ArticleExperimental gerontology2012
Enteric-delivered rapamycin enhances resistance of aged mice to pneumococcal pneumonia through reduced cellular senescence.
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 52 papers, 1 of them a synthesis that pooled it.
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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.
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.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Rapamycin not dietary restriction improves resilience against pathogens: a meta-analysis.GeroScience · 2023Pooled it
- mTORC1 inhibition by sirolimus as adjunctive treatment in experimental pneumococcal meningitis.Brain communications · 2026Article
- Enhancing immunity during ageing by targeting interactions within the tissue environment.Nature reviews. Drug discovery · 2025Review
- Article
- Impact of aging on immune function in the pathogenesis of pulmonary diseases: potential for therapeutic targets.Expert review of respiratory medicine · 2023Review
- Rapamycin ExacerbatesJournal of inflammation research · 2023Article
- Cell senescence, rapamycin and hyperfunction theory of aging.Cell cycle (Georgetown, Tex.) · 2022Review
- Metformin Attenuates Inflammatory Responses and Enhances Antibody Production in an Acute Pneumonia Model ofFrontiers in aging · 2022Article
- Anti-aging: senolytics or gerostatics (unconventional view).Oncotarget · 2021Review
- Effect of rapamycin on aging and age-related diseases-past and future.GeroScience · 2021Review
- Intersection of immunometabolism and immunosenescence during aging.Current opinion in pharmacology · 2021Review
- Older but Not Wiser: the Age-Driven Changes in Neutrophil Responses during Pulmonary Infections.Infection and immunity · 2021Review
- Macrophage LC3-associated phagocytosis is an immune defense againstProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Senescence and Host-Pathogen Interactions.Cells · 2020Review
- Omega-3 fatty acids in contrast to omega-6 protect against pneumococcal pneumonia.Microbial pathogenesis · 2020Article
- Correlative imaging of ionic transport and electronic structure in nano LiChemical communications (Cambridge, England) · 2020Article
- How Inflammation Blunts Innate Immunity in Aging.Interdisciplinary topics in gerontology and geriatrics · 2020Review
- Rapamycin for the aging skin.Aging · 2019Article
- Rapamycin for longevity: opinion article.Aging · 2019Article
- Rapamycin‑induced miR‑30a downregulation inhibits senescence of VSMCs by targeting Beclin1.International journal of molecular medicine · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Rapamycin, a potent immunomodulatory drug, has shown promise in the amelioration of numerous age-associated diseases including cancer, Alzheimer's disease and cardiac hypertrophy. Yet the elderly, the population most likely to receive therapeutic rapamycin, are already at increased risk for infectious disease; thus concern exists that rapamycin may exacerbate age-associated immune dysfunctions and worsen infection outcomes. Herein, we examined the impact of enteric delivered rapamycin monotherapy (eRapa) on the susceptibility of aged (22-24month) C57BL/6 mice to Streptococcus pneumoniae, the leading bacterial cause of community-acquired pneumonia. Following challenge with S. pneumoniae, administration of eRapa conferred modest protection against mortality. Reduced mortality was the result of diminished lung damage rather than reduced bacterial burden. eRapa had no effect on basal levels of Interleukin (IL)-1α, IL-6, IL-10, IL-12p70, KC, Interferon-γ, Tumor necrosis factor α and Monocyte chemotactic protein-1 in whole lung homogenates or during pneumococcal pneumonia. Previously we have demonstrated that cellular senescence enhances permissiveness for bacterial pneumonia through increased expression of the bacterial ligands Laminin receptor (LR), Platelet-activating factor receptor (PAFr) and Cytokeratin 10 (K10). These proteins are co-opted by S. pneumoniae and other respiratory tract pathogens for host cell attachment during lung infection. UM-HET3 mice on eRapa had reduced lung cellular senescence as determined by levels of the senescence markers p21 and pRB, but not mH2A.1. Mice on eRapa also had marked reductions in PAFr, LR, and K10. We conclude that eRapa protected aged mice against pneumonia through reduced lung cellular senescence, which in turn, lowered bacterial ligand expression.
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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.