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Updated: May 16, 2025

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

Pathogen adaptation to lung metabolites.

Gaurav Kumar Lohia¹, Sebastián A Riquelme¹

¹Department of Pediatrics, Columbia University, New York, NY 10032, USA.

Current Opinion in Microbiology

|April 3, 2025

Summary

This summary is machine-generated.

Pseudomonas aeruginosa and Staphylococcus aureus hijack host metabolism for survival in the lungs. These opportunistic pathogens utilize host metabolites and form biofilms to evade immune responses and establish infection.

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Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice

Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice

Published on: March 17, 2014

Area of Science:

Microbiology
Immunology
Metabolic pathways

Background:

Opportunistic pathogens Pseudomonas aeruginosa and Staphylococcus aureus infect the respiratory tract.
Host immune cells reprogram metabolism, releasing immunometabolites like succinate and itaconate.
These bacteria adapt to the host's metabolic environment during infection.

Purpose of the Study:

To review how P. aeruginosa and S. aureus utilize host metabolic pathways.
To highlight pathogen metabolic plasticity as a survival strategy in the human lung.
To understand bacterial adaptation to host-derived metabolites.

Main Methods:

Literature review of studies on bacterial metabolism and host-pathogen interactions.
Analysis of P. aeruginosa and S. aureus metabolic strategies.
Examination of host immunometabolite roles in infection.

Main Results:

P. aeruginosa consumes succinate for growth and forms biofilms in response to itaconate.
Host ketone bodies support less immunostimulatory microbial communities.
S. aureus forms biofilms due to itaconate and consumes proline, linking survival to fibroblast metabolism.

Conclusions:

P. aeruginosa and S. aureus exhibit significant metabolic plasticity.
Hijacking host metabolic pathways is crucial for pathogen survival and colonization.
Understanding these adaptations is key to developing new therapeutic strategies.