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Infection and Immunity, April 2001, p. 2675-2683, Vol. 69, No. 4
Department of Immunology, St. Jude
Children's Research Hospital, Memphis, Tennessee
38105,2 and Department of Physiology,
University of Tuebingen, 72076 Tuebingen, Germany1
Received 6 October 2000/Returned for modification 9 November
2000/Accepted 8 January 2001
Pseudomonas aeruginosa, a gram-negative facultative
pathogen, causes severe infections in immunocompromised and cystic
fibrosis patients. However, the molecular details of the interaction
between P. aeruginosa and mammalian cells are still largely
unknown. Here we demonstrate that infection of human conjunctiva
epithelial Chang cells with the well-characterized P. aeruginosa strain PAO-I results in rapid induction of apoptosis.
Apoptosis was mediated by mitochondrial alterations, in particular
mitochondrial depolarization, synthesis of reactive oxygen
intermediates, and release of cytochrome c, as well as an
activation of Jun N-terminal kinases (JNK). Stimulation of these events
was dependent on upregulation of CD95 on infected cells, and a
deficiency of CD95 or the CD95 ligand prevented mitochondrial changes,
JNK activation, and apoptosis upon infection. Further, efficient
apoptosis of Chang epithelial cells required infection with live
P. aeruginosa, adhesion but not invasion of the bacteria, and expression of the type III secretion system in PAO-I. The data
indicate a type III secretion system-dependent, sequential activation
of several signaling pathways by P. aeruginosa PAO-I, resulting in apoptosis of the infected cell.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.4.2675-2683.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Pseudomonas aeruginosa-Induced Apoptosis
Involves Mitochondria and Stress-Activated Protein Kinases
*
Corresponding author. Mailing address: Dept. of
Immunology, St. Jude Children's Research Hospital, 332 North
Lauderdale, Memphis, TN 38105. Phone: (901) 485-3085. Fax: (901)
495-3107. E-mail: erich.gulbins{at}stjude.org.
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