In this work the mechanisms of transduction triggered in Mytilus galloprovincialis hemocytes by bacterial challenge were investigated in an in vitro model of infection of hemocyte monolayers with Escherichia coli. Western blot analyses of hemocyte extracts with phospho-specific anti-MAPK (Mitogen Activated Protein Kinase) antibodies indicate that E. coli induced a time dependent activation of different classes of MAPKs, mainly of the stress-activated p38 MAPK. P38 activation was confirmed by the use of the selective kinase inhibitor SB203580. Moreover, hemocyte pretreatment with SB203580 significantly reduced bacterial killing, whereas PD98059, an inhibitor of extracellularly regulated kinase (ERK) activation, was ineffective. Interestingly, the PI3-kinase (phosphatidylinositol-3-OH-kinase) inhibitor, Wortmannin, reduced both p38 activation and bacterial killing, indicating a critical role also for this lipid kinase in the hemocyte immune response.

Signaling pathways involved in the physiological response of mussel hemocytes to bacterial challenge: the role of stress-activated p38 MAP kinases / Laura Canesi;Michele Betti;Caterina Ciacci;Alfonso Scarpato;Barbara Citterio;Carla Pruzzo;Gabriella Gallo. - In: DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY. - ISSN 0145-305X. - STAMPA. - 26(2002), pp. 325-334.

Signaling pathways involved in the physiological response of mussel hemocytes to bacterial challenge: the role of stress-activated p38 MAP kinases

CANESI, LAURA;PRUZZO, CARLA;GALLO, GABRIELLA
2002

Abstract

In this work the mechanisms of transduction triggered in Mytilus galloprovincialis hemocytes by bacterial challenge were investigated in an in vitro model of infection of hemocyte monolayers with Escherichia coli. Western blot analyses of hemocyte extracts with phospho-specific anti-MAPK (Mitogen Activated Protein Kinase) antibodies indicate that E. coli induced a time dependent activation of different classes of MAPKs, mainly of the stress-activated p38 MAPK. P38 activation was confirmed by the use of the selective kinase inhibitor SB203580. Moreover, hemocyte pretreatment with SB203580 significantly reduced bacterial killing, whereas PD98059, an inhibitor of extracellularly regulated kinase (ERK) activation, was ineffective. Interestingly, the PI3-kinase (phosphatidylinositol-3-OH-kinase) inhibitor, Wortmannin, reduced both p38 activation and bacterial killing, indicating a critical role also for this lipid kinase in the hemocyte immune response.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11567/487718
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