ArticleVirulence2017
Pseudomonas aeruginosa proteolytically alters the interleukin 22-dependent lung mucosal defense.
Article in Virulence, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
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- Post-viral lung diseases: the microbiota as a key player.ERJ open research · 2025Review
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- Anti-Microorganisms · 2023Review
- Current Knowledge of Th22 Cell and IL-22 Functions in Infectious Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Novel Insights on Pyoverdine: From Biosynthesis to Biotechnological Application.International journal of molecular sciences · 2022Review
- Host succinate inhibits influenza virus infection through succinylation and nuclear retention of the viral nucleoprotein.The EMBO journal · 2022Article
- Review
- An In Vitro Cell Culture Model for Pyoverdine-Mediated Virulence.Pathogens (Basel, Switzerland) · 2020Article
- Participation of the IL-10RB Related Cytokines, IL-22 and IFN-λ in Defense of the Airway Mucosal Barrier.Frontiers in cellular and infection microbiology · 2020Review
- IL-22 Plays a Critical Role in Maintaining Epithelial Integrity During Pulmonary Infection.Frontiers in immunology · 2020Review
- Review
- Mechanism of Pseudomonas aeruginosa Small Protease (PASP), a Corneal Virulence Factor.Investigative ophthalmology & visual science · 2018Article
- Interleukin-22 Immunotherapy during Severe Influenza Enhances Lung Tissue Integrity and Reduces Secondary Bacterial Systemic Invasion.Infection and immunity · 2018Article
- Mechanisms and Targeted Therapies for Pseudomonas aeruginosa Lung Infection.American journal of respiratory and critical care medicine · 2018Review
- The best defense is a good (Protease) offense: How Pseudomonas aeruginosa evades mucosal immunity in the lung.Virulence · 2017Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The IL-22 signaling pathway is critical for regulating mucosal defense and limiting bacterial dissemination. IL-22 is unusual among interleukins because it does not directly regulate the function of conventional immune cells, but instead targets cells at outer body barriers, such as respiratory epithelial cells. Consequently, IL-22 signaling participates in the maintenance of the lung mucosal barrier by controlling cell proliferation and tissue repair, and enhancing the production of specific chemokines and anti-microbial peptides. Pseudomonas aeruginosa is a major pathogen of ventilator-associated pneumonia and causes considerable lung tissue damage. A feature underlying the pathogenicity of this bacterium is its capacity to persist and develop in the host, particularly in the clinical context of nosocomial lung infections. We aimed to investigate the ability of P. auruginosa to disrupt immune-epithelial cells cross-talk. We found that P. aeruginosa escapes the host mucosal defenses by degrading IL-22, leading to severe inhibition of IL-22-mediated immune responses. We demonstrated in vitro that, protease IV, a type 2 secretion system-dependent serine protease, is responsible for the degradation of IL-22 by P. aeruginosa. Moreover, the major anti-proteases molecules present in the lungs were unable to inhibit protease IV enzymatic activity. In addition, tracheal aspirates of patients infected by P. aeruginosa contain protease IV activity which further results in IL-22 degradation. This so far undescribed cleavage of IL-22 by a bacterial protease is likely to be an immune-evasion strategy that contributes to P. aeruginosa-triggered respiratory infections.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.