Comparative evaluation of apoptosis induced by Shiga toxin 1 and/or lipopolysaccharides in human monocytic and macrophage-like cells

摘要: The enteric pathogens Shigella dysenteriae serotype 1 and Shiga toxin-producing Escherichia coli share the property of expressing structurally functionally related cytotoxins that comprise toxin (Stx) family. Stx-producing bacteria are causative agents bloody diarrheal diseases may progress to life threatening complications involving destruction blood vessels in kidneys central nervous system (CNS). precise mechanisms transport across gut epithelial barrier, role innate immunity development systemic complications, remain be fully characterized. Earlier studies suggested Stxs lipopolysaccharides (LPS) induce expression proinflammatory cytokines from differentiated (macrophage-like) THP-1 cells. These exacerbate vascular damage by up-regulating receptors on endothelial Purified have also been shown apoptosis cells vitro, but a comparative evaluation Stx-induced monocytes macrophages has not reported. We used FACS, TUNEL, DNA laddering analyses show toxin-1 (Stx1) LPS undifferentiated cells, although kinetics extent induction differ between monocytic macrophage-like Stx1-induced is A-subunit-dependent. Stx1 trigger fragmentation caspase-3 activation, as evidenced cleavage poly(ADP-ribose) polymerase (PARP). Induction response and/or treatment occurs without widespread transcriptional activation apoptosis-related genes. Finally, we present model pathogenesis disease caused Stxs.