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  • 1
    Language: English
    In: Biochemistry, 09 August 2011, Vol.50(31), pp.6730-7
    Description: Degradation of specific native proteins allows bacteria to rapidly adapt to changing environments when the activity of those proteins is no longer required. Although these processes are vital to bacterial survival, relatively little is known regarding how bacterial proteins are recognized and targeted for degradation. Staphylococcus aureus is an important human pathogen that requires iron for growth and pathogenesis. In the vertebrate host, S. aureus fulfills its iron requirement by obtaining heme iron from host hemoproteins via IsdG- and IsdI-mediated heme degradation. IsdG and IsdI are structurally and mechanistically analogous but are differentially regulated by iron and heme availability. Specifically, IsdG is targeted for degradation in the absence of heme. Therefore, we utilized the differential regulation of IsdG and IsdI to investigate the mechanism of regulated proteolysis. In contrast to canonical protease recognition sequences, we show that IsdG is targeted for degradation by internally coded sequences. Specifically, a flexible loop near the heme-binding pocket is required for IsdG degradation in the absence of heme.
    Keywords: Heme -- Deficiency ; Oxygenases -- Chemistry ; Staphylococcus Aureus -- Chemistry
    ISSN: 00062960
    E-ISSN: 1520-4995
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  • 2
    Language: English
    In: Journal of Bacteriology, Sept, 2011, Vol.193(17-18), p.4749(9)
    Description: Staphylococcus lugdunensis is often found as part of the normal flora of human skin but has the potential to cause serious infections even in healthy individuals. It remains unclear what factors enable S. lugdunensis to transition from a skin commensal to an invasive pathogen. Analysis of the complete genome reveals a putative iron-regulated surface determinant (Isd) system encoded within S. lugdunensis. In other bacteria, the Isd system permits the utilization of host heme as a source of nutrient iron to facilitate bacterial growth during infection. In this study, we establish that S. lugdunensis expresses an iron-regulated IsdG-family heme oxygenase that binds and degrades heme. Heme degradation by IsdG results in the release of free iron and the production of the chromophore staphylobilin. IsdG-mediated heme catabolism enables the use of heme as a sole source of iron, establishing IsdG as a pathophysiologically relevant heme oxygenase in S. lugdunensis. Together these findings offer insight into how S. lugdunensis fulfills its nutritional requirements while invading host tissues and establish the S. lugdunensis Isd system as being involved in heme-iron utilization. doi: 10.1128/JB.00436-11
    Keywords: Iron (Metal) -- Research ; Iron (Metal) -- Health Aspects ; Heme -- Physiological Aspects ; Heme -- Research ; Staphylococcus -- Physiological Aspects ; Staphylococcus -- Research
    ISSN: 0021-9193
    Source: Cengage Learning, Inc.
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  • 3
    Language: English
    In: Microbes and Infection, March, 2012, Vol.14(3), p.217(11)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.micinf.2011.11.001 Byline: Kathryn P. Haley, Eric P. Skaar Abstract: The use of iron as an enzymatic cofactor is pervasive in biological systems. Consequently most living organisms, including pathogenic bacteria, require iron to survive and replicate. To combat infection vertebrates have evolved sophisticated iron sequestration systems against which, pathogenic bacteria have concomitantly evolved equally elaborate iron acquisition mechanisms. Author Affiliation: Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, 1161 21st Ave., South, A5102 MCN, Nashville, TN 37232-2363, USA Article History: Received 27 July 2011; Accepted 2 November 2011
    Keywords: Staphylococcus Aureus
    ISSN: 1286-4579
    Source: Cengage Learning, Inc.
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  • 4
    Language: English
    In: Journal of Bacteriology, 2016, Vol.198(17-18), p.2536(13)
    Description: Helicobacter pylori must be able to rapidly respond to fluctuating conditions within the stomach. Despite this need for constant adaptation, H. pylori encodes few regulatory proteins. Of the identified regulators, the ferric uptake regulator (Fur), the nickel response regulator (NikR), and the two-component acid response system (ArsRS) are each paramount to the success of this pathogen. While numerous studies have individually examined these regulatory proteins, little is known about their combined effect. Therefore, we constructed a series of isogenic mutant strains that contained all possible single, double, and triple regulatory mutations in Fur, NikR, and ArsS. A growth curve analysis revealed minor variation in growth kinetics across the strains; these were most pronounced in the triple mutant and in strains lacking ArsS. Visual analysis showed that strains lacking ArsS formed large aggregates and a biofilm-like matrix at the air-liquid interface. Biofilm quantification using crystal violet assays and visualization via scanning electron microscopy (SEM) showed that all strains lacking ArsS or containing a nonphosphorylatable form of ArsR (ArsR-D52N mutant) formed significantly more biofilm than the wild-type strain. Molecular characterization of biofilm formation showed that strains containing mutations in the ArsRS pathway displayed increased levels of cell aggregation and adherence, both of which are key to biofilm development. Furthermore, SEM analysis revealed prevalent coccoid cells and extracellular matrix formation in the ArsR-D52N, ?nikR ?arsS, and ?fur ?nikR ?arsS mutant strains, suggesting that these strains may have an exacerbated stress response that further contributes to biofilm formation. Thus, H. pylori ArsRS has a previously unrecognized role in biofilm formation.
