Publications by authors named "Wolz C"

acts both as a colonizing commensal bacterium and invasive pathogen. Nasal colonization is associated with an increased risk of infection caused by the identical strain. In patients with atopic dermatitis (AD), the degree of colonization is associated with the severity of the disease.

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Background: The cell envelope of Staphylococcus aureus contains 2 major secondary cell wall glycopolymers: capsular polysaccharide (CP) and wall teichoic acid (WTA). Both CP and WTA are attached to the cell wall and play distinct roles in S. aureus colonization, pathogenesis, and bacterial evasion of host immune defenses.

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Staphylococcus aureus are gram-positive bacteria responsible for a wide array of diseases, ranging from skin and soft tissue infections to more chronic illnesses such as toxic shock syndrome, osteomyelitis, and endocarditis. Vancomycin is currently one of the most effective antibiotics available in treating patients infected with methicillin-resistant S. aureus (MRSA), however the emergence of vancomycin-resistant S.

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The success of as a major cause for endovascular infections depends on effective interactions with blood-vessel walls. We have previously shown that uses its wall teichoic acid (WTA), a surface glycopolymer, to attach to endothelial cells. However, the endothelial WTA receptor remained unknown.

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Staphylococcus aureus is considered an extracellular pathogen, yet the bacterium is able to survive within and escape from host cells. An agr/sae mutant of strain USA300 is unable to escape from macrophages but can replicate and survive within. We questioned whether such "non-toxic" S.

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The stringent response and its signalling nucleotides, pppGpp and ppGpp, have been the subject of intense research since the discovery of (p)ppGpp in 1969. Recent studies have revealed that the downstream events that follow (p)ppGpp accumulation vary among species. Consequently, the stringent response as initially characterized in largely differs from the response in Firmicutes (Bacillota), wherein synthesis and degradation of the messengers (p)ppGpp are orchestrated by the bifunctional Rel enzyme with synthetase and hydrolase activity and the two synthetases SasA/RelP and SasB/RelQ.

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Keratinocytes (KCs) form the outer epithelial barrier of the body, protecting against invading pathogens. Mice lacking the IL-17RA or both IL-17A and IL-17F develop spontaneous Staphylococcusaureus skin infections. We found a marked expansion of T cells, comprised of RORγt-expressing γδ T cells and T helper 17 cells in the skin-draining lymph nodes of these mice.

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Staphylococci are commensals of human skin and mucous membranes, but some species can also cause serious infections. Host niches during both colonization and infection differ greatly and are characterized by specific environmental conditions (pH, temperature, oxygen, nutrient availability, and microbiota) that can affect gene expression and virulence of microbes. To successfully occupy extremely different habitats at different anatomical sites, Staphylococci are equipped with a variety of regulatory elements that allow specific adaptation to the changing environments.

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Introduction: Malnutrition in cancer patients often remains undetected and underestimated in clinical practice despite studies revealing prevalences from 20 to 70%. Therefore, this study aimed to identify patient groups exposed to an increased nutritional risk in a university oncological outpatient center.

Methods: Between May 2017 and January 2018 we screened oncological patients there using the malnutrition universal screening tool (MUST).

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Article Synopsis
  • The text discusses the dual nature of certain bacteria that colonize mammalian nasal cavities but can also cause severe infections, highlighting the role of Sa3 phages found in human strains.
  • It emphasizes the importance of specific phage life cycles in different bacterial strains, classifying them into low and high transfer strains based on their ability to replicate phages.
  • The study concludes that the genetic characteristics of the bacterial hosts influence the interactions with phages, which could affect the rate of adaptation and mobilization of bacteria in response to phage presence.
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The virulence factors of the opportunistic human pathogen have been a main subject of research. In contrast, limited information is available on the mechanisms that allow the bacterium to accommodate to the conditions during carriage, a prerequisite for pathogenicity. Here, we tested the hypothesis that the adaptation of at different anatomical sites is reflected by differential gene regulation.

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Background: Toxins are key virulence determinants of pathogens and can impair the function of host immune cells, including platelets. Insights into pathogen toxin interference with platelets will be pivotal to improve treatment of patients with bacterial bloodstream infections.

