Modelling staphylococcal pneumonia in a human 3D lung tissue model system delineates toxin-mediated pathology

Dis Model Mech. 2015 Nov;8(11):1413-25. doi: 10.1242/dmm.021923. Epub 2015 Sep 3.

Abstract

Staphylococcus aureus necrotizing pneumonia is recognized as a toxin-mediated disease, yet the tissue-destructive events remain elusive, partly as a result of lack of mechanistic studies in human lung tissue. In this study, a three-dimensional (3D) tissue model composed of human lung epithelial cells and fibroblasts was used to delineate the role of specific staphylococcal exotoxins in tissue pathology associated with severe pneumonia. To this end, the models were exposed to the mixture of exotoxins produced by S. aureus strains isolated from patients with varying severity of lung infection, namely necrotizing pneumonia or lung empyema, or to purified toxins. The necrotizing pneumonia strains secreted high levels of α-toxin and Panton-Valentine leukocidin (PVL), and triggered high cytotoxicity, inflammation, necrosis and loss of E-cadherin from the lung epithelium. In contrast, the lung empyema strain produced moderate levels of PVL, but negligible amounts of α-toxin, and triggered limited tissue damage. α-toxin had a direct damaging effect on the epithelium, as verified using toxin-deficient mutants and pure α-toxin. Moreover, PVL contributed to pathology through the lysis of neutrophils. A combination of α-toxin and PVL resulted in the most severe epithelial injury. In addition, toxin-induced release of pro-inflammatory mediators from lung tissue models resulted in enhanced neutrophil migration. Using a collection of 31 strains from patients with staphylococcal pneumonia revealed that strains producing high levels of α-toxin and PVL were cytotoxic and associated with fatal outcome. Also, the strains that produced the highest toxin levels induced significantly greater epithelial disruption. Of importance, toxin-mediated lung epithelium destruction could be inhibited by polyspecific intravenous immunoglobulin containing antibodies against α-toxin and PVL. This study introduces a novel model system for study of staphylococcal pneumonia in a human setting. The results reveal that the combination and levels of α-toxin and PVL correlate with tissue pathology and clinical outcome associated with pneumonia.

Keywords: 3D lung tissue model; Pneumonia; Staphylococcus aureus.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bacterial Toxins / immunology
  • Bacterial Toxins / metabolism*
  • Cell Line, Tumor
  • Chemotaxis
  • Coculture Techniques
  • Empyema, Pleural / immunology
  • Empyema, Pleural / metabolism
  • Empyema, Pleural / microbiology*
  • Empyema, Pleural / pathology
  • Epithelial Cells / drug effects
  • Epithelial Cells / immunology
  • Epithelial Cells / metabolism
  • Epithelial Cells / microbiology*
  • Epithelial Cells / pathology
  • Exotoxins / immunology
  • Exotoxins / metabolism*
  • Fibroblasts / metabolism
  • Fibroblasts / microbiology
  • Fibroblasts / pathology
  • Hemolysin Proteins / immunology
  • Hemolysin Proteins / metabolism*
  • Humans
  • Immunoglobulins, Intravenous / pharmacology
  • Immunologic Factors / pharmacology
  • Inflammation Mediators / metabolism
  • Leukocidins / immunology
  • Leukocidins / metabolism*
  • Lung / drug effects
  • Lung / immunology
  • Lung / metabolism
  • Lung / microbiology*
  • Lung / pathology
  • Necrosis
  • Neutrophil Infiltration
  • Pneumonia, Staphylococcal / drug therapy
  • Pneumonia, Staphylococcal / immunology
  • Pneumonia, Staphylococcal / metabolism
  • Pneumonia, Staphylococcal / microbiology*
  • Pneumonia, Staphylococcal / pathology
  • Staphylococcus aureus / classification
  • Staphylococcus aureus / drug effects
  • Staphylococcus aureus / immunology
  • Staphylococcus aureus / metabolism
  • Staphylococcus aureus / pathogenicity*
  • Time Factors

Substances

  • Bacterial Toxins
  • Exotoxins
  • Hemolysin Proteins
  • Immunoglobulins, Intravenous
  • Immunologic Factors
  • Inflammation Mediators
  • Leukocidins
  • Panton-Valentine leukocidin
  • staphylococcal alpha-toxin