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Updated: May 28, 2026
Pseudomonas aeruginosa Induced Lung Injury Model
Published on: October 29, 2014
Interleukin-23-mediated inflammation in Pseudomonas aeruginosa pulmonary infection
Patricia J Dubin1, Ashley Martz, Jessica R Eisenstatt
1Department of Pediatrics, Children’s Hospital of Pittsburgh of UPMC, Pittsburgh, PA, USA. dubipj@chp.edu
Abstract:
Pseudomonas aeruginosa is an opportunistic pathogen that is capable of causing acute and chronic pulmonary infection in the immunocompromised host. In the case of cystic fibrosis (CF), chronic P. aeruginosa infection causes increased mortality by promoting overly exuberant airway inflammation and cumulative lung damage. Identifying the key regulators of this inflammation may lead to the development of new therapies that improve P. aeruginosa-related mortality. We report here that interleukin-23 (IL-23), the cytokine most clearly tied to IL-17-mediated inflammation, also promotes IL-17-independent inflammation during P. aeruginosa pulmonary infection. During the early innate immune response, prior to IL-17 induction, IL-23 acts synergistically with IL-1β to promote early neutrophil (polymorphonuclear leukocyte [PMN]) recruitment. However, at later time points, IL-23 also promoted IL-17 production by lung γδ T cells, which was greatly augmented in the presence of IL-1β. These studies show that IL-23 controls two independent phases of neutrophil recruitment in response to P. aeruginosa infection: early PMN emigration that is IL-17 independent and later PMN emigration regulated by IL-17.
Insights
Interleukin-23 (IL-23) drives both early, IL-17-independent and later, IL-17-dependent neutrophil recruitment during Pseudomonas aeruginosa lung infections. Understanding these pathways may improve therapies for cystic fibrosis patients.
Area of Science:
- Immunology
- Pulmonary Medicine
- Microbiology
Background:
- Pseudomonas aeruginosa infection, common in cystic fibrosis (CF), increases mortality via inflammation and lung damage.
- Identifying inflammation regulators is crucial for developing new P. aeruginosa therapies.
Purpose of the Study:
- To investigate the role of interleukin-23 (IL-23) in P. aeruginosa pulmonary infection.
- To determine if IL-23 influences IL-17-independent and IL-17-dependent inflammatory responses.
Main Methods:
- The study examined the effects of IL-23 on neutrophil recruitment during P. aeruginosa infection in a host model.
- Investigated the synergistic effects of IL-23 with IL-1β on immune cell responses.
- Analyzed IL-17 production by lung γδ T cells in the presence of IL-23 and IL-1β.
Main Results:
- IL-23 promotes early neutrophil (polymorphonuclear leukocyte [PMN]) recruitment independently of IL-17, working with IL-1β.
- IL-23 also drives later IL-17 production by γδ T cells, especially with IL-1β.
- IL-23 controls two distinct phases of PMN recruitment during P. aeruginosa infection.
Conclusions:
- IL-23 plays a dual role in regulating neutrophil recruitment during P. aeruginosa lung infection.
- These findings highlight IL-23 as a key mediator in both early and late inflammatory phases.
- Targeting IL-23 pathways could offer novel therapeutic strategies for P. aeruginosa-induced lung disease.
