BOCCO JOSE LUIS
Congresos y reuniones científicas
Título:
Integrity of JNK pathway is required to protect against cytoxicity triggered by Vibrio cholerae El Tor haemolysin.
Autor/es:
SAKA, HECTOR A.; ANDREOLI, VERONICA; SOLA CLAUDIA; BOCCO, JOSE LUIS
Lugar:
Pinamar, Buenos Aires. ARGENTINA
Reunión:
Congreso; XLI Reunión Anual de la Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular. 10th Congress Panamerican Association for Biochemistry and Molecular Biology. 20th Reunión Anual Sociedad Argentina de Neuroquímica.; 2005
Institución organizadora:
Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular.
Resumen:

In previous studies we have shown that El Tor Haemolysin (ETH), a highly conserved pore forming toxin secreted by most Vibrio cholerae (VC)isolates, could be involved in the pathogenesis of VC strains lacking cholera toxin. Additionally, we demonstrated that this toxin induces intracellular calcium increase and apoptosis in human intestinal cells.

It is well established that several MAPK pathways senses cell injuries caused by different bacterial toxins, leading to a protective response or to cell damage. Preliminary results suggested the induction of c-Jun activation upon cell exposure to ETH. Hence, to study the involvement of the JNK pathway in response to this toxin, we exposed human intestinal CaCo-2 cells to different doses of wt or ETH-defective mutant VC culture supernatants, or to purified ETH, in the presence or absence of the specific JNK inhibitor SP600125. After different times post-exposition, cell survival was determined. JNK blockade lead to decreased cell survival upon exposure to the toxin. Furthermore, the same result was observed using wt -MEF (Mouse Embryo Fibroblasts)and their JNK-deficient derivative cells in similar experiments. Moreover, ETH induced rapid c-Jun phosphorylation, indicating that the JNK/ c-Jun pathway is involved in cellular response to this toxin. Taken altogether, our results demonstrate that integrity of JNK pathway provides a cell protective response against cytotoxicity triggered by ETH.