Adhesiveness and invasiveness of staphylococcal species in a cell culture model

Schmidt, Heidrun; Bukholm, Geir; Holberg-Petersen, Mona

doi:10.1111/j.1699-0463.1989.tb00457.x

Cited by 18 publications

(4 citation statements)

References 23 publications

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“…aureus is generally not considered to be a significant intracellular pathogen. However, there is growing evidence that it can enter into nonprofessional phagocytic cells such as fibroblasts (34), osteoblasts (16), and endothelial (6,30,33) and epithelial cells (4,7,15,23). It has also been reported that bacteria can persist intracellularly (29) and induce apoptosis in infected cells as early as 4 h after internalization (25).…”

Section: Discussionmentioning

confidence: 99%

Dynamic interaction between airway epithelial cells andStaphylococcus aureus

Silva¹,

Zahm²,

Gras³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Staphylococcus aureus is a major cause of pulmonary infection, particularly in cystic fibrosis (CF) patients. However, few aspects of the interplay between S. aureus and host airway epithelial cells have been investigated thus far. We investigated by videomicroscopy the time- and bacterial concentration-dependent (104, 106, and 108CFU/ml) effect of S. aureus on adherence, internalization, and the associated damage of the airway epithelial cells. The balance between the secretion by S. aureus of the α-toxin virulence factor and by the airway cells of the antibacterial secretory leukoproteinase inhibitor (SLPI) was also analyzed. After 1 h of interaction, whatever the initial bacterial concentration, a low percentage of S. aureus (<8%) adhered to airway cells, and no airway epithelial cell damage was observed. In contrast, after 24 h of incubation, more bacteria adhered to airway epithelial cells, internalized bacteria were observed, and a bacterial concentration-dependent effect on airway cell damage was observed. At 24 h, most airway cells incubated with bacteria at 108CFU/ml exhibited a necrotic phenotype. The necrosis was preceded by a transient apoptotic process. In parallel, we observed a time- and bacterial concentration-dependent decrease in SLPI and increase in α-toxin expression. These results suggest that airway cells can defend against S. aureus in the early stages of infection. However, in later phases, there is a marked imbalance between the bactericidal capacity of host cells and bacterial virulence. These findings reinforce the potential importance of S. aureus in the pathogenicity of airway infections, including those observed early in CF patients.

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Section: Discussionmentioning

confidence: 99%

Dynamic interaction between airway epithelial cells andStaphylococcus aureus

Silva¹,

Zahm²,

Gras³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…We therefore sought to analyse internalization of S. saprophyticus into the human urinary bladder carcinoma cell line 5637 (5637 cells). Although S. saprophyticus shows strong adhesion to various epithelial cell lines, such as renal tubular epithelial cells and HEp2 cells (Gatermann et al , 1988; Hell et al , 1998), internalization of S. saprophyticus has only been suspected through the use of conventional microscopy but not proven in an older publication (Schmidt et al , 1989).…”

Section: Introductionmentioning

confidence: 99%

Staphylococcus saprophyticusATCC 15305 is internalized into human urinary bladder carcinoma cell line 5637

Szabados

Kleine

Anders

et al. 2008

FEMS Microbiology Letters

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Invasion of bacteria into nonphagocytic host cells is an important pathogenicity factor for escaping the host defence system. Gram-positive organisms, for example Staphylococcus aureus and Listeria monocytogenes, are invasive in nonphagocytic cells, and this mechanism is discussed as an important part of the infection process. Uropathogenic Escherichia coli and Staphylococcus saprophyticus can cause acute and recurrent urinary tract infections as well as bloodstream infections. Staphylococcus saprophyticus shows strong adhesion to human urinary bladder carcinoma and Hep2 cells and expresses the 'Microbial Surface Components Recognizing Adhesive Matrix molecule' (MSCRAMM)-protein SdrI with collagen-binding activity. MSCRAMMs are responsible for adhesion and collagen binding in S. aureus and are discussed as an important pathogenicity factor for invasion. To investigate internalization in S. aureus, several fluorescence activated cell sorting (FACS) assays have been described recently. We used a previously described FACS assay, with slight modifications, in addition to an antibiotic protection assay and transmission electron microscopy to show that S. saprophyticus ATCC 15305 and the wild-type strain 7108 were internalized into the human urinary bladder carcinoma cell line 5637. The discovery of the internalization of S. saprophyticus may be an important step for understanding the pathogenicity of recurrent infections caused by this organism.

