Effect of Bitis gabonica and Dendroaspis angusticeps snake venoms on apoptosis-related genes in human thymic epithelial cells

Certain environmental toxins permanently damage the thymic epithelium, accelerate immune senescence and trigger secondary immune pathologies. However, the exact underlying cellular mechanisms and pathways of permanent immune intoxication remain unknown. The aim of the present study was to demonstrat...

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Veröffentlicht in:The journal of venomous animals and toxins including tropical diseases 2020-12, Vol.26, p.e20200057-e20200057
Hauptverfasser: Boda, Francisc, Banfai, Krisztina, Garai, Kitti, Kovacs, Bela, Almasi, Attila, Scheffer, Dalma, Sinkler, Reka Lambertne, Csonka, Robert, Czompoly, Tamas, Kvell, Krisztian
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Sprache:eng
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Zusammenfassung:Certain environmental toxins permanently damage the thymic epithelium, accelerate immune senescence and trigger secondary immune pathologies. However, the exact underlying cellular mechanisms and pathways of permanent immune intoxication remain unknown. The aim of the present study was to demonstrate gene expressional changes of apoptosis-related cellular pathways in human thymic epithelial cells following exposure to snake venom from and Snake venoms were characterized by analytical methods including reversed phase high-performance liquid chromatography and sodium dodecyl sulphate-polyacrylamide gel electrophoresis, then applied on human thymic epithelial cells (1889c) for 24 h at 10 μg/mL (as used in previous TaqMan Array study). Gene expressional changes restricted to apoptosis were assayed by TaqMan Array (Human Apoptosis Plate). The most prominent gene expressional changes were shown by (≈ 2.5 million-fold, confirmed by dedicated quantitative polymerase chain reaction) and (0.016-fold) for and (6.46-fold) and (0.30-fold) for The observed apoptotic environment suggests that pyroptosis may be the dominant pathway through which and snake venoms trigger thymic epithelial apoptosis following envenomation.
ISSN:1678-9199
1678-9199
DOI:10.1590/1678-9199-JVATITD-2020-0057