ArticleScientific reports2016
The host genetic background defines diverse immune-reactivity and susceptibility to chronic Pseudomonas aeruginosa respiratory infection.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Chronic infection by nontypeableERJ open research · 2021Article
- Mice Lacking γδ T Cells Exhibit Impaired Clearance of Pseudomonas aeruginosa Lung Infection and Excessive Production of Inflammatory Cytokines.Infection and immunity · 2020Article
- Susceptibility Analysis in Several Mouse Strains Reveals Robust T-Cell Responses AfterFrontiers in cellular and infection microbiology · 2020Article
- The impact of host genetic background in the Pseudomonas aeruginosa respiratory infections.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Synthesized Heparan Sulfate Competitors Attenuate Pseudomonas aeruginosa Lung Infection.International journal of molecular sciences · 2018Article
- The Collaborative African Genomics Network (CAfGEN): Applying Genomic technologies to probe host factors important to the progression of HIV and HIV-tuberculosis infection in sub-Saharan Africa.AAS open research · 2018Article
- Inflammation: A Double-Edged Sword in the Response to Pseudomonas aeruginosa Infection.Journal of innate immunity · 2017Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with P. aeruginosa airways infection show markedly variable clinical phenotypes likely influenced by genetic backgrounds. Here, we investigated the cellular events involved in resistance and susceptibility to P. aeruginosa chronic infection using genetically distinct inbred mouse strains. As for patients, different murine genotypes revealed variable susceptibility to infection. When directly compared, resistant C3H/HeOuJ and susceptible A/J strains revealed distinct immune responsiveness to the pathogen. In C3H/HeOuJ resistant mice, IL17-producing cells rapidly and transiently infiltrated the infected lung, and this was paralleled by the acute accumulation of alveolar macrophages, bacterial clearance and resolution of infection. In contrast, A/J susceptible mice revealed a more delayed and prolonged lung infiltration by IL17
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