Materials And Methods: In this study, we deciphered the effects of Staphylococcus aureus toxins α-hemolysin, LukAB, LukDE, and LukSF on human platelets and compared the effects with the pore forming toxin pneumolysin of Streptococcus pneumoniae.

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encodes 16 two-component systems (TCSs) that enable the bacteria to sense and respond to changing environmental conditions. Considering the function of these TCSs in bacterial survival and their potential role as drug targets, it is important to understand the exact mechanisms underlying signal perception. The differences between the sensing of appropriate signals and the transcriptional activation of the TCS system are often not well described, and the signaling mechanisms are only partially understood.

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The healthy human epidermis provides physical protection and is impenetrable for pathogenic microbes. Nevertheless, commensal and pathogen bacteria such as are able to colonize the skin surface, which may subsequently lead to infection. To identify and characterize regulatory elements facilitating adaptation of to the human skin environment we used tissue explants and quantified gene transcription during co-culture.

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During antibiotic persistence, bacterial cells become transiently tolerant to antibiotics by restraining their growth and metabolic activity. Detailed molecular characterization of antibiotic persistence is hindered by low count of persisting cells and the need for their isolation. Here, we used sustained addition of stable isotope-labeled lysine to selectively label the proteome during -induced persistence and -induced resuscitation of Escherichia coli cells in minimal medium after antibiotic treatment.

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As an opportunistic pathogen of humans and animals, Staphylococcus aureus asymptomatically colonizes the nasal cavity but is also a leading cause of life-threatening acute and chronic infections. The evolution of S. aureus resulting from short- and long-term adaptation to diverse hosts is tightly associated with mobile genetic elements.

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Stapylococcus aureus colonises the nose of healthy individuals but can also cause a wide range of infections. Amino acid (AA) synthesis and their availability is crucial to adapt to conditions encountered in vivo. Most S.

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Staphylococcus aureus commonly infects the skin, but the host-pathogen interactions controlling bacterial growth remain unclear. S. aureus virulence is regulated by the Agr quorum-sensing system that controls factors including phenol-soluble modulins (PSMs), a group of cytotoxic peptides.

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A large proportion of clinical isolates that carry an inactive Agr system are associated with persistent infection that is difficult to treat. Once is inside the bloodstream, it can cross the endothelial barrier and invade almost every organ in the human body. Endothelial cells can either be lysed by this pathogen or they serve as a niche for its intracellular long-term survival.

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The stringent response is characterized by the synthesis of the messenger molecules pppGpp, ppGpp or pGpp (here collectively designated (pp)pGpp). The phenotypic consequences resulting from (pp)pGpp accumulation vary among species and can be mediated by different underlying mechanisms. Most genome-wide analyses have been performed under stress conditions, which often mask the immediate effects of (pp)pGpp-mediated regulatory circuits.

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Slow growing stationary phase bacteria are often tolerant to multiple stressors and antimicrobials. Here, we show that the pathogen Staphylococcus aureus develops a non-specific tolerance towards oxidative stress during the stationary phase, which is mediated by the nucleotide second messenger (p)ppGpp. The (p)ppGpp mutant was highly susceptible to HOCl stress during the stationary phase.

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The stringent response is characterized by the synthesis of the alarmone (p)ppGpp. The phenotypic consequences resulting from (p)ppGpp accumulation vary among species, and for several pathogenic bacteria, it has been shown that the activation of the stringent response strongly affects biofilm formation and maintenance. In , (p)ppGpp can be synthesized by the RelA/SpoT homolog Rel upon amino acid deprivation or by the two small alarmone synthetases RelP and RelQ under cell wall stress.

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The stringent response enables metabolic adaptation of bacteria under stress conditions and is governed by RelA/SpoT Homolog (RSH)-type enzymes. Long RSH-type enzymes encompass an N-terminal domain (NTD) harboring the second messenger nucleotide (p)ppGpp hydrolase and synthetase activity and a stress-perceiving and regulatory C-terminal domain (CTD). CTD-mediated binding of Rel to stalled ribosomes boosts (p)ppGpp synthesis.

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