ArticleExperimental gerontology2012
Age-related defects in TLR2 signaling diminish the cytokine response by alveolar macrophages during murine pneumococcal pneumonia.
Article in Experimental gerontology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 116 citations in OpenAlex.
- Respiratory virus immune response in the aged host.Immunity & ageing : I & A · 2026Review
- Targeting senescence-associated secretory phenotype macrophage: apigenin inhibits DOT1L-dependent H3K79me2 atFrontiers in molecular biosciences · 2026Article
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Glabridin attenuates LTA‑induced alveolar macrophage migration via activation of the Nrf2/HO‑1 pathway.Molecular medicine reports · 2026Article
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- Aging-associated changes in immunological parameters: Implications for COVID-19 immune response in the elderly.Physiological reports · 2025Review
- Innate immunosenescence and sepsis in the elderly: mechanisms and innate immune modulation strategies.Central-European journal of immunology · 2025Review
- Immunosenescence, Physical Exercise, and their Implications in Tumor Immunity and Immunotherapy.International journal of biological sciences · 2025Review
- Healthy and premature aging of monocytes and macrophages.Frontiers in immunology · 2025Review
- Ageing results in an exacerbated inflammatory response to LPS by resident lung cells.Immunity & ageing : I & A · 2024Article
- Unveiling mechanisms of lung aging in COPD: A promising target for therapeutics development.Chinese medical journal pulmonary and critical care medicine · 2024Review
- Activating A1 adenosine receptor signaling boosts early pulmonary neutrophil recruitment in aged mice in response to Streptococcus pneumoniae infection.Immunity & ageing : I & A · 2024Article
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- FocalJournal of inflammation research · 2024Article
- The aging lung: microenvironment, mechanisms, and diseases.Frontiers in immunology · 2024Review
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- Clinical risk factors and blood protein biomarkers of 10-year pneumonia risk.medRxiv : the preprint server for health sciences · 2023Article
- The Impact of Aging and Toll-like Receptor 2 Deficiency on the Clinical Outcomes of Staphylococcus aureus Bacteremia.The Journal of infectious diseases · 2023Article
- Age-related exacerbation of lung damage after trauma is associated with increased expression of inflammasome components.Frontiers in immunology · 2023Article
- Mitochondrial dysfunction at the cornerstone of inflammatory exacerbation in aged macrophages.Exploration of immunology · 2023Article
10 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Alveolar macrophages (AMs) are the first immune cells to respond to an invading pathogen and coordinate the inflammatory response within the lungs. Studies suggest that macrophages exhibit age-related deficiencies in Toll-like receptor (TLR) function; however, the impact of this dysfunction during pneumonia, the leading cause of infectious death in the elderly, and the underlying mechanisms responsible remain unclear. We examined disease severity in young, mature, and aged BALB/cBy mice following intratracheal infection with the Gram-positive bacteria Streptococcus pneumoniae (Spn). Both mature and aged mice failed to clear bacteria and as a result had increased mortality, tissue damage and vascular leakage. Early production of TNFα, IL-1β, and IL-6 during pneumonia declined with age and was associated with an inability of isolated AMs to respond to pneumococcal cell wall (CW) and ethanol-killed Spn ex vivo. Total levels of TLR1 were unaffected by age and TLR2 surface expression was slightly yet significantly increased on aged AMs suggesting that intracellular TLR signaling defects were responsible for the age-related decline in cytokine responsiveness. Following infection of isolated AMs with live Spn, a significant age-related decline in TLR2-induced phosphorylation of p65 NFκB, JNK and p38 MAPK, and an increase in ERK phosphorylation was observed by immunoblotting. These data are the first to demonstrate that TLR2-dependent recognition of Spn by aged AMs is impaired and is associated with a delayed pro-inflammatory cytokine response in vivo along with enhanced susceptibility to pneumococcal pneumonia.
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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.