureuspathogenicity and demonstrates that the transcriptional response ofS. aureusto NO˙ is highly pleiotropic and intrinsically tied to metabolism and virulence regulation.

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Wu, Shizhou, Junqi Zhang, Qi Peng, Yunjie Liu, Lei Lei, and Hui Zhang. "The Role of Staphylococcus aureus YycFG in Gene Regulation, Biofilm Organization and Drug Resistance." Antibiotics 10, no. 12 (December 19, 2021): 1555. http://dx.doi.org/10.3390/antibiotics10121555.

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Antibiotic resistance is a serious global health concern that may have significant social and financial consequences. Methicillin-resistant Staphylococcus aureus (MRSA) infection is responsible for substantial morbidity and leads to the death of 21.8% of infected patients annually. A lack of novel antibiotics has prompted the exploration of therapies targeting bacterial virulence mechanisms. The two-component signal transduction system (TCS) enables microbial cells to regulate gene expression and the subsequent metabolic processes that occur due to environmental changes. The YycFG TCS in S. aureus is essential for bacterial viability, the regulation of cell membrane metabolism, cell wall synthesis and biofilm formation. However, the role of YycFG-associated biofilm organization in S. aureus antimicrobial drug resistance and gene regulation has not been discussed in detail. We reviewed the main molecules involved in YycFG-associated cell wall biosynthesis, biofilm development and polysaccharide intercellular adhesin (PIA) accumulation. Two YycFG-associated regulatory mechanisms, accessory gene regulator (agr) and staphylococcal accessory regulator (SarA), were also discussed. We highlighted the importance of biofilm formation in the development of antimicrobial drug resistance in S. aureus infections. Data revealed that inhibition of the YycFG pathway reduced PIA production, biofilm formation and bacterial pathogenicity, which provides a potential target for the management of MRSA-induced infections.

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Bischoff, Markus, Paul Dunman, Jan Kormanec, Daphne Macapagal, Ellen Murphy, William Mounts, Brigitte Berger-Bächi, and Steven Projan. "Microarray-Based Analysis of the Staphylococcus aureus σB Regulon." Journal of Bacteriology 186, no. 13 (July 1, 2004): 4085–99. http://dx.doi.org/10.1128/jb.186.13.4085-4099.2004.

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ABSTRACT Microarray-based analysis of the transcriptional profiles of the genetically distinct Staphylococcus aureus strains COL, GP268, and Newman indicate that a total of 251 open reading frames (ORFs) are influenced by σB activity. While σB was found to positively control 198 genes by a factor of ≥2 in at least two of the three genetic lineages analyzed, 53 ORFs were repressed in the presence of σB. Gene products that were found to be influenced by σB are putatively involved in all manner of cellular processes, including cell envelope biosynthesis and turnover, intermediary metabolism, and signaling pathways. Most of the genes and/or operons identified as upregulated by σB were preceded by a nucleotide sequence that resembled the σB consensus promoter sequence of Bacillus subtilis. A conspicuous number of virulence-associated genes were identified as regulated by σB activity, with many adhesins upregulated and prominently represented in this group, while transcription of various exoproteins and toxins were repressed. The data presented here suggest that the σB of S. aureus controls a large regulon and is an important modulator of virulence gene expression that is likely to act conversely to RNAIII, the effector molecule of the agr locus. We propose that this alternative transcription factor may be of importance for the invading pathogen to fine-tune its virulence factor production in response to changing host environments.

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Kluthe, Kennedy Elizabeth, Trevor Daubert, Alexis Page, Kim Carlson, and Austin Nuxoll. "Investigating Staphylococcus aureus tolerance to innate immunity." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 156.28. http://dx.doi.org/10.4049/jimmunol.204.supp.156.28.

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Abstract S. aureus accounts for approximately 80,000 infections every year, resulting in 11,000 deaths. While antibiotic resistance has been researched heavily, antibiotic tolerance has not. Persister cells are dormant like cells that are tolerant to antibiotic treatment. Persister cells could be the cause of many chronic and relapsing infections. Recent experiments have shown central metabolism is a critical component of persister cell formation. Results suggest that interruptions in the tricarboxylic acid (TCA) cycle increase persister cell formation. While many studies have been performed concerning the mechanism of formation of persister cells, few have been done to analyze how persister cells react in in vivo models or against aspects of the innate immune system. Antimicrobial peptides (AMPs) are a key component of the innate immune system. Challenging wild type S. aureus with AMPs, LL-37 and hBD-3, showed several logs of killing. Interruption of the TCA cycle (fumC) resulted in 100-fold more surviving cells compared to wild type. Following infection in Drosophila melanogaster, the fumC knockout exhibited increased survival. Furthermore, D. melanogaster that were infected with fumC had reduced survival. Interruption of the TCA cycle also led to increased survival within a macrophage suggesting persister cells represent a multifaceted problem for the immune system. These data suggest that persisters not only present a challenge during antimicrobial therapy but also for the innate immune system.

