INVESTIGADORES
PARAJE Maria Gabriela
artículos
Título:
Nitric oxide-mediated apoptosis in rat macrophages
Autor/es:
JOSE´ LUIS BARONETTI, NATALIA ANGEL VILLEGAS, MARIA GABRIELA PARAJE AND INES ALBESA
Revista:
MICROBIOLOGY AND IMMUNOLOGY
Editorial:
WILEY-BLACKWELL PUBLISHING, INC
Referencias:
Lugar: Tokyo, Japan; Año: 2011 vol. 55 p. 231 - 238
ISSN:
0385-5600
Resumen:
ABSTRACT
Shiga toxin-producing Escherichia coli are important food-borne pathogens. Themain 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 andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
Peritoneal macrophages incubated in the presence of E. coli supernatants showed an increase in the
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
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 andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
Peritoneal macrophages incubated in the presence of E. coli supernatants showed an increase in the
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
Escherichia coli are important food-borne pathogens. Themain 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 andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
Peritoneal macrophages incubated in the presence of E. coli supernatants showed an increase in the
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
E. coli.
Peritoneal macrophages incubated in the presence of E. coli supernatants showed an increase in the
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
E. coli supernatants showed an increase in the
amounts of apoptosis andNOproduction. Furthermore, inhibition ofNOsynthesis 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.
apoptosis of macrophages.
E. coli supernatants or Stx2 induces NO-mediated
apoptosis of macrophages.
Key words Escherichia coli, hemolytic uremic syndrome, Shiga toxin 2.Escherichia coli, hemolytic uremic syndrome, Shiga toxin 2.