The fibronectin binding proteins of Staphylococcus aureus are required for adhesion to and invasion of bovine mammary gland cells

Lammers, A.; Nuijten, Piet J. M.; Smith, Hilde E.

doi:10.1111/j.1574-6968.1999.tb08783.x

Cited by 93 publications

(44 citation statements)

References 15 publications

(13 reference statements)

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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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“…The lack of response towards S. aureus is unclear. It may reside in a differential presence of humoral milk factors which may alter the ability of bacteria to attach to MEC [1,16], or to survive intracellular in macrophages [15] or epithelial cells [25].…”

Section: Discussionmentioning

confidence: 99%

Escherichia coli, but notStaphylococcus aureustriggers an early increased expression of factors contributing to the innate immune defense in the udder of the cow

et al. 2008

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-The outcome of an udder infection is influenced by the pathogen species. We established a strictly defined infection model to better analyze the unknown molecular causes for these pathogen-specific effects, using Escherichia coli and Staphylococcus aureus strains previously asseverated from field cases of mastitis. Inoculation of quarters with 500 CFU of E. coli (n = 4) was performed 6 h, 12 h, and 24 h before culling. All animals showed signs of acute clinical mastitis 12 h after challenge: increased somatic cell count (SCC), decreased milk yield, leukopenia, fever, and udder swelling. Animals inoculated with 10 000 CFU of S. aureus for 24 h (n = 4) showed no or only modest clinical signs of mastitis. However, S. aureus caused clinical signs in animals, inoculated for 72 h-84 h. Real-time PCR proved that E. coli inoculation strongly and significantly upregulated the expression of β-defensins, TLR2 and TLR4 in the pathogen inoculated udder quarters as well as in mammary lymph nodes. TLR3 and TLR6 were not significantly regulated by the infections. Immuno-histochemistry identified mammary epithelial cells as sites for the upregulated TLR2 and β-defensin expression. S. aureus, in contrast, did not significantly regulate the expression of any of these genes during the first 24 h after pathogen inoculation. Only 84 h after inoculation, the expression of β-defensins, but not of TLRs was significantly (> 20 fold) upregulated in five out of six pathogen inoculated quarters. Using the established mastitis model, the data clearly demonstrate a pathogen-dependent difference in the time kinetics of induced pathogen receptors and defense molecules.toll-like receptor / mastitis / beta-defensin / mammary epithelial cell

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“…However, Hayakawa et al (29) have described two isolates of S. aureus from milk from cows with mastitis wherein the ORFs agrB and agrD were closely similar to those from agr-2 Sa for one strain and from agr-3 Sa for the other one, whereas the agrC ORF from the two strains was clearly an agr-1 Sa type. These variants would be expected to show possible agr inhibition but not activation, and their pathogenic potential is surprising because virulence is usually associated with a functional agr system (10,25,34).…”

Section: S Haemolyticusmentioning

confidence: 99%

High Genetic Variability of the agr Locus in Staphylococcus Species

Dufour¹,

Jarraud²,

Vandenesch³

et al. 2002

J Bacteriol

191

176

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The agr quorum-sensing and signal transduction system was initially described in Staphylococcus aureus, where four distinct allelic variants have been sequenced. Western blotting suggests the presence of homologous loci in many other staphylococci, and this has been confirmed for S. epidermidis and S. lugdunensis. In this study we isolated agr-like loci from a range of staphylococci by using PCR amplification from primers common to the six published agr sequences and bracketing the most variable region, associated with quorum-sensing specificity. Positive amplifications were obtained from 14 of 34 staphylococcal species or subspecies tested. Sequences of the amplicons identified 24 distinct variants which exhibited extensive sequence divergence with only 10% of the nucleotides absolutely conserved on multiple alignment. This variability involved all three open reading frames involved in quorum sensing and signal transduction. However, these variants retained several protein signatures, including the conserved cysteine residue of the autoinducing peptide, with the exception of S. intermedius of pigeon origin, which contained a serine in place of cysteine at this position. We discuss hypotheses on the mode of action and the molecular evolution of the agr locus based on comparisons between the newly determined sequences.

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The fibronectin binding proteins of Staphylococcus aureus are required for adhesion to and invasion of bovine mammary gland cells

Cited by 93 publications

References 15 publications

Dynamic interaction between airway epithelial cells andStaphylococcus aureus

Dynamic interaction between airway epithelial cells andStaphylococcus aureus

Escherichia coli, but notStaphylococcus aureustriggers an early increased expression of factors contributing to the innate immune defense in the udder of the cow

High Genetic Variability of the agr Locus in Staphylococcus Species

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