TY - JOUR T1 - Inefficient immune response is associated with microbial permissiveness in juvenile oysters affected by mass mortalities on field A1 - de Lorgeril,Julien A1 - Escoubas,Jean Michel A1 - Loubiere,Vincent A1 - Pernet,Fabrice A1 - Le Gall,Patrik A1 - Vergnes,Agnes A1 - Aujoulat,Fabien A1 - Jeannot,Jean-Luc A1 - Jumas-Bilak,Estelle A1 - Got,Patrice A1 - Gueguen,Yannick A1 - Destoumieux-Garzon,Delphine A1 - Bachere,Evelyne AD - Univ Perpignan, Univ Montpellier, IHPE, CNRS,Ifremer, Via Domitia, Perpignan, France. AD - Ifremer, LEMAR UMR6539, CNRS UBO IRD Ifremer, F-29280 Plouzane, France. AD - CNRS IRD Ifremer UM, MARBEC UMR 9190, F-34203 Sete, France. AD - Univ Montpellier, CNRS, IRD, UMR HydroSci Montpellier 5569,Equipe Pathogens Hy, Montpellier, France. AD - CNRS IRD Ifremer UM, MARBEC UMR 9190, F-34095 Montpellier, France. AD - Univ Montpellier, CNRS, UMR 9002, Inst Human Genet, Montpellier, France. UR - https://doi.org/10.1016/j.fsi.2018.03.027 DO - 10.1016/j.fsi.2018.03.027 KW - Host pathogen interaction KW - Innate immunity KW - Invertebrate KW - Mollusk KW - In situ mortality KW - Total bacteria KW - Crassostrea gigas N2 - Since 2008, juvenile Crassostrea gigas oysters have suffered from massive mortalities in European farming areas. This disease of complex etiology is still incompletely understood. Triggered by an elevated seawater temperature, it has been associated to infections by a herpes virus named OsHV-1 as well as pathogenic vibrios of the Splendidus clade. Ruling out the complexity of the disease, most of our current knowledge has been acquired in controlled experiments. Among the many unsolved questions, it is still ignored what role immunity plays in the capacity oysters have to survive an infectious episode. Here we show that juvenile oysters susceptible to the disease mount an inefficient immune response associated with microbial permissiveness and death. We found that, in contrast to resistant adult oysters having survived an earlier episode of mortality, susceptible juvenile oysters never exposed to infectious episodes died by more than 90% in a field experiment. Susceptible oysters were heavily colonized by OsHV-1 herpes virus as well as bacteria including vibrios potentially pathogenic for oysters, which proliferated in oyster flesh and body fluids during the mortality event. Nonetheless, susceptible oysters were found to sense microbes as indicated by an overexpression of immune receptors and immune signaling pathways. However, they did not express important immune effectors involved in antimicrobial immunity and apoptosis and showed repressed expression of genes involved in ROS and metal homeostasis. This contrasted with resistant oysters, which expressed those important effectors, controlled bacterial and viral colonization and showed 100% survival to the mortality event. Altogether, our results demonstrate that the immune response mounted by susceptible oysters lacks some important immune functions and fails in controlling microbial proliferation. This study opens the way to more holistic studies on the “mass mortality syndrome”, which are now required to decipher the sequence of events leading to oyster mortalities and determine the relative weight of pathogens, oyster genetics and oyster-associated microbiota in the disease. Y1 - 2018/06 PB - Academic Press Ltd- Elsevier Science Ltd JF - Fish & Shellfish Immunology SN - 1050-4648 VL - 77 SP - 156 EP - 163 ID - 54470 ER -