ArticleToxins2015
Diverse profiles of ricin-cell interactions in the lung following intranasal exposure to ricin.
Article in Toxins, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 38 citations in OpenAlex.
- NET degradation attenuates ricin-induced acute lung injury and protects mice from ARDS.Molecular medicine (Cambridge, Mass.) · 2025Article
- LRP1 Shedding in Ricin-Induced Lung Injury: A Cell-Specific Response to Toxin Exposure.International journal of molecular sciences · 2025Article
- Article
- Inflammatory Profiles Induced by Intranasal Immunization with Ricin Toxin-immune Complexes.ImmunoHorizons · 2024Article
- Short- and long-term outcomes of pulmonary exposure to a sublethal dose of ricin in mice.Scientific reports · 2024Article
- Long-Term Pulmonary Damage in Surviving Antitoxin-Treated Mice following a Lethal Ricin Intoxication.Toxins · 2024Article
- Article
- Comparative Aspects of Ricin Toxicity by Inhalation.Toxins · 2023Review
- New Insights into the Alveolar Epithelium as a Driver of Acute Respiratory Distress Syndrome.Biomolecules · 2022Review
- Characterization of Lung Injury following Abrin Pulmonary Intoxication in Mice: Comparison to Ricin Poisoning.Toxins · 2022Article
- Differential ER stress as a driver of cell fate following ricin toxin exposure.FASEB bioAdvances · 2022Article
- The low density receptor-related protein 1 plays a significant role in ricin-mediated intoxication of lung cells.Scientific reports · 2020Article
- Post-Exposure Anti-Ricin Treatment Protects Swine Against Lethal Systemic and Pulmonary Exposures.Toxins · 2020Article
- An intranasally administered monoclonal antibody cocktail abrogates ricin toxin-induced pulmonary tissue damage and inflammation.Human vaccines & immunotherapeutics · 2020Article
- Article
- Equal Neutralization Potency of Antibodies Raised against Abrin Subunits.Antibodies (Basel, Switzerland) · 2020Article
- Sites of vulnerability on ricin B chain revealed through epitope mapping of toxin-neutralizing monoclonal antibodies.PloS one · 2020Article
- Effects of ricin on primary pulmonary alveolar macrophages.The Journal of international medical research · 2019Article
- Intramuscular Ricin Poisoning of Mice Leads to Widespread Damage in the Heart, Spleen, and Bone Marrow.Toxins · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ricin, a plant-derived exotoxin, inhibits protein synthesis by ribosomal inactivation. Due to its wide availability and ease of preparation, ricin is considered a biothreat, foremost by respiratory exposure. We examined the in vivo interactions between ricin and cells of the lungs in mice intranasally exposed to the toxin and revealed multi-phasic cell-type-dependent binding profiles. While macrophages (MΦs) and dendritic cells (DCs) displayed biphasic binding to ricin, monophasic binding patterns were observed for other cell types; epithelial cells displayed early binding, while B cells and endothelial cells bound toxin late after intoxication. Neutrophils, which were massively recruited to the intoxicated lung, were refractive to toxin binding. Although epithelial cells bound ricin as early as MΦs and DCs, their rates of elimination differed considerably; a reduction in epithelial cell counts occurred late after intoxication and was restricted to alveolar type II cells only. The differential binding and cell-elimination patterns observed may stem from dissimilar accessibility of the toxin to different cells in the lung and may also reflect unequal interactions of the toxin with different cell-surface receptors. The multifaceted interactions observed in this study between ricin and the various cells of the target organ should be considered in the future development of efficient post-exposure countermeasures against ricin intoxication.
Indexed as
Identifiers
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.