ArticleRespiratory research2024
Age-dependent inflammatory response is altered in an ex vivo model of bacterial pneumonia.
Article in Respiratory research, 2024. 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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Who cites it
7 citing papers in PubMed, 4 citations in OpenAlex.
- Bronchiectasis in Older Adults: Distinctive Epidemiology, Etiology, Diagnosis, and Clinical Evolution Compared with Younger Populations.Drugs & aging · 2026Review
- Machine learning-based precision subtyping and risk prediction in sepsis: a retrospective analysis using MIMIC-IV database.BMC infectious diseases · 2026Article
- The Inflammation-Metabolism Axis in Preserved Ratio Impaired Spirometry: Pathogenic Mechanisms and Translational Implications.Journal of inflammation research · 2026Review
- RNA modifications shape innate immunity and cellular adaptation during bacterial respiratory infection.Frontiers in immunology · 2026Review
- Lower respiratory tract microbiota characteristics in patients withFrontiers in cellular and infection microbiology · 2026Article
- Global, regional, and national burden of autoimmune disease in older adults (≥60 years) from 1990 to 2021: Results from the Global Burden of Disease Study 2021.The journal of nutrition, health & aging · 2025Article
- Precision cut lung slices: an integrated ex vivo model for studying lung physiology, pharmacology, disease pathogenesis and drug discovery.Respiratory research · 2024Review
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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
backgroundAging is associated with an increased incidence and mortality of Pseudomonas aeruginosa-induced pneumonias. This might be partly due to age-dependent increases in inflammatory mediators, referred to as inflamm-aging and a decline in immune functions, known as immunosenescence. Still, the impact of dysregulated immune responses on lung infection during aging is poorly understood. Here, we aimed to mimic inflamm-aging using ex vivo precision-cut lung slices (PCLS) and neutrophils - as important effector cells of innate immunity - from young and old mice and investigated the influence of aging on inflammation upon infection with P. aeruginosa bacteria.
methodsMurine PCLS were infected with the P. aeruginosa standard lab strain PAO1 and a clinical P. aeruginosa isolate D61. After infection, whole-transcriptome analysis of the tissue as well as cytokine expression in supernatants and tissue lysates were performed. Responses of isolated neutrophils towards the bacteria were investigated by quantifying neutrophil extracellular trap (NET) formation, cytokine secretion, and analyzing expression of surface activation markers using flow cytometry.
resultsInflamm-aging was observed by transcriptome analysis, showing an enrichment of biological processes related to inflammation, innate immune response, and chemotaxis in uninfected PCLS of old compared with young mice. Upon P. aeruginosa infection, the age-dependent pro-inflammatory response was even further promoted as shown by increased production of cytokines and chemokines such as IL-1β, IL-6, CXCL1, TNF-α, and IL-17A. In neutrophil cultures, aging did not influence NET formation or cytokine secretion during P. aeruginosa infection. However, expression of receptors associated with inflammatory responses such as complement, adhesion, phagocytosis, and degranulation was lower in neutrophils stimulated with bacteria from old mice as compared to young animals.
conclusionsBy using PCLS and neutrophils from young and old mice as immunocompetent ex vivo test systems, we could mimic dysregulated immune responses upon aging on levels of gene expression, cytokine production, and receptor expression. The results furthermore reflect the exacerbation of inflammation upon P. aeruginosa lung infection as a result of inflamm-aging in old age.
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