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Background:   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  Bitis gabonica  and  Dendroaspis angusticeps.Methods:   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).    Results:   The most prominent gene expressional changes were shown by  CASP5  (≈ 2.5 million-fold, confirmed by dedicated quantitative polymerase chain reaction) and  CARD9  (0.016-fold) for  B. gabonica,  and  BIRC7  (6.46-fold) and  CASP1  (0.30-fold) for  D. angusticeps.Conclusion:   The observed apoptotic environment suggests that pyroptosis may be the dominant pathway through which  B. gabonica  and  D. angusticeps  snake venoms trigger thymic epithelial apoptosis following envenomation.

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