Binding of a Staphylococcus aureus bone pathogen to type I collagen

Buxton, Thomas B.; Rissing, J. Peter; Horner, Jack A.; Plowman, Kent M.; Scott, David F.; Sprinkle, T.J.; Best, Gary K.

doi:10.1016/0882-4010(90)90031-k

Cited by 35 publications

(19 citation statements)

References 26 publications

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“…Together with the elastin degradation by ScpA (Potempa et al, 1988), the collagenolytic activity of staphopains could injure the endocardium, causing endocarditis. Binding of S. aureus to collagen (Speziale et al, 1986;Holderbaum et al, 1987;Naidu et al, 1989;Buxton et al, 1990;Switalski et al, 1989) possibly augments the collagenolysis. Besides the collagen-binding protein (Switalski et al, 1989), a staphylococcal surface protein capable of binding to several extracellular matrix glycoproteins (McGavin et al, 1993) facilitates adherence of S. aureus to the matrix of various tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, interaction of S. aureus with fibrinogen plays a crucial role in the pathogenicity of endocarditis caused by this bacterium. Moreover, a 135 kDa cell surface protein of S. aureus (Switalski et al, 1989) binds specifically to collagen (Speziale et al, 1986;Holderbaum et al, 1987;Naidu et al, 1989;Buxton et al, 1990), constituting another important virulence trait in experimental endocarditis (Hienz et al, 1996). …”

Section: Discussionmentioning

confidence: 99%

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Degradation of fibrinogen and collagen by staphopains, cysteine proteases released from Staphylococcus aureus

et al. 2011

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Staphylococcus aureus is the most frequently isolated pathogen in Gram-positive sepsis often complicated by a blood clotting disorder, and is the leading cause of infective endocarditis induced by bacterial destruction of endocardial tissues. The bacterium secretes cysteine proteases referred to as staphopain A (ScpA) and staphopain B (SspB). To investigate virulence activities of staphopains pertinent to clotting disorders and tissue destruction, we examined their effects on collagen, one of the major tissue components, and on plasma clotting. Both staphopains prolonged the partial thromboplastin time of plasma in a dose-and activitydependent manner, with SspB being threefold more potent than ScpA. Staphopains also prolonged the thrombin time of both plasma and fibrinogen, indicating that these enzymes can cause impaired plasma clotting through fibrinogen degradation. Whereas SspB cleaved the fibrinogen Aa-chain at the C-terminal region very efficiently, ScpA degraded it rather slowly. This explains the superior ability of the former enzyme to impair fibrinogen clottability. Enzymically active staphopains, at concentrations as low as 10 nM, degraded collagen with comparable efficiency. These results show novel virulence activities of staphopains in degrading fibrinogen and collagen, and suggest an involvement of staphopains in the clotting impairment and tissue destruction caused by staphylococcal infection. INTRODUCTIONSepsis is a serious medical condition, in which living bacteria are present in the bloodstream. Shock and disseminated intravascular coagulation (DIC) are common and potentially fatal consequences of sepsis. DIC occurs in as many as 40 % of sepsis patients, often leading to multiple organ failure (Levi & ten Cate, 1999), and is directly linked to a high mortality rate. Clinical studies have shown that Gram-positive micro-organisms are as common as Gram-negative bacteria in causing sepsis (Ahmed et al., 1991;Kieft et al., 1993).Staphylococcus aureus is the most frequently isolated pathogen in Gram-positive sepsis (Ahmed et al., 1991;Bone, 1993). In addition, this bacterium is the leading cause of infective endocarditis in many regions of the world (Fowler et al., 2005). The development of endocarditis increases the mortality rate of patients with bacteraemia (Chang et al., 2003) et al., 2005). These findings suggest that staphopains contribute to S. aureus septic shock, one of the major fatal complications of sepsis.Clotting induction and a subsequent tendency to bleeding are prominent clinical features of DIC, another lethal outcome of sepsis. Staphopains may participate in the onset of the clotting disorder through activation or inactivation of clotting factors in plasma by proteolytic cleavage. However, the ability of staphopains to affect plasma clotting has not been studied. Invasion of S. aureus into the endocardium to cause infective endocarditis requires the degradation of connective tissue including extracellular matrix proteins, and is facilitated by proteases. In this context, staphy...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Degradation of fibrinogen and collagen by staphopains, cysteine proteases released from Staphylococcus aureus