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Lin, Yuqi, Li Huang, Xiaoyong Zhang, Jiajia Yang, Xiaodan Chen, Fengming Li, Jun Liu, and Riming Huang. "Multi-Omics Analysis Reveals Anti-Staphylococcus aureus Activity of Actinomycin D Originating from Streptomyces parvulus." International Journal of Molecular Sciences 22, no. 22 (November 12, 2021): 12231. http://dx.doi.org/10.3390/ijms222212231.

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Staphylococcus aureus (S. aureus) is a common pathogen that causes various serious diseases, including chronic infections. Discovering new antibacterial agents is an important aspect of the pharmaceutical field because of the lack of effective antibacterial drugs. In our research, we found that one anti-S. aureus substance is actinomycin D, originating from Streptomyces parvulus (S. parvulus); then, we further focused on the anti-S. aureus ability and the omics profile of S. aureus in response to actinomycin D. The results revealed that actinomycin D had a significant inhibitory activity on S. aureus with a minimum inhibitory concentration (MIC) of 2 μg/mL and a minimum bactericidal concentration (MBC) of 64 μg/mL. Bacterial reactive oxygen species (ROS) increased 3.5-fold upon treatment with actinomycin D, as was measured with the oxidation-sensitive fluorescent probe DCFH-DA, and H2O2 increased 3.5 times with treatment by actinomycin D. Proteomics and metabolomics, respectively, identified differentially expressed proteins in control and treatment groups, and the co-mapped correlation network of proteomics and metabolomics annotated five major pathways that were potentially related to disrupting the energy metabolism and oxidative stress of S. aureus. All findings contributed to providing new insight into the mechanisms of the anti-S. aureus effects of actinomycin D originating from S. parvulus.

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Maltarollo, Vinicius Gonçalves. "Classification of Staphylococcus Aureus FabI Inhibitors by Machine Learning Techniques." International Journal of Quantitative Structure-Property Relationships 4, no. 4 (October 2019): 1–14. http://dx.doi.org/10.4018/ijqspr.2019100101.

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Enoyl-acyl carrier protein reductase (FabI) is a key enzyme in the fatty acid metabolism of gram-positive bacteria and is considered a potential target for new antibacterial drugs development. Indeed, triclosan is a widely employed antibacterial and AFN-1252 is currently under phase-II clinical trials, both are known as FabI inhibitors. Nowadays, there is an urgent need for new drug discovery due to increasing antibacterial resistance. In the present study, classification models using machine learning techniques were generated to distinguish SaFabI inhibitors from non-inhibitors successfully (e.g., Mathews correlation coefficient values equal to 0.837 and 0.789 calculated with internal and external validations). The interpretation of a selected model indicates that larger compounds, number of N atoms and the distance between central amide and naphthyridinone ring are important to biological activity, corroborating previous studies. Therefore, these obtained information and generated models can be useful for design/discovery of novel bioactive ligands as potential antibacterial agents.

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Pohl, Konstanze, Patrice Francois, Ludwig Stenz, Frank Schlink, Tobias Geiger, Silvia Herbert, Christiane Goerke, Jacques Schrenzel, and Christiane Wolz. "CodY in Staphylococcus aureus: a Regulatory Link between Metabolism and Virulence Gene Expression." Journal of Bacteriology 191, no. 14 (July 15, 2009): 4695. http://dx.doi.org/10.1128/jb.00542-09.

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Krismer, Bernhard, Manuel Liebeke, Daniela Janek, Mulugeta Nega, Maren Rautenberg, Gabriele Hornig, Clemens Unger, Christopher Weidenmaier, Michael Lalk, and Andreas Peschel. "Nutrient Limitation Governs Staphylococcus aureus Metabolism and Niche Adaptation in the Human Nose." PLoS Pathogens 10, no. 1 (January 16, 2014): e1003862. http://dx.doi.org/10.1371/journal.ppat.1003862.