    Keywords: Helicobacter Pylori – Research ; Helicobacter Pylori – Physiological Aspects ; Microbial Mats – Research
    ISSN: 0021-9193
    Source: Cengage Learning, Inc.
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  • 5
    Language: English
    In: Journal of bacteriology, 15 September 2016, Vol.198(18), pp.2536-48
    Description: Helicobacter pylori must be able to rapidly respond to fluctuating conditions within the stomach. Despite this need for constant adaptation, H. pylori encodes few regulatory proteins. Of the identified regulators, the ferric uptake regulator (Fur), the nickel response regulator (NikR), and the two-component acid response system (ArsRS) are each paramount to the success of this pathogen. While numerous studies have individually examined these regulatory proteins, little is known about their combined effect. Therefore, we constructed a series of isogenic mutant strains that contained all possible single, double, and triple regulatory mutations in Fur, NikR, and ArsS. A growth curve analysis revealed minor variation in growth kinetics across the strains; these were most pronounced in the triple mutant and in strains lacking ArsS. Visual analysis showed that strains lacking ArsS formed large aggregates and a biofilm-like matrix at the air-liquid interface. Biofilm quantification using crystal violet assays and visualization via scanning electron microscopy (SEM) showed that all strains lacking ArsS or containing a nonphosphorylatable form of ArsR (ArsR-D52N mutant) formed significantly more biofilm than the wild-type strain. Molecular characterization of biofilm formation showed that strains containing mutations in the ArsRS pathway displayed increased levels of cell aggregation and adherence, both of which are key to biofilm development. Furthermore, SEM analysis revealed prevalent coccoid cells and extracellular matrix formation in the ArsR-D52N, ΔnikR ΔarsS, and Δfur ΔnikR ΔarsS mutant strains, suggesting that these strains may have an exacerbated stress response that further contributes to biofilm formation. Thus, H. pylori ArsRS has a previously unrecognized role in biofilm formation. Despite a paucity of regulatory proteins, adaptation is key to the survival of H. pylori within the stomach. While prior studies have focused on individual regulatory proteins, such as Fur, NikR, and ArsRS, few studies have examined the combined effect of these factors. Analysis of isogenic mutant strains that contained all possible single, double, and triple regulatory mutations in Fur, NikR, and ArsS revealed a previously unrecognized role for the acid-responsive two-component system ArsRS in biofilm formation.
    Keywords: Bacterial Proteins -- Metabolism ; Biofilms -- Growth & Development ; Gene Expression Regulation, Bacterial -- Physiology ; Helicobacter Pylori -- Physiology ; Trans-Activators -- Metabolism
    ISSN: 00219193
    E-ISSN: 1098-5530
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  • 6
    Language: English
    In: Infection and immunity, September 2015, Vol.83(9), pp.3578-89
    Description: Bacteria alter their cell surface in response to changing environments, including those encountered upon invasion of a host during infection. One alteration that occurs in several Gram-positive pathogens is the presentation of cell wall-anchored components of the iron-regulated surface determinant (Isd) system, which extracts heme from host hemoglobin to fulfill the bacterial requirement for iron. Staphylococcus lugdunensis, an opportunistic pathogen that causes infective endocarditis, encodes an Isd system. Unique among the known Isd systems, S. lugdunensis contains a gene encoding a putative autolysin located adjacent to the Isd operon. To elucidate the function of this putative autolysin, here named IsdP, we investigated its contribution to Isd protein localization and hemoglobin-dependent iron acquisition. S. lugdunensis IsdP was found to be iron regulated and cotranscribed with the Isd operon. IsdP is a specialized peptidoglycan hydrolase that cleaves the stem peptide and pentaglycine crossbridge of the cell wall and alters processing and anchoring of a major Isd system component, IsdC. Perturbation of IsdC localization due to isdP inactivation results in a hemoglobin utilization growth defect. These studies establish IsdP as an autolysin that functions in heme acquisition and describe a role for IsdP in cell wall reorganization to accommodate nutrient uptake systems during infection.
