Trial reportMucosal immunology2014
Dendritic cells from aged subjects contribute to chronic airway inflammation by activating bronchial epithelial cells under steady state.
Trial report in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 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
32 citing papers in PubMed, 40 citations in OpenAlex.
- Chronic IL-21 exposure reshapes pulmonary environment, elevating risk of respiratory diseases.Cellular and molecular life sciences : CMLS · 2026Article
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Age-Related Impairment of Innate and Adaptive Immune Responses Exacerbates Herpes Simplex Viral Infection.Pathogens (Basel, Switzerland) · 2025Article
- Zinc deficiency as possible link between immunosenescence and age-related diseases.Immunity & ageing : I & A · 2025Review
- Therapy-induced senescence is a transient drug resistance mechanism in breast cancer.Molecular cancer · 2025Article
- CCL26 as a prognostic biomarker in hepatocellular carcinoma: integrating bioinformatics analysis, clinical validation, and radiomics score.Discover oncology · 2025Article
- Influence of Aging and Immune Alterations on Susceptibility to Pneumococcal Pneumonia in the Elderly.Pathogens (Basel, Switzerland) · 2025Review
- Epithelial Barrier Theory: The Role of Exposome, Microbiome, and Barrier Function in Allergic Diseases.Allergy, asthma & immunology research · 2023Review
- Review
- Short palate, lung, and nasal epithelial clone 1 (SPLUNC1) level determines steroid-resistant airway inflammation in aging.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Cellular senescence is a key mediator of lung aging and susceptibility to infection.Frontiers in immunology · 2022Review
- Immunosenescence: A Critical Factor Associated With Organ Injury After Sepsis.Frontiers in immunology · 2022Review
- Age-related changes in ocular mucosal tolerance: Lessons learned from gut and respiratory tract immunity.Immunology · 2021Review
- The ocular surface immune system through the eyes of aging.The ocular surface · 2021Review
- Discovery of core gene families associated with liver metastasis in colorectal cancer and regulatory roles in tumor cell immune infiltration.Translational oncology · 2021Article
- Review
- NETs Are Double-Edged Swords with the Potential to Aggravate or Resolve Periodontal Inflammation.Cells · 2020Review
- Immunogenetic Association Underlying Severe COVID-19.Vaccines · 2020Review
- An Inflamed Human Alveolar Model for Testing the Efficiency of Anti-inflammatory DrugsFrontiers in bioengineering and biotechnology · 2020Article
- Age-associated antigen-presenting cell alterations promote dry-eye inducing Th1 cells.Mucosal immunology · 2019Article
Corrections and comments
- Erratum issuedBenMohamad, L [corrected to BenMohamed, L]
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms underlying the increased susceptibility of the elderly to respiratory infections are not well understood. The crosstalk between the dendritic cells (DCs) and epithelial cells is essential in maintaining tolerance as well as in generating immunity in the respiratory mucosa. DCs from aged subjects display an enhanced basal level of activation, which can affect the function of epithelial cells. Our results suggest that this is indeed the scenario as exposure of primary bronchial epithelial cells (PBECs) to supernatants from unstimulated DCs of aged subjects resulted in activation of PBECs. The expression of CCL20, CCL26, CXCL10, mucin, and CD54 was significantly increased in the PBECs exposed to aged DC supernatants, but not to young DC supernatants. Furthermore, aged DC supernatants also enhanced the permeability of the PBEC barrier. We also found that DCs from aged subjects spontaneously secreted increased levels of pro-inflammatory mediators, interleukin-6, tumor necrosis factor (TNF)-α, and metalloproteinase A disintegrin family of metalloproteinase 10, which can affect the functions of PBECs. Finally, we demonstrated that TNF-α, present in the supernatant of DCs from aged subjects, was the primary pro-inflammatory mediator that affected PBEC functions. Thus, age-associated alterations in DC-epithelial interactions contribute to chronic airway inflammation in the elderly, increasing their susceptibility to respiratory diseases.
Indexed as
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What OpenQuestion holds
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.