ArticleCell death & disease2021
Impairment in inflammasome signaling by the chronic Pseudomonas aeruginosa isolates from cystic fibrosis patients results in an increase in inflammatory response.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Molecular exploration of host-pathogen interactions in severeFrontiers in medicine · 2025Pooled it
- Identification of DksA as a novel pro-inflammatory mediator ofVirulence · 2026Article
- Bridging bench and bedside: translational omics ofEuropean respiratory review : an official journal of the European Respiratory Society · 2026Review
- Inflammasome Dynamics in the High-Risk Clone ST235 with Altered Pyoverdine Structures.International journal of molecular sciences · 2026Article
- Article
- Unraveling the immunosuppressive role of Elastase B produced by cystic fibrosis isolates ofVirulence · 2025Article
- Article
- Effects of influenza A infection on liberation of bacteria from biofilms and inflammatory response in anMicrobiology (Reading, England) · 2025Article
- Establishment and characterization of persistentInfection and immunity · 2025Article
- Isolation, Characterization, and Genomic Analysis of Bacteriophages AgainstMicroorganisms · 2025Article
- Article
- Uncovering a new family of conserved virulence factors that promote the production of host-damaging outer membrane vesicles in gram-negative bacteria.Journal of extracellular vesicles · 2025Article
- Neutrophil extracellular traps and interleukin-1β in cystic fibrosis lung disease.Frontiers in immunology · 2025Review
- Regulation of Zfp36 by ISGF3 and MK2 restricts the expression of inflammatory cytokines during necroptosis stimulation.Cell death & disease · 2024Article
- Secreted Metabolites fromMicroorganisms · 2024Article
- Quercetin attenuates Pseudomonas aeruginosa-induced acute lung inflammation by inhibiting PI3K/AKT/NF-κB signaling pathway.Inflammopharmacology · 2024Article
- Early host immune responses in a human organoid-derived gallbladder monolayer toFrontiers in immunology · 2024Article
- Review
- Deacetylation of Histones and Non-histone Proteins in Inflammatory Diseases and Cancer Therapeutic Potential of Histone Deacetylase Inhibitors.Current genomics · 2023Review
- AtbFinder Diagnostic Test System Improves Optimal Selection of Antibiotic Therapy in Persons with Cystic Fibrosis.Journal of clinical microbiology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Pseudomonas aeruginosa is a common respiratory pathogen in cystic fibrosis (CF) patients which undergoes adaptations during chronic infection towards reduced virulence, which can facilitate bacterial evasion of killing by host cells. However, inflammatory cytokines are often found to be elevated in CF patients, and it is unknown how chronic P. aeruginosa infection can be paradoxically associated with both diminished virulence in vitro and increased inflammation and disease progression. Thus, we investigated the relationship between the stimulation of inflammatory cell death pathways by CF P. aeruginosa respiratory isolates and the expression of key inflammatory cytokines. We show that early respiratory isolates of P. aeruginosa from CF patients potently induce inflammasome signaling, cell death, and expression of IL-1β by macrophages, yet little expression of other inflammatory cytokines (TNF, IL-6 and IL-8). In contrast, chronic P. aeruginosa isolates induce relatively poor macrophage inflammasome signaling, cell death, and IL-1β expression but paradoxically excessive production of TNF, IL-6 and IL-8 compared to early P. aeruginosa isolates. Using various mutants of P. aeruginosa, we show that the premature cell death of macrophages caused by virulent bacteria compromises their ability to express cytokines. Contrary to the belief that chronic P. aeruginosa isolates are less pathogenic, we reveal that infections with chronic P. aeruginosa isolates result in increased cytokine induction due to their failure to induce immune cell death, which results in a relatively intense inflammation compared with early isolates.
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