Neither microcystin, nor nodularin, nor cylindrospermopsin directly interact with human toll-like receptors

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Publikace nespadá pod Ekonomicko-správní fakultu, ale pod Přírodovědeckou fakultu. Oficiální stránka publikace je na webu muni.cz.
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HANSEN John D. LOFTIN Keith A. LAUGHREY Zachary ADAMOVSKÝ Ondřej

Rok publikování 2021
Druh Článek v odborném periodiku
Časopis / Zdroj Chemosphere
Fakulta / Pracoviště MU

Přírodovědecká fakulta

Citace
www https://www.sciencedirect.com/science/article/pii/S0045653521000928?via%3Dihub
Doi http://dx.doi.org/10.1016/j.chemosphere.2021.129623
Klíčová slova Cyanotoxin; Toll-like receptor; Inflammation; NF-kappa B
Popis Various stressors including temperature, environmental chemicals, and toxins can have profound impacts on immunity to pathogens. Increased eutrophication near rivers and lakes coupled with climate change are predicted to lead to increased algal blooms. Currently, the effects of cyanobacterial toxins on disease resistance in mammals is a largely unexplored area of research. Recent studies have suggested that freshwater cyanotoxins can elicit immunomodulation through interaction with specific components of innate immunity, thus potentially altering disease susceptibility parameters for fish, wildlife, and human health owing to the conserved nature of the vertebrate immune system. In this study, we investigated the effects of three microcystin congeners (LR, LA, and RR), nodularin-R, and cylin-drospermopsin for their ability to directly interact with nine different human Toll-like receptors (TLRs)-key pathogen recognition receptors for innate immunity. Toxin concentrations were verified by LC/MS/MS prior to use. Using an established HEK293-hTLR NF-kappa B reporter assay, we concluded that none of the tested toxins (29-90 nM final concentration) directly interacted with human TLRs in either an agonistic or antagonistic manner. These results suggest that earlier reports of cyanotoxin-induced NF-kappa B responses likely occur through different surface receptors to mediate inflammation. Published by Elsevier Ltd.
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