ArticleEnvironment international2019
Low-dose cadmium potentiates lung inflammatory response to 2009 pandemic H1N1 influenza virus in mice.
Article in Environment international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Toxic metal exposure as a possible risk factor for COVID-19 and other respiratory infectious diseases.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Pooled it
- Single-cell RNA sequencing reveals dysregulation of innate immune signaling in early-life respiratory syncytial virus infection with subsequent low-level cadmium exposure.Toxicology reports · 2026Article
- Research Progress on Heavy Metals as Regulators of Bacterial Virulence in aPathogens (Basel, Switzerland) · 2026Review
- Association between heavy metal exposure and chronic cough: the mediating roles of inflammation.Annals of medicine · 2025Article
- Cadmium exposure following early-life respiratory syncytial virus infection promotes lung fibrosis through autophagy inhibition.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Cadmium toxicity and autophagy: a review.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- Study on the relationship between selenium and cadmium in diseased human lungs.Advances in redox research · 2023Article
- Can PPARBiomolecules · 2022Article
- Low-Dose Cadmium Potentiates Metabolic Reprogramming Following Early-Life Respiratory Syncytial Virus Infection.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Understanding the relationship between viral infections and trace elements from a metallomics perspective: implications for COVID-19.Metallomics : integrated biometal science · 2020Review
- Environmental Cadmium and Mortality from Influenza and Pneumonia in U.S. Adults.Environmental health perspectives · 2020Article
- Bioactive Natural Antivirals: An Updated Review of the Available Plants and Isolated Molecules.Molecules (Basel, Switzerland) · 2020Review
- Environmental Cadmium Enhances Lung Injury by Respiratory Syncytial Virus Infection.The American journal of pathology · 2019Article
- Redox Systems Biology of Nutrition and Oxidative Stress.The Journal of nutrition · 2019Article
- Low-dose cadmium disrupts mitochondrial citric acid cycle and lipid metabolism in mouse lung.Free radical biology & medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Cadmium (Cd) is a toxic, pro-inflammatory metal ubiquitous in the diet that accumulates in body organs due to inefficient elimination. Responses to influenza virus infection are variable, particularly severity of pneumonia. We used a murine model of chronic low-dose oral exposure to Cd to test if increased lung tissue Cd worsened inflammation in response to sub-lethal H1N1 infection. The results show that Cd-treated mice had increased lung tissue inflammatory cells, including neutrophils, monocytes, T lymphocytes and dendritic cells, following H1N1 infection. Lung genetic responses to infection (increasing TNF-α, interferon and complement, and decreasing myogenesis) were also exacerbated. To reveal the organization of a network structure, pinpointing molecules critical to Cd-altered lung function, global correlations were made for immune cell counts, leading edge gene transcripts and metabolites. This revealed that Cd increased correlation of myeloid immune cells with pro-inflammatory genes, particularly interferon-γ and metabolites. Together, the results show that Cd burden in mice increased inflammation in response to sub-lethal H1N1 challenge, which was coordinated by genetic and metabolic responses, and could provide new targets for intervention against lethal inflammatory pathology of clinical H1N1 infection.
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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.