<i>Pseudomonas aeruginosa</i> cytotoxin stimulates prostacyclin production in cultured pulmonary artery endothelial cells: Membrane attack and calcium influx

Suttorp, Norbert; Seeger, Werner; Uhl, J.; Lutz, F.; Róka, L

doi:10.1002/jcp.1041230111

Cited by 67 publications

(26 citation statements)

References 37 publications

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“…The consequence is increased plasma membrane permeability to small molecules and ions. Such intoxication has been documented in granulocytes (Baltch et al 1985), endothelial cells (Suttorp et al 1985), Ehrlich ascites tumor cells , and human leukemic cells (Sasak and Lutz 1985). In the case of granulocytes, treatment with the cytotoxin causes an inhibition of the ability of granulocytes to kill P. aeruginosa cells (Baltch et al 1985).…”

Section: Invasionmentioning

confidence: 99%

Contribution of an arsenal of virulence factors to pathogenesis of Pseudomonas aeruginosa infections

2011

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Pseudomonas aeruginosa is an increasingly prevalent opportunistic pathogen that causes a variety of nosocomial infections, life-threatening diseases in immunocompromised persons and chronic pulmonary infections in cystic fibrosis patients. The organism's virulence depends on an arsenal of cell-associated and extracellular factors determining the pathogenesis of infections as multifactorial. Most P. aeruginosa infections are both invasive and toxinogenic. Many of the extracellular virulence factors (proteases, exotoxin A, pyocyanin, siderophores, hemolysins) required for tissue invasion and dissemination of P. aeruginosa are controlled by quorum sensing (QS) that enable the bacteria to produce these factors in a coordinated, cell-density-dependent manner and overwhelm the host defense mechanisms during acute infection. Sometimes, QS also contributes to biofilm formation and thus participates in pathogenesis of chronic infection. This system is recognized to be a global regulatory network controlling the expression of a large number of virulence genes either directly or indirectly. Two-component sensor kinases such as RetS, LadS and GacS are also controlling the production of virulence factors as well as the switch from acute to chronic infection. The present review describes the known virulence determinants of P. aeruginosa, the stages of infection as well as the importance of QS in the pathogenesis of P. aeruginosa infection.

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Section: Invasionmentioning

confidence: 99%

Contribution of an arsenal of virulence factors to pathogenesis of Pseudomonas aeruginosa infections

2011

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“…To screen for ToxB-1470, standard cytotoxicity tests were carried out with CHO cells (EicheI-Streiber et aL, 1987). Morphological changes were assayed on endothelial cells from the pulmonary artery of pigs (Suttorp et aL, 1985). F-actin was stained with fluorescein-labelled phalloidin (Oksche et aL, 1992).…”

Section: Functional Testsmentioning

confidence: 99%

Closing in on the toxic domain through analysis of a variant Clostridium difficile cytotoxin B

Eichel-Streiber

Heringdorf

Habermann

et al. 1995

Molecular Microbiology

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Strain 1470 is the standard typing strain for serogroup F of Clostridium difficile containing both toxin genes, toxA-1470 and toxB-1470. A polymerase chain reaction (PCR)-based approach to the sequencing of the total toxB-1470 gene identified an open reading frame (ORF) of 7104 nucleotides. In comparison with the previously sequenced toxB of C. difficile VP10463, the toxB-1470 gene has 16 additional nucleotides, 13 within the 5'-untranslated region and three within the coding region. The M(r) of ToxB-1470 is 269,262, with an isoelectric point (IP) of 4.16. The equivalent values for ToxB are M(r) 269,709 and IP 4.13. In comparison with ToxB, ToxB-1470 differs primarily in the N-terminal region between positions 1 and 868 where 148 amino acids residues are changed. The C-terminal region between residues 869-2367 is highly conserved with only six amino acid alterations. Dot matrix comparison of ToxB-1470 with ToxA and ToxB reveals the highest homology between ToxB-1470 and ToxB. Thus ToxB-1470 did not originate from recombination between ToxA and ToxB. On cultured endothelial cells, from porcine pulmonary artery, purified ToxB-1470 is less potent than ToxB. The cytopathic effects of ToxB-1470 are indistinguishable from those caused by the lethal toxin (LT) of Clostridium sordellii, but are clearly different from the patterns observed after exposure of endothelial cells to ToxA and ToxB of C. difficile (VPI10463) or alpha-toxin (Tcn alpha) of Clostridium novyi. The LT-like action of ToxB-1470 was not due to altered internalization processes, as microinjection and addition to the medium induced identical effects on the cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Endothelial cells were isolated, characterized, maintained, and dispersed as previously described (37)(38)(39).…”

Section: Introductionmentioning

confidence: 99%

Adenosine diphosphate-ribosylation of G-actin by botulinum C2 toxin increases endothelial permeability in vitro.

Suttorp¹,

Polley²,

Seybold³

et al. 1991

J. Clin. Invest.

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The endothelial cytoskeleton is believed to play an important role in the regulation ofendothelial permeability. We used botulinum C2 toxin to perturb cellular actin and determined its effect on the permeability of endothelial cell monolayers derived from porcine pulmonary arteries. The substrate for botulinum C2 toxin is nonmuscle monomeric actin which becomes ADPribosylated. This modified actin cannot participate in actin polymerization and, in addition, acts as a capping protein. Exposure of endothelial cell monolayers to botulinum C2 toxin resulted in a dose-(3-100 ng/ml) and time-dependent (30-120 min) increase in the hydraulic conductivity and decrease in the selecfivity ofthe cell monolayers. The effects ofC2 toxin were accompanied by a time-and dose-dependent increase in ADP-ribosylatin of G-actin. G-Actin content increased and F-actin content decreased time-and dose-dependently in C2 toxin-treated endothelial cells. Phalloidin which stabilizes filamentous actin prevented the effects of botulinum C2 toxin on endothelial permeability. Botulinum C2 toxin induced interendothelial gaps. The effects occurred in the absence of overt cell damage and were not reversible within 2 h. The data suggest that the endothelial microfilament system is important for the regulation ofendothelial permeability. (J. Clin. Invest. 1991. 87:1575-1584

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Pseudomonas aeruginosa cytotoxin stimulates prostacyclin production in cultured pulmonary artery endothelial cells: Membrane attack and calcium influx

Cited by 67 publications

References 37 publications

Contribution of an arsenal of virulence factors to pathogenesis of Pseudomonas aeruginosa infections

Contribution of an arsenal of virulence factors to pathogenesis of Pseudomonas aeruginosa infections

Closing in on the toxic domain through analysis of a variant Clostridium difficile cytotoxin B

Adenosine diphosphate-ribosylation of G-actin by botulinum C2 toxin increases endothelial permeability in vitro.

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