Porin from Pseudomonas aeruginosa induces apoptosis in an epithelial cell line derived from rat seminal vesicles

Micromolar concentrations of porin, purified from the outer membranes of Pseudomonas aeruginosa, induced in vitro the classic morphological and biochemical signs of apoptosis in an epithelial cell line (SVC1) derived from the rat seminal vesicle secretory epithelium. The programmed cell death (PCD)...

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Bibliographic Details
Published in:Infection and immunity 1999-09, Vol.67 (9), p.4794-4800
Main Authors: BUOMMINO, E, MORELLI, F, METAFORA, S, ROSSANO, F, PERFETTO, B, BARONI, A, TUFANO, M. A
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Bacteriology
Biological and medical sciences
Calcium - metabolism
Cell Line
Cell Membrane - physiology
Epithelial Cells - pathology
Fundamental and applied biological sciences. Psychology
Humans
Male
Microbiology
Molecular and Cellular Pathogenesis
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Porins - metabolism
Porins - pharmacology
Proto-Oncogene Proteins c-myc - metabolism
Pseudomonas aeruginosa
Rats
Seminal Vesicles - pathology
Tumor Suppressor Protein p53 - metabolism
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Summary:Micromolar concentrations of porin, purified from the outer membranes of Pseudomonas aeruginosa, induced in vitro the classic morphological and biochemical signs of apoptosis in an epithelial cell line (SVC1) derived from the rat seminal vesicle secretory epithelium. The programmed cell death (PCD) was p53 independent and associated with significant decrease of bcl-2 expression, a marked increase of c-myc transcriptional activity, and an absence of the mRNA coding for tissue transglutaminase. The Ca(2+) influx, caused by the porin treatment of SVC1 cells, appears to play an important role in the triggering of apoptosis in our biological model. The possibility that the porin property of inducing PCD plays a role in the infertility of individuals chronically infected by gram-negative bacteria is discussed.
ISSN:0019-9567
1098-5522
DOI:10.1128/IAI.67.9.4794-4800.1999