Nitric oxide-mediated apoptosis in rat macrophages subjected to Shiga toxin 2 from Escherichia coli.

Autor: Baronetti JL; Department of Pharmacy, Faculty of Chemical Sciences, National University of Córdoba, Haya de la Torre y Medina Allende, University Campus, 500 Córdoba, Argentina. jbaronetti@bioclin.fcq.unc.edu.ar, Villegas NA, Paraje MG, Albesa I
Jazyk: angličtina
Zdroj: Microbiology and immunology [Microbiol Immunol] 2011 Apr; Vol. 55 (4), pp. 231-8.
DOI: 10.1111/j.1348-0421.2011.00310.x
Abstrakt: Shiga toxin-producing Escherichia coli are important food-borne pathogens. The main factor conferring virulence on this bacterium is its capacity to secrete Shiga toxins (Stxs), which have been reported to induce apoptosis in several cell types. However, the mechanisms of this apoptosis have not yet been fully elucidated. In addition, Stxs have been shown to stimulate macrophages to produce nitric oxide (NO), a well-known apoptosis inductor.The aim of this study was to investigate the participation of NO in apoptosis of rat peritoneal macrophages induced by culture supernatants or Stx2 from E. coli. Peritoneal macrophages incubated in the presence of E. coli supernatants showed an increase in the amounts of apoptosis and NO production. Furthermore, inhibition of NO synthesis induced by addition of aminoguanidine (AG) was correlated with a reduction in the percentage of apoptotic cells, indicating participation of this metabolite in the apoptotic process. Similarly, treatment of cells with Stx2 induced an increase in NO production and amount of apoptosis, these changes being reversed by addition of AG. In summary, these data show that treatment with E. coli supernatants or Stx2 induces NO-mediated apoptosis of macrophages.
(© 2011 The Societies and Blackwell Publishing Asia Pty Ltd.)
Databáze: MEDLINE
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