Related Experiment Video
Updated: Mar 22, 2026
Pseudomonas aeruginosa Induced Lung Injury Model
Published on: October 29, 2014
The great escape: Pseudomonas breaks out of the lung
Angelica Zhang1, Stephanie M Rangel1, Alan R Hauser2
1Department of Microbiology/Immunology, Northwestern University, Feinberg School of Medicine, Chicago Illinois, USA.
Abstract:
The Gram-negative bacterium Pseudomonas aeruginosa is a major cause of hospital-acquired infections and the focus of much attention due to its resistance to many conventional antibiotics. It harbors a wide range of disease-promoting virulence factors, including a type III secretion system. Here we review our recent study of ExoS, one of the effector proteins exported by this type III secretion system. Using a mouse model of pneumonia, we showed that the ADP-ribosyltransferase (ADPRT) activity of ExoS caused formation of "fields of cell injection" (FOCI) in the lungs. These FOCI represented ExoS-injected clusters of type I pneumocytes that became compromised, leading to disruption of the pulmonary-vascular barrier and subsequent bacterial dissemination from the lungs to the bloodstream. We discuss the potential mechanisms by which these processes occur as well as the novel techniques used to study ExoS function in vivo.
Insights
Pseudomonas aeruginosa infections cause hospital-acquired pneumonia. Its ExoS toxin disrupts lung cells, breaching the pulmonary-vascular barrier and spreading bacteria to the bloodstream.
Area of Science:
- Microbiology and Immunology
- Infectious Diseases
- Pulmonary Medicine
Background:
- Pseudomonas aeruginosa is a Gram-negative bacterium frequently causing hospital-acquired infections.
- Antibiotic resistance in P. aeruginosa necessitates understanding its virulence mechanisms.
- The type III secretion system (T3SS) is a key virulence factor, delivering effector proteins like ExoS into host cells.
Purpose of the Study:
- To investigate the role of ExoS, a T3SS effector protein, in P. aeruginosa-induced pneumonia.
- To elucidate the mechanisms by which ExoS contributes to lung injury and bacterial dissemination.
- To explore novel in vivo techniques for studying ExoS function.
Main Methods:
- Utilized a mouse model of P. aeruginosa pneumonia.
- Assessed the impact of ExoS ADP-ribosyltransferase (ADPRT) activity on host cells.
- Employed advanced techniques to visualize and analyze ExoS function in vivo.
Main Results:
- ExoS ADPRT activity induced the formation of 'fields of cell injection' (FOCI) in lung tissue.
- FOCI comprised ExoS-injected type I pneumocytes, exhibiting compromised integrity.
- ExoS-mediated damage led to pulmonary-vascular barrier disruption and bacterial dissemination to the bloodstream.
Conclusions:
- ExoS is a critical virulence factor in P. aeruginosa pneumonia, directly impacting lung cell function.
- The disruption of the pulmonary-vascular barrier by ExoS facilitates systemic bacterial spread.
- Novel in vivo methodologies provide valuable insights into T3SS effector protein function during infection.
Related Concept Videos
01:14Atypical Pneumonia
01:30Pneumonia I: Introduction
Risk Factors
Various factors influence the likelihood of developing pneumonia. Age plays a crucial role, with infants, children under two, and individuals over 65 at increased risk due to their...
01:29Pneumonia II: Pathophysiology
01:30Pneumonia III: Complications and Assessment
01:28Pneumonia IV: Management
Bacterial Pneumonia Treatment
For bacterial pneumonia, antibiotics serve as the cornerstone of therapy. Initial treatment often begins with empirical antibiotics, tailored to the anticipated causative organism and adjusted based on culture results. Key antibiotic choices include:
01:30Pneumonia V: Nursing management and Prevention
The nurse must practice strict medical asepsis and adhere to infection control guidelines to minimize healthcare-associated infections.
Enhance airway patency
Position the patient correctly to facilitate drainage of the affected lung segments. Manual or mechanical percussion and vibration can also be employed....