et al. 2011

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“…In one study, it was shown that a small capsule was necessary for fibroblast attachment by protein A of S. aureus and that a fully encapsulated strain reduced the binding efficiency (104). In another study, the thin capsule was shown to be necessary for binding to bone collagen type 1, since high capsular expression actually inhibited binding (23). Once these microorganisms adhere to solid surfaces (such as bone), both in vitro and in vivo, staphylococci produce larger quantities of cell-associated capsule than do those grown in liquid cultures (95).…”

Section: Nongonococcal Arthritismentioning

confidence: 99%

Acute Septic Arthritis

2002

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Acute septic arthritis may develop as a result of hematogenous seeding, direct introduction, or extension from a contiguous focus of infection. The pathogenesis of acute septic arthritis is multifactorial and depends on the interaction of the host immune response and the adherence factors, toxins, and immunoavoidance strategies of the invading pathogen. Neisseria gonorrhoeae and Staphylococcus aureus are used in discussing the host-pathogen interaction in the pathogenesis of acute septic arthritis. While diagnosis rests on isolation of the bacterial species from synovial fluid samples, patient history, clinical presentation, laboratory findings, and imaging studies are also important. Acute nongonococcal septic arthritis is a medical emergency that can lead to significant morbidity and mortality. Therefore, prompt recognition, rapid and aggressive antimicrobial therapy, and surgical treatment are critical to ensuring a good prognosis. Even with prompt diagnosis and treatment, high mortality and morbidity rates still occur. In contrast, gonococcal arthritis is often successfully treated with antimicrobial therapy alone and demonstrates a very low rate of complications and an excellent prognosis for full return of normal joint function. In the case of prosthetic joint infections, the hardware must be eventually removed by a two-stage revision in order to cure the infection

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“…Although there is no direct evidence suggesting that either mammalian actin ®laments contain an SPA-binding domain, or that actin receptors are found in the surface of S. aureus, it is possible that the binding of SPA and actin ®laments may regulate S. aureus infection of mammalian epithelial cells. This suggestion may be related, in part, to the previous report that intracellular pathogens develop a common mechanism to exploit the actin cytoskeleton as a means of facilitating their direct spread between cells [13]. [6, 7, 13, 19±21].…”

Section: Discussionmentioning

confidence: 95%

Involvement of staphylococcal protein A and cytoskeletal actin in Staphylococcus aureus invasion of cultured human oral epithelial cells

Jung

Dan

Lee

et al. 2001

Journal of Medical Microbiology

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Following the coincidental discovery that â-actin isolated from renal epithelial cells was precipitated by staphylococcal protein A (SPA), the possibility that SPA and cytoskeletal actin ®laments may be involved in Staphylococcus aureus infection of epithelial cells was considered. Therefore, to clarify the potential role of SPA and actin ®laments in S. aureus infection, the invasion ef®ciency of S. aureus was determined quantitatively by measuring the number of cfu of viable organisms recovered from cultured KB cells. S. aureus invasion was found to be time dependent (0±60 min) and increased linearly when increasing numbers of bacteria were added (10 4 ±10 6 cfu/ml). However, signi®cant variation in the level of invasion was noted in protein A-de®cient S. aureus Wood 46. Cytochalasin B inhibited the invasion ef®ciency of S. aureus in a dose-dependent manner. The present study suggests that interaction of staphylococcal protein A and cytoskeletal actin ®laments is involved in the S. aureus invasion of cultured KB cells, and this process may contribute, in part, to the intracellular movement, cell-to-cell spread and dissemination of S. aureus within human oral epithelial cells in vivo.

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Binding of a Staphylococcus aureus bone pathogen to type I collagen

Cited by 35 publications

References 26 publications

Degradation of fibrinogen and collagen by staphopains, cysteine proteases released from Staphylococcus aureus

Degradation of fibrinogen and collagen by staphopains, cysteine proteases released from Staphylococcus aureus

Acute Septic Arthritis

Involvement of staphylococcal protein A and cytoskeletal actin in Staphylococcus aureus invasion of cultured human oral epithelial cells

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