ArticleThe American journal of pathology2009
Staphylococcus aureus beta-toxin induces lung injury through syndecan-1.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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67 citing papers in PubMed, 114 citations in OpenAlex.
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- CNP-miR146a Decreases Inflammation in Murine Acute Infectious Lung Injury.Pharmaceutics · 2023Article
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- Release of extracellular superoxide dismutase into alveolar fluid protects against acute lung injury and inflammation inAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
- In Silico Genome-Scale Analysis of Molecular Mechanisms Contributing to the Development of a Persistent Infection with Methicillin-ResistantInternational journal of molecular sciences · 2022Article
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- MRSA-induced endothelial permeability and acute lung injury are attenuated by FTY720 S-phosphonate.American journal of physiology. Lung cellular and molecular physiology · 2022Article
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- Glycan-dependent cell adhesion mechanism of Tc toxins.Nature communications · 2020Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
In pneumonia caused by the bacterium Staphylococcus aureus, the intense inflammatory response that is triggered by this infection can lead to the development of lung injury. Little is known, however, about the impact of specific virulence factors on this inflammatory disorder, which causes both significant mortality and morbidity. In this study, we examined the role of beta-toxin, a neutral sphingomyelinase, in S. aureus-induced lung injury. Our results showed that the central features of lung injury--specifically, increased neutrophilic inflammation, vascular leakage of serum proteins into the lung tissue, and exudation of proteins into the airway--are significantly attenuated in mice infected intranasally with S. aureus deficient in beta-toxin compared with mice infected with S. aureus expressing beta-toxin. In addition, intranasal administration of beta-toxin evoked the characteristic features of lung injury in wild-type mice whereas neutropenic mice were protected from such injury. However, mutant beta-toxin mice deficient in sphingomyelinase activity failed to trigger features of lung injury. Ablation of sphingomyelinase activity also interfered with the ability of beta-toxin to stimulate ectodomain shedding of syndecan-1, a major heparan sulfate proteoglycan found in epithelial cells. Moreover, syndecan-1-null mice were significantly protected from beta-toxin-induced lung injury relative to wild-type mice. These data indicate that S. aureus beta-toxin is a critical virulence factor that induces neutrophil-mediated lung injury through both its sphingomyelinase activity and syndecan-1.
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