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Sun, Jinchun, Jinshan Jin, Richard D. Beger, Carl E. Cerniglia, and Huizhong Chen. "Evaluation of metabolism of azo dyes and their effects on Staphylococcus aureus metabolome." Journal of Industrial Microbiology & Biotechnology 44, no. 10 (August 7, 2017): 1471–81. http://dx.doi.org/10.1007/s10295-017-1970-8.

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Zhang, Wenwen, Gomez Escalada Margarita, Di Wu, Wenqin Yuan, Sha Yan, Suzhen Qi, Xiaofeng Xue, Kai Wang, and Liming Wu. "Antibacterial Activity of Chinese Red Propolis against Staphylococcus aureus and MRSA." Molecules 27, no. 5 (March 4, 2022): 1693. http://dx.doi.org/10.3390/molecules27051693.

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The antibacterial activity of propolis has long been of great interest, and the chemical composition of propolis is directly dependent on its source. We recently obtained a type of propolis from China with a red color. Firstly, the antibacterial properties of this unusual propolis were determined against Staphylococcus aureus and methicillin-resistant Staphylococcus aureus (MRSA). Studies on its composition identified and quantified 14 main polyphenols of Chinese red propolis extracts (RPE); quantification was carried out using liquid chromatography triple quadrupole tandem mass spectrometry (LC-QQQ-MS/MS) and RPE was found to be rich in pinobanksin, pinobanksin-3-acetate, and chrysin. In vitro investigations of its antibacterial activity revealed that its activity against S. aureus and MRSA is due to disruption of the cell wall and cell membrane, which then inhibits bacterial growth. Despite its similar antibacterial activities against S. aureus and MRSA, metabolomic analysis further revealed the effects of RPE on bacteria metabolism were different. The untargeted metabolomic results showed that a total of 7 metabolites in 12 metabolic pathways had significant changes (Fold change > 2, p < 0.05 *) after RPE treatment in S. aureus, while 11 metabolites in 9 metabolic pathways had significant changes (Fold change > 2, p < 0.05 *) after RPE treated on MRSA. Furthermore, RPE downregulated several specific genes related to bacterial biofilm formation, autolysis, cell wall synthesis, and bacterial virulence in MRSA. In conclusion, the data obtained indicate that RPE may be a promising therapeutic agent against S. aureus and MRSA.

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Reilly, S. S., M. C. Hudson, J. F. Kellam, and W. K. Ramp. "In vivo internalization of Staphylococcus aureus by embryonic chick osteoblasts." Bone 26, no. 1 (January 2000): 63–70. http://dx.doi.org/10.1016/s8756-3282(99)00239-2.

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Elasri, M. O., J. R. Thomas, R. A. Skinner, J. S. Blevins, K. E. Beenken, C. L. Nelson, and M. S. Smelter. "Staphylococcus aureus collagen adhesin contributes to the pathogenesis of osteomyelitis." Bone 30, no. 1 (January 2002): 275–80. http://dx.doi.org/10.1016/s8756-3282(01)00632-9.

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Weinrick, Brian, Paul M. Dunman, Fionnuala McAleese, Ellen Murphy, Steven J. Projan, Yuan Fang, and Richard P. Novick. "Effect of Mild Acid on Gene Expression in Staphylococcus aureus." Journal of Bacteriology 186, no. 24 (December 15, 2004): 8407–23. http://dx.doi.org/10.1128/jb.186.24.8407-8423.2004.

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ABSTRACT During staphylococcal growth in glucose-supplemented medium, the pH of a culture starting near neutrality typically decreases by about 2 units due to the fermentation of glucose. Many species can comfortably tolerate the resulting mildly acidic conditions (pH, ∼5.5) by mounting a cellular response, which serves to defend the intracellular pH and, in principle, to modify gene expression for optimal performance in a mildly acidic infection site. In this report, we show that changes in staphylococcal gene expression formerly thought to represent a glucose effect are largely the result of declining pH. We examine the cellular response to mild acid by microarray analysis and define the affected gene set as the mild acid stimulon. Many of the genes encoding extracellular virulence factors are affected, as are genes involved in regulation of virulence factor gene expression, transport of sugars and peptides, intermediary metabolism, and pH homeostasis. Key results are verified by gene fusion and Northern blot hybridization analyses. The results point to, but do not define, possible regulatory pathways by which the organism senses and responds to a pH stimulus.

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Journal articles on the topic 'Staphylococcus aureus Metabolism'

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