Effects of α‐Toxin of <i>Staphylococcus aureus</i> on the Ciliary Activity and Ultrastructure of Human Nasal Ciliated Epithelial Cells

Yun, Yeong Seok; Min, Yang Gi; Rhee, Chae Seo; Jung, In Ho; Koh, Young Yull; Jang, Tae Young; Jung, Dong Hak

doi:10.1097/00005537-199912000-00024

Cited by 18 publications

(11 citation statements)

References 16 publications

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“…Hla expression is Agr-dependent and increased upon interaction with epithelial cells, infection in vivo, and is higher in USA300 strains [3, 19, 32, 74]. In airway epithelial cells α-hemolysin has been associated with calcium fluxes, pro-inflammatory signaling [75], and alteration of ciliary beat frequency of cells (Fig. 2) [76].…”

Section: α-Hemolysinmentioning

confidence: 99%

Immunopathogenesis of Staphylococcus aureus pulmonary infection

2011

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Staphylococcus aureus is a common human pathogen highly evolved as both a component of the commensal flora and as a major cause of invasive infection. Severe respiratory infection due to staphylococci has been increasing due to the prevalence of more virulent USA300 CA-MRSA strains in the general population. The ability of S. aureus to adapt to the milieu of the respiratory tract has facilitated its emergence as a respiratory pathogen. Its metabolic versatility, the ability to scavenge iron, coordinate gene expression, and the horizontal acquisition of useful genetic elements have all contributed to its success as a component of the respiratory flora, in hospitalized patients, as a complication of influenza and in normal hosts. The expression of surface adhesins facilitates its persistence in the airways. In addition, the highly sophisticated interactions of the multiple S. aureus virulence factors, particularly the α-hemolysin and protein A, with diverse immune effectors in the lung such as ADAM10, TNFR1, EGFR, immunoglobulin, and complement all contribute to the pathogenesis of staphylococcal pneumonia.

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Section: α-Hemolysinmentioning

confidence: 99%

Immunopathogenesis of Staphylococcus aureus pulmonary infection

2011

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“…While there is now clear evidence that the cystic fibrosis transmembrane conductance regulator (CFTR), which had been previously implicated with release of ATP from airway epithelial cells [19], does not provide an exit pathway for ATP [20,21], pannexin channels, specifically Panx1, have been shown to serve as potential exit pathways for ATP in stressed cells [22,23,24,25]. Alternatively, cell stress induced by exposing cells to pore-forming toxins, such as α-toxin, may result in alterations in mitochondrial integrity and reduction of ATP production, which may contribute to lowering cellular ATP content [26,27]. Thus, it is still unclear whether ATP production is attenuated in toxin-exposed cells or ATP gets lost from the cytosol to the external space through the Hla pore or other pathways that may be activated by signals elicited by attachment of Hla monomers or pore formation.…”

Section: Introductionmentioning

confidence: 99%

ATP Release from Human Airway Epithelial Cells Exposed to Staphylococcus aureus Alpha-Toxin

Baaske

Richter

Möller

et al. 2016

Toxins

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Airway epithelial cells reduce cytosolic ATP content in response to treatment with S. aureus alpha-toxin (hemolysin A, Hla). This study was undertaken to investigate whether this is due to attenuated ATP generation or to release of ATP from the cytosol and extracellular ATP degradation by ecto-enzymes. Exposure of cells to rHla did result in mitochondrial calcium uptake and a moderate decline in mitochondrial membrane potential, indicating that ATP regeneration may have been attenuated. In addition, ATP may have left the cells through transmembrane pores formed by the toxin or through endogenous release channels (e.g., pannexins) activated by cellular stress imposed on the cells by toxin exposure. Exposure of cells to an alpha-toxin mutant (H35L), which attaches to the host cell membrane but does not form transmembrane pores, did not induce ATP release from the cells. The Hla-mediated ATP-release was completely blocked by IB201, a cyclodextrin-inhibitor of the alpha-toxin pore, but was not at all affected by inhibitors of pannexin channels. These results indicate that, while exposure of cells to rHla may somewhat reduce ATP production and cellular ATP content, a portion of the remaining ATP is released to the extracellular space and degraded by ecto-enzymes. The release of ATP from the cells may occur directly through the transmembrane pores formed by alpha-toxin.

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“…More than one-third of the general population (37.2%) are carriers of Staphylococcus aureus in the nasal cavity [3], this organism is frequently isolated in chronic rhinosinusitis [4]. It is known that bacterial toxins reduce mucociliary transport, and alpha-toxin causes acute rhinosinusitis [5,6]. It has been demonstrated that exotoxins secreted by colonizing S. aureus are capable of triggering the inflammatory infiltrate characteristic of chronic rhinosinusitis with nasal polyp [7,8].…”

Section: Introductionmentioning

confidence: 99%

“…It has been demonstrated that exotoxins secreted by colonizing S. aureus are capable of triggering the inflammatory infiltrate characteristic of chronic rhinosinusitis with nasal polyp [7,8]. Previous studies indicate that exotoxins produced by bacteria can decrease ciliary activity, subsequently inducing acute rhinosinusitis [6,9].…”

Section: Introductionmentioning

confidence: 99%

Effects of staphylococcal enterotoxin on ciliary activity and histology of the sinus mucosa

Min

Won

et al. 2006

Acta Oto-Laryngologica

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After exposure to low doses of SEA (0.03 and 0.3 ng/ml), CBF did not decrease, but after exposure to high doses of SEA (1.5, 3, and 30 ng/ml), CBF decreased significantly as a function of time. At 24 h after instillation of high-dose SEA (30 ng/ml) into the sinus, CBF decreased significantly and rhinosinusitis was induced after 7 days. Although no alteration was observed in the CBF of the sinus mucosa after instillation of low-dose SEA (0.3 ng/ml), histological findings of rhinosinusitis including subepithelial edema and inflammatory cell infiltration were observed.

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Effects of α‐Toxin of Staphylococcus aureus on the Ciliary Activity and Ultrastructure of Human Nasal Ciliated Epithelial Cells

Abstract: CBF increased at first, but with increasing incubation time ciliary movements decreased gradually and stopped eventually. This loss of CBF may be an irreversible change associated with ultrastructural changes in the mitochondria and the plasma membrane of the cilia.

Cited by 18 publications

References 16 publications

Immunopathogenesis of Staphylococcus aureus pulmonary infection

Immunopathogenesis of Staphylococcus aureus pulmonary infection

ATP Release from Human Airway Epithelial Cells Exposed to Staphylococcus aureus Alpha-Toxin

Effects of staphylococcal enterotoxin on ciliary activity and histology of the sinus mucosa

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