<i>Staphylococcus aureus</i>
            pathogenesis in diverse host environments

Balasubramanian, Divya; Harper, Lamia; Shopsin, Bo; Torres, Victor J.

doi:10.1093/femspd/ftx005

Cited by 203 publications

(182 citation statements)

References 194 publications

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“…Similarly, Said-Salim et al used casamino acids-yeast extract—glycerolphosphate broth for their studies. Here, the addition of glycerol, as well as the use of an entirely different complex media, would alter the activity of other transcriptional regulators such as CodY, CcpE, CcpA and RpiRC, which are known to sense the carbon status of the cell [44]. Therefore, whilst Rot has the potential to regulate all four protease loci, our data suggests that Rot primarily controls expression of aur and sspAB , likely in an agr- dependent manner.…”

Section: Resultsmentioning

confidence: 99%

Mapping the Global Network of Extracellular Protease Regulation inStaphylococcus aureus

Gimza

Larias

Budny

et al. 2019

Preprint

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Section: Resultsmentioning

confidence: 99%

Mapping the Global Network of Extracellular Protease Regulation inStaphylococcus aureus

Gimza

Larias

Budny

et al. 2019

Preprint

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“…The superficial skin is a major infection site for S. aureus , which normally resides in 10–20% of healthy individuals (Lowy, 1998). The S. aureus causing skin infections often originate from resident bacteria that colonize the mucosal surfaces of the skin (Balasubramanian et al, 2017; Lowy, 1998). How S. aureus produces virulence factors to transform from a skin commensal to a pathogen is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Staphylococcus aureus Virulent PSMα Peptides Induce Keratinocyte Alarmin Release to Orchestrate IL-17-Dependent Skin Inflammation

Nakagawa

Matsumoto

Katayama

et al. 2017

Cell Host & Microbe

219

176

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Summary Staphylococcus aureus commonly colonizes the epidermis, but the mechanisms by which the host senses virulent but not commensal S. aureus to trigger inflammation remain unclear. Using a murine epicutaneous infection model, we found that S. aureus expressed phenol-soluble modulin (PSM)α, a group of secreted virulence peptides, is required to trigger cutaneous inflammation. PSMα induces the release of keratinocyte IL-1α and IL-36α, and signaling via IL-1R and IL-36R was required for induction of the pro-inflammatory cytokine IL-17. The levels of released IL-1α and IL-36α, as well as IL-17 production by γδ T cells and ILC3 and neutrophil infiltration to the site of infection were greatly reduced in mice with total or keratinocyte-specific deletion of the IL-1R and IL-36R signaling adaptor Myd88. Further, Il17a−/−f−/− mice showed blunted S. aureus-induced inflammation. Thus, keratinocyte Myd88 signaling in response to S. aureus PSMα drives an IL-17-mediated skin inflammatory response to epicutaneous S. aureus infection.

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“…Pathogenicity in S. aureus is both diverse and tightly controlled, being highly adaptive to the surrounding environment and available resources (1). In order to survive and persist within the host, this pathogen produces a wide array of virulence factors throughout the different stages of infection (2).…”

Section: Introductionmentioning

confidence: 99%

MroQ is a Novel Abi-domain Protein That Influences Virulence Gene Expression in Staphylococcus aureus via Modulation of Agr Activity

Marroquin

Gimza

Tomlinson

et al. 2019

Preprint

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17Numerous factors have to date been identified as playing a role in the regulation of Agr 18 activity in S. aureus, including transcription factors, antisense RNAs, and host elements. 19Herein we investigate the product of SAUSA300_1984 (termed MroQ), a transmembrane 20Abi-domain/M79 protease-family protein, as a novel effector of this system. Using a 21 USA300 mroQ mutant we observed a drastic reduction in proteolysis, hemolysis and 22 pigmentation that was fully complementable. This appears to result from diminished agr 23 activity, as transcriptional analysis revealed significant decreases in expression of both 24 RNAII and RNAIII in the mroQ mutant. Such effects appear to be direct, rather than 25 indirect, as known agr effectors demonstrated limited alterations in their activity upon 26 mroQ disruption. A comparison of RNA-sequencing datasets for both mroQ and agr 27 mutants reveal a profound overlap in their regulomes, with the majority of factors affected 28 being known virulence determinants. Importantly, the preponderance of alterations in 29 expression were more striking in the agr mutant, indicating that MroQ is necessary, but 30 not sufficient, for Agr function. Mechanism profiling revealed that putative residues for 31 metalloprotease activity within MroQ are required for its Agr controlling effect, however 32 this is not wielded at the level of AgrD processing. Virulence assessment demonstrated 33 that mroQ and agr mutants both exhibited increased formation of renal abscesses, but 34 decreased skin abscess formation, alongside diminished dermonecrosis. Collectively, we 35 present the characterization of a novel agr effector in S. aureus, which would appear to 36 be a direct regulator, potentially functioning via interaction with the AgrC histidine kinase. 37Pathogenicity in S. aureus is both diverse and tightly controlled, being highly adaptive to 39 the surrounding environment and available resources (1). In order to survive and persist 40 within the host, this pathogen produces a wide array of virulence factors throughout the 41 different stages of infection (2). For example, during earlier phases of growth, adhesins 42 and other binding proteins are actively synthesized (e.g. Spa, FnbAB), which play a role 43 in colonization (2, 3). In contrast, in later phases, these surface proteins are repressed, 44 whilst secreted toxins, proteases, and exoenzymes are produced to facilitate invasion and 45 dissemination (2, 4). This coordination is facilitated by an array of global regulators of 46 gene expression (2, 5-10). 47 48The agr quorum sensing system is one of the most important regulators of virulence in S. 49 aureus (11). It is a quorum sensing system comprised of two transcriptional units, RNAII 50 and RNAIII, each controlled by its own promoter, P2 and P3, respectively. RNAII encodes 51 the agr operon, which is comprised of four genes, agrBDCA (12). The quorum sensing 52 system functions in three parts: i) a quorum sensing module comprised of AgrB and AgrD; 53ii) a two-component system (TCS) Agr...

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Staphylococcus aureus pathogenesis in diverse host environments

Cited by 203 publications

References 194 publications

Mapping the Global Network of Extracellular Protease Regulation inStaphylococcus aureus

Mapping the Global Network of Extracellular Protease Regulation inStaphylococcus aureus

Staphylococcus aureus Virulent PSMα Peptides Induce Keratinocyte Alarmin Release to Orchestrate IL-17-Dependent Skin Inflammation

MroQ is a Novel Abi-domain Protein That Influences Virulence Gene Expression in Staphylococcus aureus via Modulation of Agr Activity

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