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Updated: Sep 24, 2025

Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
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Lung-Adapted Staphylococcus aureus Isolates With Dysfunctional Agr System Trigger a Proinflammatory Response.

Elodie Ramond1,2, Agathe Lepissier1,3, Xiongqi Ding1,2

  • 1Université de Paris Cité, Paris, France.

The Journal of Infectious Diseases
|May 7, 2022
PubMed
Summary
This summary is machine-generated.

Lung-adapted Staphylococcus aureus in cystic fibrosis (CF) children promotes inflammation and disease progression. This occurs through acquired agr dysfunction, leading to increased staphylococcal protein A expression and a proinflammatory response.

Keywords:
Staphylococcus aureusadaptationchronic infectioncystic fibrosisinflammation

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Area of Science:

  • Microbiology
  • Immunology
  • Pulmonology

Background:

  • Staphylococcus aureus is prevalent in the lungs of children with cystic fibrosis (CF).
  • Persistent S. aureus clones can cause chronic infections, negatively impacting lung function.
  • The precise role of S. aureus in respiratory decline in CF patients remains unclear.

Purpose of the Study:

  • To investigate how persistent Staphylococcus aureus clones contribute to cystic fibrosis disease progression.
  • To elucidate the mechanisms by which S. aureus impacts lung function in CF patients.

Main Methods:

  • Analysis of sequential isogenic S. aureus isolates from 15 young CF patients.
  • Utilized an air-liquid infection model to study bacterial adaptation and host response.
  • Investigated the role of staphylococcal protein A (Spa) and the agr quorum-sensing system.

Main Results:

  • Lung-adapted S. aureus (late isolates) showed low toxicity but high proinflammatory cytokine secretion, unlike early isolates.
  • Cytokine secretion was linked to staphylococcal protein A (Spa) expression, which was higher in late isolates.
  • Dysfunctional agr quorum-sensing system in late isolates led to increased Spa expression.
  • TNF-α receptor 1 signaling was involved in the airway epithelial cell response to lung-adapted S. aureus.

Conclusions:

  • Bacterial adaptation in the lung plays a direct role in chronic lung disease progression in CF.
  • Acquired agr dysfunction in S. aureus promotes a proinflammatory response, contributing to CF lung disease.
  • This study reveals an unexpected mechanism linking bacterial adaptation to increased inflammation in CF lungs.