Immunomodulatory Potency of Microcystin, an Important Water-Polluting Cyanobacterial Toxin
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Cell Line drug effects MeSH
- Water Pollutants, Chemical toxicity MeSH
- Immunologic Factors toxicity MeSH
- Interleukin-6 metabolism MeSH
- Macrophages drug effects metabolism pathology MeSH
- Microcystins toxicity MeSH
- Marine Toxins MeSH
- Mice MeSH
- NF-kappa B metabolism MeSH
- Immunity, Innate drug effects MeSH
- Protein Phosphatase 2 metabolism MeSH
- Cyanobacteria pathogenicity MeSH
- Toxicity Tests, Chronic methods MeSH
- Tumor Necrosis Factor-alpha metabolism MeSH
- Inflammation chemically induced immunology metabolism MeSH
- Water Supply MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Water Pollutants, Chemical MeSH
- cyanoginosin LR MeSH Browser
- Immunologic Factors MeSH
- interleukin-6, mouse MeSH Browser
- Interleukin-6 MeSH
- Microcystins MeSH
- Marine Toxins MeSH
- NF-kappa B MeSH
- Protein Phosphatase 2 MeSH
- Tumor Necrosis Factor-alpha MeSH
Microcystins (MCs) are primarily hepatotoxins produced by cyanobacteria and are responsible for intoxication in humans and animals. There are many incidents of chronic exposure to MCs, which have been attributed to the inappropriate treatment of water supplies or contaminated food. Using RAW 264.7 macrophages, we showed the potency of microcystin-LR (MC-LR) to stimulate production of pro-inflammatory cytokines (tumor necrosis factor α and interleukin-6) as a consequence of fast nuclear factor κB and nitrogen-activated protein kinase activation. In contrast to other studies, the observed effects were not attributed to the intracellular inhibition of protein phosphatases 1/2A due to lack of specific transmembrane transporters for MCs. However, the MC-LR-induced activation of macrophages was effectively inhibited by a specific peptide that blocks signaling of receptors, which play a pivotal role in the innate immune responses. Taken together, we showed for the first time that MC-LR could interfere with macrophage receptors that are responsible for triggering the above-mentioned signaling pathways. These findings provide an interesting mechanistic explanation of some adverse health outcomes associated with toxic cyanobacteria and MCs.
Faculty of Science RECETOX Masaryk University Kamenice 753 5 62500 Brno Czech Republic
Institute of Biophysics Academy of Sciences Královopolská 135 612 65 Brno Czech Republic
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