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- W2783010245 abstract "Ocean acidification (OA) and pathogenic diseases pose a considerable threat to key species of marine ecosystem. However, few studies have investigated the combined impact of reduced seawater pH and pathogen challenge on the immune responses of marine invertebrates. In this study, Pacific oysters, Crassostrea gigas, were exposed to OA (~2000 ppm) for 28 days and then challenged with Vibrio splendidus for another 72 h. Hemocyte parameters showed that V. splendidus infection exacerbated the impaired oyster immune responses under OA exposure. An iTRAQ-based quantitative proteomic analysis revealed that C. gigas responded differently to OA stress and V. splendidus challenge, alone or in combination. Generally, OA appears to act via a generalized stress response by causing oxidative stress, which could lead to cellular injury and cause disruption to the cytoskeleton, protein turnover, immune responses and energy metabolism. V. splendidus challenge in oysters could suppress the immune system directly and lead to a disturbed cytoskeleton structure, increased protein turnover and energy metabolism suppression, without causing oxidative stress. The combined OA- and V. splendidus-treated oysters ultimately presented a similar, but stronger proteomic response pattern compared with OA treatment alone. Overall, the impaired oyster immune functions caused by OA exposure may have increased the risk of V. splendidus infection. These results have important implications for the impact of OA on disease outbreaks in marine invertebrates, which would have significant economic and ecological repercussions." @default.
- W2783010245 created "2018-01-26" @default.
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- W2783010245 date "2018-06-01" @default.
- W2783010245 modified "2023-10-18" @default.
- W2783010245 title "CO2-induced ocean acidification impairs the immune function of the Pacific oyster against Vibrio splendidus challenge: An integrated study from a cellular and proteomic perspective" @default.
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- W2783010245 doi "https://doi.org/10.1016/j.scitotenv.2018.01.056" @default.
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