Pathogenic <i>Vibrio harveyi</i>, in contrast to non‐pathogenic strains, intervenes with the p38 MAPK pathway to avoid an abalone haemocyte immune response

Journal of Cellular Biochemistry - Tập 106 Số 1 - Trang 152-160 - 2009
Marie‐Agnès Travers1,2, Ronan Le Bouffant3, Carolyn S. Friedman4, Florence Buzin1, Bertrand Cougard1, Sylvain Huchette2, Marcel Koken1, Christine Paillard1
1LEMAR - Laboratoire des Sciences de l'Environnement Marin (LEMAR) (IUEM Technopôle Brest-Iroise - rue Dumont d'Urville - 29280 Plouzané - FRANCE - France)
2Scea France Haliotis (Lieu dit Kerazan 29880 Plouguernau - France)
3UMR_S_566 - Gametogenèse et génotoxicité (CEA Route de Panorama 92265 FONTENAY-AUX-ROSES CEDEX - France)
4School of Aquatic and Fishery Sciences (University of Washington, Box 355020, Seattle, WA 98195 - United States)

Tóm tắt

AbstractVibrio harveyi is a marine bacterial pathogen responsible for episodic abalone epidemics associated with massive mortalities in France, Japan, and Australia. The aim of this study was the understanding of a possible role of the p38 MAPK in abalone haemocyte responses towards this bacterium. First, the pathogenicity of different V. harveyi strains was compared in both immersion and injection trials, and clear differences were detected. The three strains, ORM4, 04/092, and 05/053, all isolated from moribund abalone, induced up to 80% mortalities in immersion or injection challenges (LD50 (ORM4) = 2.5 × 102 CFU animal−1). The two strains, LMG 4044T and LMG 7890 were non‐pathogenic towards abalone in immersion trials, and needed very high numbers for killing by intramuscular injections (LD50 = 8.9 × 104 and 1.6 × 105 CFU animal−1, respectively). To start unraveling the mechanism explaining these differences, the p38‐MAPK, a keyplayer in antimicrobial immune response, was studied. The non‐pathogenic strain, LMG 7890 can be eliminated by abalone haemocytes and induces haemocyte phagocytosis and high ROS production. With different concentrations of a p38‐specific inhibitor, SB203580, p38 implication was shown. This inhibitor reduced phagocytosis and ROS induction leading to LMG 7890 proliferation. In the case of the pathogenic ORM4 which can not be eliminated by abalone haemocytes, no phagocytosis and ROS production was induced, and a retarded p38 activation was observed. Taken together, our results suggest that p38 MAPK modulation may be one of the ways of virulent V. harveyi to attack its host and escape abalone immune response. J. Cell. Biochem. 106: 152–160, 2009. © 2008 Wiley‐Liss, Inc.

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Thông tin xuất bản

Journal of Cellular Biochemistry

Tập 106 Số 1

152-160

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