ArticlePloS one2014
Toll-like receptor 9 deficiency protects mice against Pseudomonas aeruginosa lung infection.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Cytosolic nucleic acid sensing as driver of critical illness: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2025Review
- Acid ceramidase regulates CD8+ T-cell exhaustion via type I interferon-mediated upregulation of PD-L1.Frontiers in immunology · 2025Article
- DNA at the center of mammalian innate immune recognition of bacterial biofilms.Trends in immunology · 2024Review
- Battle royale: Immune response on biofilms - host-pathogen interactions.Current research in immunology · 2023Review
- TLR9 Negatively Regulates Intracellular Bacterial Killing by Pyroptosis in Burkholderia pseudomalleiMicrobiology spectrum · 2022Article
- LACpG10-HL Functions Effectively in Antibiotic-Free and Healthy Husbandry by Improving the Innate Immunity.International journal of molecular sciences · 2022Article
- Isthmin 1 is Expressed by Progenitor-Like Cells in the Lung: Phenotypical Analysis of Isthmin 1Journal of immunology research · 2022Article
- Bacteriocin BacSp222 and Its Succinylated Forms Exhibit Proinflammatory Activities Toward Innate Immune Cells .Journal of inflammation research · 2022Article
- Extracellular DNA (eDNA). A Major Ubiquitous Element of the Bacterial Biofilm Architecture.International journal of molecular sciences · 2021Review
- The Role of Innate Immunity in Pulmonary Infections.BioMed research international · 2021Review
- Neutrophil-Dependent Immunity During Pulmonary Infections and Inflammations.Frontiers in immunology · 2021Review
- UnderstandingCells · 2020Review
- The Role of Insulin Regulated Aminopeptidase in Endocytic Trafficking and Receptor Signaling in Immune Cells.Frontiers in molecular biosciences · 2020Review
- Pf Bacteriophage and Their Impact on Pseudomonas Virulence, Mammalian Immunity, and Chronic Infections.Frontiers in immunology · 2020Review
- Article
- IRAPNature immunology · 2017Article
- Inflammation: A Double-Edged Sword in the Response to Pseudomonas aeruginosa Infection.Journal of innate immunity · 2017Review
- TLR9 expression is required for the development of cigarette smoke-induced emphysema in mice.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Current Concepts and Controversies in Innate Immunity of Cystic Fibrosis Lung Disease.Journal of innate immunity · 2016Review
- Microbial Nucleic Acid Sensing in Oral and Systemic Diseases.Journal of dental research · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudomonas aeruginosa is an opportunistic pathogen involved in nosocomial infections. While a number of studies have demonstrated the roles of TLR2, TLR4 and TLR5 in host defense againt P. aeruginosa infection, the implication of TLR9 in this process has been overlooked. Here, we show that P. aeruginosa DNA stimulates the inflammatory response through TLR9 pathway in both a cell line and primary alveolar macrophages (AMs). This activation requires asparagine endopeptidase- and endosomal acidification. Interestingly, TLR9-/- mice resisted to lethal lung infection by P. aeruginosa, compared to WT C57BL/6 mice. The resistance of TLR9-/- mice to P. aeruginosa infection was associated with: (i) a higher ability of TLR9-/- AMs to kill P. aeruginosa; (ii) a rapid increase in the pro-inflammatory cytokines such as TNFα, IL-1β and IL-6 production; and (iii) an increase in nitric oxide (NO) production and inductible NO synthase expression in AMs. In addition, inhibition of both IL-1β and NO production resulted in a significant decrease of P. aeruginosa clearance by AMs. Altogether these results indicate that TLR9 plays a detrimental role in pulmonary host defense toward P. aeruginosa by reducing the AMs clearance activity and production of IL-1β and NO necessary for bacteria killing.
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Registered trials
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.