Expression of Clumping and Fibrinogen‐Binding Activities of <i>Staphylococcus aureus</i> at Various Growth Stages

Yonemasu, Kunio; Sasaki, Takako; Ohmae, Riichi; Kashiba, Syuzo

doi:10.1111/j.1348-0421.1991.tb01571.x

Cited by 5 publications

(4 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, only one strain, Wood 46, did not show strong aggregation. Because that strain does not adhere to fibrinogen or fibronectin [20,21], these results are in good accordance with our findings described below, attributing a key contribution of fibrinogenand fibronectinbinding proteins to aggregation in SF. Light (Figure 2D and 2E) and electron microscopic (Figure 2F ) examination verified the extreme clumping behavior of S. aureus USA300 grown in SF.…”

Section: Formation Of S Aureus Aggregates In Sfsupporting

confidence: 92%

Effect of Biofilms on Recalcitrance of Staphylococcal Joint Infection to Antibiotic Treatment

Dastgheyb

Parvızı

Shapiro

et al. 2014

Journal of Infectious Diseases

145

153

View full text Add to dashboard Cite

The pathogenesis of joint infections is not well understood. In particular, we do not know why these infections respond poorly to antibiotic treatment. Here we show that methicillin-resistant Staphylococcus aureus, a major cause of joint infections, forms exceptionally strong biofilmlike aggregates in human synovial fluid (SF), to an extent significantly exceeding biofilm formation observed in growth medium or serum. Screening a transposon bank identified bacterial fibronectin- and fibrinogen-binding proteins as important for the formation of macroscopic clumps in SF, suggesting an important role of fibrin-containing clots in the formation of bacterial aggregates during joint infection. Pretreatment of SF with plasmin led to a strongly reduced formation of aggregates and increased susceptibility to antibiotics. These results give important insight into the pathogenesis of staphylococcal joint infection and the mechanisms underlying resistance to treatment. Furthermore, they point toward a potential novel approach for treating joint infections.

show abstract

Section: Formation Of S Aureus Aggregates In Sfsupporting

confidence: 92%

Effect of Biofilms on Recalcitrance of Staphylococcal Joint Infection to Antibiotic Treatment

Dastgheyb

Parvızı

Shapiro

et al. 2014

Journal of Infectious Diseases

145

153

View full text Add to dashboard Cite

show abstract

“…The wild type S. aureus that we used in this study was Newman D2C, which has been reported as a new reference strain for SrtA studies ( Miller et al, 1977 ) due to its being coagulase-negative ( Yonemasu et al, 1987 , 1991 ) and non-hemolytic ( Chen et al, 2013 ). To our current knowledge, SrtA is the most important virulence factor in this strain, and therefore this strain has an advantage for studying the function of SrtA and the activity of SrtA inhibitors.…”

Section: Discussionmentioning

confidence: 99%

The therapeutic effect of chlorogenic acid against Staphylococcus aureus infection through sortase A inhibition

Wang

Cai

et al. 2015

Front. Microbiol.

View full text Add to dashboard Cite

The emergence and wide spread of multi-drug resistant Staphylococcus aureus (S. aureus) requires the development of new therapeutic agents with alternative modes of action. Anti-virulence strategies are hoped to meet that need. Sortase A (SrtA) has attracted great interest as a potential drug target to treat infections caused by S. aureus, as many of the surface proteins displayed by SrtA function as virulence factors by mediating bacterial adhesion to specific organ tissues, invasion of host cells, and evasion of the host-immune responses. It has been suggested that inhibitors of SrtA might be promising candidates for the treatment and/or prevention of S. aureus infections. In this study, we report that chlorogenic acid (CHA), a natural compound that lacks significant anti-S. aureus activity, inhibit the activity of SrtA in vitro (IC50 = 33.86 ± 5.55 μg/ml) and the binding of S. aureus to fibrinogen (Fg). Using molecular dynamics simulations and mutagenesis assays, we further demonstrate that CHA binds to the binding sites of C184 and G192 in the SrtA. In vivo studies demonstrated that CHA prevent mice from S. aureus-induced renal abscess, resulting in a significant survival advantage. These findings indicate that CHA is a promising therapeutic compound against SrtA during S. aureus infections.

show abstract

“…To address this question, we chose S. aureus Newman D2C as a new reference strain for SrtA studies (Miller et al ., ). Because this strain is coagulase‐negative (Yonemasu et al ., , ), we could exclude the effects of coagulase and focus just on the functions of SrtA. Here, we investigated the roles of SrtA in the pathogenesis of S. aureus ‐induced mastitis.…”

Section: Introductionmentioning

confidence: 99%

Role of sortase A in the pathogenesis ofStaphylococcus aureus-induced mastitis in mice

Chen

Liu

Wang

et al. 2014

FEMS Microbiol Lett

View full text Add to dashboard Cite

Sortase A (SrtA), a transpeptidase, anchors surface proteins with an LPXTG-motif sorting signal to the cell envelope. To determine the role of SrtA in the pathogenesis of Staphylococcus aureus, we constructed a mutant strain, ∆SrtA, by genetic techniques and identified its functions in a S. aureus-induced mastitis mouse model. The histological and myeloperoxidase (MPO) level results showed that the ∆SrtA strain attenuated the inflammatory reaction in the mammary tissue of mice compared with wild-type S. aureus challenge. Additionally, the ELISA results showed that the ∆SrtA strain impaired the induction of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), and the Western blot results showed that the mutant strain blocked the activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) by attenuating the degradation and phosphorylation of signaling pathway molecules such as IκBα, p65 and p38. These results suggest that SrtA is a key virulence factor in the pathogenesis of S. aureus-induced mastitis in mice. It appears that the srtA mutant affected the attachment of S. aureus to host cells, thus attenuating the activation of the NF-κB and MAPK signaling pathways, which regulated the expression of pro-inflammatory cytokines and decreased the susceptibility to mastitis.

show abstract

Expression of Clumping and Fibrinogen‐Binding Activities of Staphylococcus aureus at Various Growth Stages

Cited by 5 publications

References 9 publications

Effect of Biofilms on Recalcitrance of Staphylococcal Joint Infection to Antibiotic Treatment

Effect of Biofilms on Recalcitrance of Staphylococcal Joint Infection to Antibiotic Treatment

The therapeutic effect of chlorogenic acid against Staphylococcus aureus infection through sortase A inhibition

Role of sortase A in the pathogenesis ofStaphylococcus aureus-induced mastitis in mice

Contact Info

Product

Resources

About