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Table 1 Selected in vitro studies implicating lethal (LT) or edema toxin (ET) in endothelial cell dysfunction

From: B. anthracisassociated cardiovascular dysfunction and shock: the potential contribution of both non-toxin and toxin components

Study Toxin Cell type Toxin effect
Rolando, M. 2010 LT HUVEC Exerted cytotoxic effects on endothelial cell monolayers with elongation and redistribution of VE-cadherin and subsequent cell death; increased caspase-3, 8 and 9 activity. Up-regulation of TNF-related apoptosis-inducing ligand (TRAIL) and down-regulation of xaf1 (XIAP associated factor-1) participated in LT-induced caspase-3 activation; increased caspase-3 dependent cortactin and rhophilin-2 activity in combination with calponin-1 expression appeared necessary for LT mediated actin cable formation.
Guichard, A. 2010 LT Human brain, dermal and lung microvascular endothelial cells (HBMEC, HDMEC and HMVEC-Ls, respectively) Lethal factor (LF) worked synergistically with edema factor (EF) to reduce DE-cadherin levels at adherens junctions in HBMEC, HDMECs and HMVEC-Ls.
Warfel, J. 2011 LT Human lung microvascular endothelial cells Increased monolayer permeability, effects on permeability associated with the activation of Rho associated kinase (ROCK-1) and increased myosin light chain (MLC) phosphorylation and subsequent actin stress fiber formation and VE-cadherin gene and protein expression inhibition.
Liu, T. 2012 LT Rat pulmonary microvascular endothelial cells Increased gap formation and permeability of endothelial cell monolayers; decreased p38 signaling; permeability effects overcome by pmHSP27 over-expression.
Guichard, A. 2010 ET Human brain, dermal and lung microvascular endothelial cells (HBMEC, HDMEC and HMVEC-Ls, respectively) Edema factor (EF) worked synergistically with lethal factor (LF) to reduce DE-cadherin levels at adherens junctions in HBMEC, HDMECs and HMVEC-Ls.
EF increased the permeability of HBMEC trans-well monolayers.
Maddugoda, M. 2011 ET Mouse endothelial cells, HUVEC Stimulated trans-endothelial macro-aperture (TEM) tunnel formation and increased endothelial permeability potentially via cAMP mediated mechanisms.
Ebrahimi, C. 2011 ET HBMEC Disrupted tight junction formation and barrier function and monolayer integrity; contributed to disruption of endothelial cells and ZO-1, a primary regulatory protein of tight junction formation in the blood?brain barrier.