ArticleScientific reports2017
Stingray venom activates IL-33 producing cardiomyocytes, but not mast cell, to promote acute neutrophil-mediated injury.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Isolation and Characterization of the First Antigen-Specific EGFRvIII vNAR from Freshwater Stingray (International journal of molecular sciences · 2025Article
- Histopathological characterization of skin and muscle lesions induced by lionfish (The journal of venomous animals and toxins including tropical diseases · 2025Article
- A comprehensive overview of fish envenomation and venom toxicity in Brazil.The journal of venomous animals and toxins including tropical diseases · 2025Article
- Effective Pre-Clinical Treatment of Fish Envenoming with Polyclonal Antiserum.International journal of molecular sciences · 2023Article
- Review
- Natterin-Induced Neutrophilia Is Dependent on cGAS/STING Activation via Type I IFN Signaling Pathway.International journal of molecular sciences · 2022Article
- Cytokine Production Is Differentially Modulated in Malignant and Non-malignant Tissues in ST2-Receptor Deficient Mice.Inflammation · 2018Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the hallmarks of acute inflammation is neutrophil infiltration of tissues. We investigated molecular mechanisms implicated in acute neutrophilic inflammation induced by the venom of a freshwater stingray (Potamotrygon cf. henlei) in mice. Ray venom induced early mobilization of neutrophil in the microvasculature of cremaster mice and infiltration of the peritoneal cavity 2 hours after injury, in a dose-response manner. IL-1β, IL-6, TNF-α, and KC were produced. The neutrophilic infiltration did not occur in mice with ST2 receptor and MyD88 adapters neutralized, or in those with PI3K and p38 MAPK signaling blocked. Drastic reduction of neutrophil infiltration to peritoneal cavities was observed in ST2
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