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“…Many studies have used cells of nonhuman origin, mainly bovine endothelial cells. S. aureus invasion of human cells has been described so far for endothelial cells (8,38), epithelial cells (7,47,50), osteoblasts (24), and fibroblasts (50).…”

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confidence: 99%

Heterologously Expressed Staphylococcus aureus Fibronectin-Binding Proteins Are Sufficient for Invasion of Host Cells

et al. 2000

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Staphylococcus aureus is generally considered an extracellular pathogen (12, 44). However, it was shown in vitro over several years that S. aureus can invade a variety of nonprofessional phagocytes of different species. Many studies have used cells of nonhuman origin, mainly bovine endothelial cells. S. aureus invasion of human cells has been described so far for endothelial cells (8,38), epithelial cells (7,47,50), osteoblasts (24), and fibroblasts (50).S. aureus is among the most important bacterial pathogens for humans. It commonly causes superficial skin infections. Upon bloodstream dissemination or by continuous spread, it can readily survive in various deep tissues and cause, among others, abscess formation, osteomyelitis, endocarditis, and sepsis. Since these S. aureus infections are frequently long lasting, are difficult to eradicate, and often relapse after antibiotic treatment, prolonged treatment, including the use of cell-permeating antimicrobial drugs, is often required (30, 31). Invasion of nonprofessional phagocytes may provide a protected niche for S. aureus, but the precise role of invasion of host cells in S. aureus pathology in vivo is still not known.We have previously analyzed the process of cellular S. aureus invasion and elucidated the molecular mechanism of the internalization step (50). Bacterial entry proceeds by a "zippertype" mechanism, which resembles professional phagocytosis, and requires bacterial surface proteins, namely, adhesins (also termed microbial surface components recognizing adhesive matrix molecules [MSCRAMMs] [13]). The internalization process if F actin dependent, as demonstrated by complete inhibition by cytochalasin D. By use of isogenic deletion mutants, we identified fibronectin-binding protein (FnBP) as the necessary S. aureus invasin. Using competition experiments, we mapped the region of interaction with the host cell to the major fibronectin-binding domain of the FnBP, the D1 to D4 repeats. Fibronectin acts as a bridging molecule between the FnBP and the fibronectin receptor integrin ␣ 5 ␤ 1 , an adhesion molecule on the host cell. Cellular invasion is highly conserved in clinical S. aureus isolates (15 out of 15 tested were invasive), and the mechanism elucidated for the epithelial cell model of 293 cells is also valid for ECV304 cells, skin fibroblasts (50), and human umbilical vein endothelial cells (B. Sinha, unpublished data). These data are compatible with the results obtained by four different groups, who found that FnBPs are essential either for adhesion to or invasion of human endothelial cells (42), bovine mammary epithelial cells (9, 27), and mouse fibroblastic cells (14).Our previous data did not support a role for S. aureus invasins other than FnBPs but could not exclude necessary (S. aureus-specific) coreceptors. However, they largely excluded an efficient second invasin in S. aureus (50), unlike the situation found for streptococcal M proteins. This study was performed to address the questions of whether S. aureus FnBPs are sufficient to confer...

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Adhesiveness and invasiveness of staphylococcal species in a cell culture model

Cited by 18 publications

References 23 publications

Dynamic interaction between airway epithelial cells andStaphylococcus aureus

Dynamic interaction between airway epithelial cells andStaphylococcus aureus

Staphylococcus saprophyticusATCC 15305 is internalized into human urinary bladder carcinoma cell line 5637

Heterologously Expressed Staphylococcus aureus Fibronectin-Binding Proteins Are Sufficient for Invasion of Host Cells

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