SOLA CLAUDIA DEL VALLE
Congresos y reuniones científicas
Título:
Staphylococcus aureus á-TOXIN ACTIVATES MAPKS AND
Autor/es:
MOYANO A.J; ANDREOLI, VERONICA; RACA AC; SOLA C; PANZETTA-DUTARI G; BOCCO JL
Lugar:
Potrero de los Funes, San Luis
Reunión:
Congreso; Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y. Biología Molecular (SAIB 2011).; 2011
Institución organizadora:
Sociedad Argentina de Investigación en Bioquímica y. Biología Molecular
Resumen:
The Staphylococcus aureus á-toxin is a key virulence factor
involved in the onset of diverse and often fatal infections, such us
necrotizing pneumonia. However, its molecular mechanisms are not
well understood. The biochemical response mediated by the main
group of Mitogen-Activated-Protein Kinases (MAPKs) JNK, p38
and ERK in A549 lung epithelial cells intoxicated with á-toxin was
analyzed. Distribution of c-Jun and KLF6 transcription factors,
which are key regulators of cell fate upon diverse stimuli, including
microbial infections was additionally investigated. Western-Blot
(WB) analyses of cells treated with S. aureus culture supernatants or
with purified á-toxin, showed the activation of the three MAPKs –
JNK, p38 and ERK – phenomenon which was not observed in cells
treated with supernatants from an isogenic á-toxin-deficient srain.
Pharmacological inhibition of MAPKs indicates that activation of
the three pathways were important for cell survival. Furthermore, á-
toxin increase phosphorylation and decreased the c-Jun protein
level. Finally, WB of nuclear and cytoplasmic fractions, as well as
confocal microscopy, showed that á-toxin provoked a fast decrease
of KLF6 at the nucleus, while gaining a more cytoplasmic
distribution. These results shed light on the role MAPKs pathways
and the involvement of c-Jun and KLF6 in the complex cell
response upon S. aureus á-toxin intoxication.
involved in the onset of diverse and often fatal infections, such us
necrotizing pneumonia. However, its molecular mechanisms are not
well understood. The biochemical response mediated by the main
group of Mitogen-Activated-Protein Kinases (MAPKs) JNK, p38
and ERK in A549 lung epithelial cells intoxicated with á-toxin was
analyzed. Distribution of c-Jun and KLF6 transcription factors,
which are key regulators of cell fate upon diverse stimuli, including
microbial infections was additionally investigated. Western-Blot
(WB) analyses of cells treated with S. aureus culture supernatants or
with purified á-toxin, showed the activation of the three MAPKs –
JNK, p38 and ERK – phenomenon which was not observed in cells
treated with supernatants from an isogenic á-toxin-deficient srain.
Pharmacological inhibition of MAPKs indicates that activation of
the three pathways were important for cell survival. Furthermore, á-
toxin increase phosphorylation and decreased the c-Jun protein
level. Finally, WB of nuclear and cytoplasmic fractions, as well as
confocal microscopy, showed that á-toxin provoked a fast decrease
of KLF6 at the nucleus, while gaining a more cytoplasmic
distribution. These results shed light on the role MAPKs pathways
and the involvement of c-Jun and KLF6 in the complex cell
response upon S. aureus á-toxin intoxication.
