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

Abstract

Vibrio 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 (LD(50) (ORM4) = 2.5 x 10(2) 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 (LD(50) = 8.9 x 10(4) and 1.6 x 10(5) 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.

Characterization of abalone Haliotis tuberculata–Vibrio harveyi interactions in gill primary cultures

“…In vitro immunity assays based on hemocyte cultures allowed to evidence the antibacterial activity of abalone hemocytes exposed to Vibrio species (Vakalia and Benkendorff 2005;Dang et al 2011b;Travers et al 2009). Significant variations of antibacterial activity of hemocytes were observed depending on environmental conditions such as temperature, quality of seawater, diet, or spawning period (Travers et al 2008b;Mottin et al 2010;Dang et al 2011a, b).…”

“…Significant variations of antibacterial activity of hemocytes were observed depending on environmental conditions such as temperature, quality of seawater, diet, or spawning period (Travers et al 2008b;Mottin et al 2010;Dang et al 2011a, b). Furthermore, immune depression and antibacterial activity were reported in abalones affected by viruses or bacteria in hemolymph but also in the digestive gland (Travers et al 2009;Dang et al 2011a). …”

“…Since 1998, summer mass mortality outbreaks of the European abalone H. tuberculata reported along the north coast of Britanny (France) have been associated with Vibrio bacteria . Bacterial strains were isolated from both farmed and wild abalones, allowing in vivo and in vitro studies on the interactions between abalone H. tuberculata and V. harveyi Travers et al 2008bTravers et al , 2009. Vibrio harveyi is an opportunistic bacterium becoming pathogenic if immunity is compromised due to summer heat stress, poor water quality or reproduction period (Cheng et al 2004a, b;Vakalia and Benkendorff 2005;Hooper et al 2007;Travers et al 2008b;Mottin et al 2010;Dang et al 2011a, b;Latire et al 2012).…”

“…Antibacterial activity of abalone hemolymph has been demonstrated against Vibrio using in vitro assays (Vakalia and Benkendorff 2005;Travers et al 2009;Dang et al 2011a, b) such as phagocytosis, ROS activity or phenoloxidase activity, and secretion of antibacterial peptides or lipophilic antibacterial compounds. The immune response of abalone hemocytes has been previously shown to change according to the pathogenicity of bacterial strains (Travers et al 2009).…”

“…The immune response of abalone hemocytes has been previously shown to change according to the pathogenicity of bacterial strains (Travers et al 2009). Thus pathogen strains would be able to proliferate in contact with hemolymph avoiding phagocytosis and preventing immune response.…”