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Interactions between Mytilus haemocytes and different strains of Escherichia coli and Vibrio cholerae O1 El Tor: role of kinase‐mediated signalling
Author(s) -
Canesi Laura,
Betti Michele,
Ciacci Caterina,
Lorusso Lucia Cecilia,
Gallo Gabriella,
Pruzzo Carla
Publication year - 2005
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2005.00499.x
Subject(s) - vibrio cholerae , biology , microbiology and biotechnology , escherichia coli , bacteria , hemolymph , mutant , vibrio , biochemistry , genetics , gene
Summary Marine bivalves accumulate large amounts of bacteria from the environment (mainly Vibrionaceae and coliforms). Although persistence of different bacteria in bivalve tissues largely depends on their sensitivity to the bactericidal activity of circulating haemocytes and haemolymph soluble factors, the mechanisms involved in bacteria–host cell interactions in these invertebrates are largely unknown. In the mussel Mytilus , differences in interactions between haemocytes and different Escherichia coli and Vibrio cholerae strains [ E. coli MG155, a wild‐type strain carrying type 1 fimbriae, and its unfimbriated derivative, AAEC072 Δ fim ; V. cholerae O1 El Tor biotype strain N16961, carrying the mannose‐sensitive haemagglutinin (MSHA), and its MSHA mutant] lead to differences in bactericidal activity in the presence of serum. Here we show that different bacteria induced distinct patterns of phosphorylation of mitogen‐activated protein kinases (MAPKs), in particular of the stress‐activated MAPKs involved in the immune response. Differences in phosphorylation of PKC‐like proteins were also observed. The results support the hypothesis that, like in mammalian host cells, different bacteria can modulate the signalling pathways of mussel haemocytes. The lower anti‐bacterial activity towards the mutant E. coli strain and wild‐type V. cholerae compared with wild E. coli may result from a reduced capacity of activating MAPKs. Moreover, the mutant V. cholerae strain that was the most resistant to the haemocyte bactericidal activity induced downregulation of cell signalling and showed the strongest effect on lysosomal membrane stability, evaluated as a marker of bivalve cell stress. These data suggest that certain bacteria could evade the bactericidal activity of mussel haemocytes through disruption of the host signalling pathways.

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