Effect of staphylococcal β toxin on the cytotoxicity, proliferation and adherence of Staphylococcus aureus to bovine mammary epithelial cells

Cifrian, E.; Guidry, A.J.; Bramley, A. J.; Norcross, N. L.; Bastida, Felix; Marquardt, W. W.

doi:10.1016/0378-1135(95)00159-x

Cited by 42 publications

(27 citation statements)

References 18 publications

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“…Interaction between alpha and beta toxins increases the adherence to bovine mammary epithelial cells and the proliferation of S. aureus (Cifrian et al 1996). Furthermore, the capacity of the strains isolated from subclinical mastitis to produce both hemolysins indicates that these toxins might be necessary for the establishment of Staphylococcus strains in mammary glands as previously described by Cifrian et al (1996) and Bownik & Siwicki (2008).…”

Section: Resultsmentioning

confidence: 54%

Virulence factors and antimicrobial resistance of Staphylococcus aureus isolated from bovine mastitis in Rio de Janeiro

et al. 2009

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RESUMO.-[Fatores de virulência e resistência antimicrobiana em Staphylococcus aureus isolados de mastite bovina no Rio de Janeiro.] O presente estudo foi conduzido com o objetivo de caracterizar feno-genotipicamente os fatores de virulência e perfil de resistência aos antibióticos de Staphylococcus aureus isolados de amostras de leite de vacas com mastite clínica e subclínica. Em todos os isolados hemolíticos foi detectada a presença de beta hemolisina e 38% dos não-hemolíticos produziram hemolisinas na presença de cepa beta-hemolítica. A amplificação do gene coa apresentou quatro tipos polimórficos distintos com aproximadamente 400 bp, 600 bp, 700 bp e 900 bp. O gene spaA que codifica a região de ligação da proteína A à IgG apresentou bandas de 700 bp e 900 bp. A amplificação do gene que codifica a região X revelou um único amplicon para cada isolado sendo o tamanho The study was conducted to characterize pheno-genotypically the virulence factors and resistance pattern of Staphylococcus aureus isolates from milk samples of cows with subclinical mastitis. All hemolytic isolates presented beta-hemolysin, and 38% of the nonhemolytic isolates were able to express hemolysins in the presence of a beta-hemolytic strain. The amplification of the coa-gene displayed four different size polymorphisms with about 400 bp, 600 bp, 700 bp and 900 bp. The spaA gene that encodes the IgG-binding region of protein A revealed sizes of 700 bp and 900 bp. The amplification of region X from spaA yielded a single amplicon for each isolate with the prevalent amplicon size being of 180 bp. Amplification of sae gene yielded an amplicon size of 920 bp in 71% of the isolates. Antibiotic resistance pattern revealed that 42% S. aureus were susceptible to all antimicrobials tested. Seven different antibiotic patterns were observed. Our results indicated that 47% and 25% of S. aureus strains exhibited resistance to penicillin and oxacillin respectively. All oxacillin-resistant isolates were mecA-positive.

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Section: Resultsmentioning

confidence: 54%

Virulence factors and antimicrobial resistance of Staphylococcus aureus isolated from bovine mastitis in Rio de Janeiro

et al. 2009

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“…It is likely that two mechanisms contribute to the increased permeability. First, cellular damage by bacterial toxins [30,54,189] may result in discontinuity in the epithelial barrier. Second, pro-inflammatory mediators such as 386 P. Rainard, C. Riollet histamine, TNF-α and IFN-γ have been shown to alter epithelial tight junction efficiency [101].…”

Section: Humoral Defensesmentioning

confidence: 99%

Innate immunity of the bovine mammary gland

2006

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-Understanding the immune defenses of the mammary gland is instrumental in devising and developing measures to control mastitis, the major illness of dairy ruminants. Innate immunity is an extremely broad field for investigation, and despite decades of research, our present knowledge of the innate defenses of the udder is incomplete. Yet, information is being gained on the recognition of pathogens by the mammary gland, and on several locally inducible defenses. The contribution of mammary epithelial cells to local defenses and to the mobilization of leucocytes is under growing scrutiny. Interactions of mastitis-causing bacteria such as Escherichia coli or Staphylococcus aureus and the mammary gland represents a suitable model for studies on innate immunity at an epithelium frontier. Powerful new research tools are radically modifying the prospects for the understanding of the interplay between the mammary gland innate defenses and mastitis-causing bacteria: genetic dissection of the immune response, microarray gene technology, transcriptomic methodologies and gene silencing by RNA interference will make possible the discovery of several of the key defense mechanisms which govern the susceptibility/resistance to mastitis at the molecular and genetic levels. It should then be possible to enhance the resistance of dairy ruminants to mastitis through immunomodulation and genetic improvement. mastitis / cattle / innate immunity / inflammation / milk

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“…However, some studies have suggested that this toxin is important in intramammary infection. Purified toxin has been shown to cause moderate inflammatory changes in mouse and rabbit mammary glands (Calvinho et al, 1993;Ward et al, 1979) and to be cytotoxic for bovine mammary epithelial cells (Cifrian et al, 1996). In addition, non-beta-toxin-producing mutants have been found to be less virulent than wild-type strains in a mouse model of intramammary infection (Bramley et al, 1989) but not in non-mammary models (Nilsson et al, 1999;O'Callaghan et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Simultaneous lack of catalase and beta-toxin in Staphylococcus aureus leads to increased intracellular survival in macrophages and epithelial cells and to attenuated virulence in murine and ovine models

et al. 2009

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Staphylococcus aureus produces a variety of virulence factors that allow it to cause a wide range of infections in humans and animals. In the latter, S. aureus is a leading cause of intramammary infections. The contribution of catalase (KatA), an enzyme implicated in oxidative stress resistance, and beta-toxin (Hlb), a haemolysin, to the pathogenesis of S. aureus is poorly characterized. To investigate the role of these enzymes as potential virulence factors in S. aureus, we examined the intracellular survival of DkatA, Dhlb and DkatA Dhlb mutants in murine macrophages (J774A.1) and bovine mammary epithelial cells (MAC-T), and their virulence in different murine and ovine models. Catalase was not required for the survival of S. aureus within either J774A.1 or MAC-T cells. However, it was necessary for the intracellular proliferation of the bacterium after invasion of MAC-T cells. In addition, catalase was not needed for the full virulence of S. aureus in mice. Deletion of the hlb gene had no effect on the intracellular survival of S. aureus in J774A.1 cells but did cause a slight increase in survival in MAC-T cells. Furthermore, like catalase, beta-toxin was not required for complete virulence of S. aureus in murine models. Unexpectedly, the DkatA Dhlb mutant showed a notably increased persistence in both cell lines, and was significantly less virulent for mice than were the wild-type strain and single mutants. Most interestingly, it was also markedly attenuated in intramammary and subcutaneous infections in ewes and lambs.

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Effect of staphylococcal β toxin on the cytotoxicity, proliferation and adherence of Staphylococcus aureus to bovine mammary epithelial cells

Cited by 42 publications

References 18 publications

Virulence factors and antimicrobial resistance of Staphylococcus aureus isolated from bovine mastitis in Rio de Janeiro

Virulence factors and antimicrobial resistance of Staphylococcus aureus isolated from bovine mastitis in Rio de Janeiro

Innate immunity of the bovine mammary gland

Simultaneous lack of catalase and beta-toxin in Staphylococcus aureus leads to increased intracellular survival in macrophages and epithelial cells and to attenuated virulence in murine and ovine models

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