    Keywords: Cell Wall -- Metabolism ; Iron -- Metabolism ; N-Acetylmuramoyl-L-Alanine Amidase -- Metabolism ; Staphylococcal Infections -- Metabolism ; Staphylococcus Lugdunensis -- Metabolism
    ISSN: 00199567
    E-ISSN: 1098-5522
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  • 7
    In: International Journal of Genomics, 2015, Vol.2015, 8 pages
    Description: The advent of genomic analyses has revolutionized the study of human health. Infectious disease research in particular has experienced an explosion of bacterial genomic, transcriptomic, and proteomic data complementing the phenotypic methods employed in traditional bacteriology. Together, these techniques have revealed novel virulence determinants in numerous pathogens and have provided information for potential chemotherapeutics. The bacterial pathogen, , has been recognized as a class 1 carcinogen and contributes to chronic inflammation within the gastric niche. Genomic analyses have uncovered remarkable coevolution between the human host and . Perturbation of this coevolution results in dysregulation of the host-pathogen interaction, leading to oncogenic effects. This review discusses the relationship of with the human host and environment and the contribution of each of these factors to disease progression, with an emphasis on features that have been illuminated by genomic tools.
    Keywords: Review Article;
    ISSN: 2314-436X
    E-ISSN: 2314-4378
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  • 8
    Language: English
    In: Journal of visualized experiments : JoVE, 07 February 2013(72)
    Description: S. aureus is a pathogenic bacterium that requires iron to carry out vital metabolic functions and cause disease. The most abundant reservoir of iron inside the human host is heme, which is the cofactor of hemoglobin. To acquire iron from hemoglobin, S. aureus utilizes an elaborate system known as the iron-regulated surface determinant (Isd) system. Components of the Isd system first bind host hemoglobin, then extract and import heme, and finally liberate iron from heme in the bacterial cytoplasm. This pathway has been dissected through numerous in vitro studies. Further, the contribution of the Isd system to infection has been repeatedly demonstrated in mouse models. Establishing the contribution of the Isd system to hemoglobin-derived iron acquisition and growth has proven to be more challenging. Growth assays using hemoglobin as a sole iron source are complicated by the instability of commercially available hemoglobin, contaminating free iron in the growth medium, and toxicity associated with iron chelators. Here we present a method that overcomes these limitations. High quality hemoglobin is prepared from fresh blood and is stored in liquid nitrogen. Purified hemoglobin is supplemented into iron-deplete medium mimicking the iron-poor environment encountered by pathogens inside the vertebrate host. By starving S. aureus of free iron and supplementing with a minimally manipulated form of hemoglobin we induce growth in a manner that is entirely dependent on the ability to bind hemoglobin, extract heme, pass heme through the bacterial cell envelope and degrade heme in the cytoplasm. This assay will be useful for researchers seeking to elucidate the mechanisms of hemoglobin-/heme-derived iron acquisition in S. aureus and possibly other bacterial pathogens.
    Keywords: Hemoglobins ; Iron ; Bacteriological Techniques -- Methods ; Staphylococcus Aureus -- Growth & Development
    E-ISSN: 1940-087X
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  • 9
    Language: English
    In: Microbes and Infection, March 2012, Vol.14(3), pp.217-227
    Description: The use of iron as an enzymatic cofactor is pervasive in biological systems. Consequently most living organisms, including pathogenic bacteria, require iron to survive and replicate. To combat infection vertebrates have evolved sophisticated iron sequestration systems against which, pathogenic bacteria have concomitantly evolved equally elaborate iron acquisition mechanisms.
    Keywords: Bacterial Pathogenesis ; Staphylococcus Aureus ; Isd System ; Nutritional Immunity ; Staphylococcal Iron Acquisition ; Biology
    ISSN: 1286-4579
    E-ISSN: 1769-714X
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  • 10
    In: Gastroenterology Research and Practice, 2016, Vol.2016, 10 pages
    Description: colonizes the stomachs of greater than 50% of the world’s human population making it arguably one of the most successful bacterial pathogens. Chronic colonization results in gastritis in nearly all patients; however in a subset of people, persistent infection with is associated with an increased risk for more severe disease outcomes including B-cell lymphoma of mucosal-associated lymphoid tissue (MALT lymphoma) and invasive adenocarcinoma. Research aimed at elucidating determinants that mediate disease progression has revealed genetic differences in both humans and which increase the risk for developing gastric cancer. Furthermore, host diet and nutrition status have been shown to influence-associated disease outcomes. In this review we will discuss how is able to create a replicative niche within the hostile host environment by subverting and modifying the host-generated immune response as well as successfully competing for limited nutrients such as transition metals by deploying an arsenal of metal acquisition proteins and virulence factors. Lastly, we will discuss how micronutrient availability or alterations in the gastric microbiome may exacerbate negative disease outcomes associated with colonization.
    Keywords: Review Article;
    ISSN: 1687-6121
    E-ISSN: 1687-630X
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