Expression of Î³-hemolysin regulated by<i>sae</i>in<i>Staphylococcus aureus</i>strain Smith 5R

Yamazaki, Kazuko; Kato, Fuminori; Kamio, Yoshiyuki; Kaneko, Jun

doi:10.1111/j.1574-6968.2006.00236.x

Cited by 14 publications

(12 citation statements)

References 22 publications

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“…On the other hand, the hlgB mRNA levels in MW2 and FRP3757 were Ͻ1/10-fold that in Newman, and the ratios of surfactant-dependent induction of hlgB mRNA were 1.3-and 1.4-fold, respectively. Recent studies demonstrated that expression of the hlgB gene is dependent on the SaeRS system (28) and that the Newman strain possesses a point mutation that leads to constitutive expression of the saeS gene (29). Based on these reports, the hlgB gene is assumed to be highly expressed in S. aureus Newman, which would account for our data showing that the expression level of the hlgB gene in S. aureus Newman was higher than those in clinical isolates.…”

Section: Resultssupporting

confidence: 56%

“…On the other hand, Malachowa et al reported only a modest contribution of Hlg to host killing by S. aureus in a sepsis model (1), and there has been little analysis of its virulence potential in a pneumonia model. Furthermore, the expression of hla and hlg genes is differentially regulated by the twocomponent systems Agr and Sae, respectively (28). Under our experimental conditions for surfactant treatment, the transcript levels of the hla and agr genes were not significantly affected, whereas the mRNA quantities of hlgB and hlgC were upregulated.…”

Section: Discussionmentioning

confidence: 79%

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Induction of Virulence Gene Expression in Staphylococcus aureus by Pulmonary Surfactant

et al. 2014

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bWe performed a genomewide analysis using a next-generation sequencer to investigate the effect of pulmonary surfactant on gene expression in Staphylococcus aureus, a clinically important opportunistic pathogen. RNA sequence (RNA-seq) analysis of bacterial transcripts at late log phase revealed 142 genes that were upregulated >2-fold following the addition of pulmonary surfactant to the culture medium. Among these genes, we confirmed by quantitative reverse transcription-PCR analysis that mRNA amounts for genes encoding ESAT-6 secretion system C (EssC), an unknown hypothetical protein (NWMN_0246; also called pulmonary surfactant-inducible factor A [PsiA] in this study), and hemolysin gamma subunit B (HlgB) were increased 3-to 10-fold by the surfactant treatment. Among the major constituents of pulmonary surfactant, i.e., phospholipids and palmitate, only palmitate, which is the most abundant fatty acid in the pulmonary surfactant and a known antibacterial substance, stimulated the expression of these three genes. Moreover, these genes were also induced by supplementing the culture with detergents. The induction of gene expression by surfactant or palmitate was not observed in a disruption mutant of the sigB gene, which encodes an alternative sigma factor involved in bacterial stress responses. Furthermore, each disruption mutant of the essC, psiA, and hlgB genes showed attenuation of both survival in the lung and host-killing ability in a murine pneumonia model. These findings suggest that S. aureus resists membrane stress caused by free fatty acids present in the pulmonary surfactant through the regulation of virulence gene expression, which contributes to its pathogenesis within the lungs of the host animal.

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Section: Resultssupporting

confidence: 56%

Section: Discussionmentioning

confidence: 79%

Induction of Virulence Gene Expression in Staphylococcus aureus by Pulmonary Surfactant

et al. 2014

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“…SaeR binding sites have been identified within the promoter regions of nearly all leucocidin genes, including lukSF, hlgA, hlgCB, lukED, and lukAB (lukHG) (309,321). Experimentally, an sae deletion mutant of S. aureus has significantly reduced transcript levels of all known leucocidins and is dramatically attenuated in murine infection models (308)(309)(310)315).…”

Section: Regulation At the Transcriptional Levelmentioning

confidence: 99%

The Bicomponent Pore-Forming Leucocidins of Staphylococcus aureus

Alonzo

Torres

2014

Microbiol Mol Biol Rev

240

290

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SUMMARY The ability to produce water-soluble proteins with the capacity to oligomerize and form pores within cellular lipid bilayers is a trait conserved among nearly all forms of life, including humans, single-celled eukaryotes, and numerous bacterial species. In bacteria, some of the most notable pore-forming molecules are protein toxins that interact with mammalian cell membranes to promote lysis, deliver effectors, and modulate cellular homeostasis. Of the bacterial species capable of producing pore-forming toxic molecules, the Gram-positive pathogen Staphylococcus aureus is one of the most notorious. S. aureus can produce seven different pore-forming protein toxins, all of which are believed to play a unique role in promoting the ability of the organism to cause disease in humans and other mammals. The most diverse of these pore-forming toxins, in terms of both functional activity and global representation within S. aureus clinical isolates, are the bicomponent leucocidins. From the first description of their activity on host immune cells over 100 years ago to the detailed investigations of their biochemical function today, the leucocidins remain at the forefront of S. aureus pathogenesis research initiatives. Study of their mode of action is of immediate interest in the realm of therapeutic agent design as well as for studies of bacterial pathogenesis. This review provides an updated perspective on our understanding of the S. aureus leucocidins and their function, specificity, and potential as therapeutic targets.

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“…One two-component regulatory system, encoded by saeRS, was originally identified as a transposon mutant system deficient in the synthesis of several exoproteins, including ␣-and ␤-hemolysin, and coagulase (21). SaeRS has subsequently been shown to regulate staphylococcal immune evasion proteins (48), adhesins (26), and ␥-hemolysin (58). Importantly, sae inactivation reduces invasion of S. aureus in several animal models and cell lines (20,35,52,57).…”

mentioning

confidence: 99%

Staphylococcus epidermidis saeR Is an Effector of Anaerobic Growth and a Mediator of Acute Inflammation

Handke¹,

Rogers²,

Olson³

et al. 2008

Infect Immun

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The saeRS two-component regulatory system regulates transcription of multiple virulence factors in Staphylococcus aureus. In the present study, we demonstrated that the saePQRS region in Staphylococcus epidermidis is transcriptionally regulated in a temporal manner and is arranged in a manner similar to that previously described for S. aureus. Studies using a mouse foreign body infection model demonstrated that the virulence of strain 1457 and the virulence of a mutant, strain 1457 saeR, were statistically equivalent. However, histological analyses suggested that the polymorphonuclear neutrophil response at 2 days postinfection was significantly greater in 1457-infected mice than in 1457 saeR-infected mice, demonstrating that SaeR influences the early, acute phases of infection. Microarray analysis demonstrated that a saeR mutation affected the transcription of 65 genes (37 genes were upregulated and 28 genes were downregulated); in particular, 8 genes that facilitate growth under anaerobic conditions were downregulated in 1457 saeR. Analysis of growth under anaerobic conditions demonstrated that 1457 saeR had a decreased growth rate compared to 1457. Further metabolic experiments demonstrated that 1457 saeR had a reduced capacity to utilize nitrate as a terminal electron acceptor and exhibited increased production of lactic acid in comparison to 1457. These data suggest that in S. epidermidis SaeR functions to regulate the transition between aerobic growth and anaerobic growth. In addition, when grown anaerobically, 1457 saeR appeared to compensate for the redox imbalance created by the lack of electron transport-mediated oxidation of NADH to NAD ؉ by increasing lactate dehydrogenase activity and the subsequent oxidation of NADH.

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Expression of Î³-hemolysin regulated bysaeinStaphylococcus aureusstrain Smith 5R

Cited by 14 publications

References 22 publications

Induction of Virulence Gene Expression in Staphylococcus aureus by Pulmonary Surfactant

Induction of Virulence Gene Expression in Staphylococcus aureus by Pulmonary Surfactant

The Bicomponent Pore-Forming Leucocidins of Staphylococcus aureus

Staphylococcus epidermidis saeR Is an Effector of Anaerobic Growth and a Mediator of Acute Inflammation

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