Ocean acidification weakens the immune response of blood clam through hampering the NF-kappa beta and toll-like receptor pathways

The impact of pCO2 driven ocean acidification on marine bivalve immunity remains poorly understood. To date, this impact has only been investigated in a few bivalve species and the underlying molecular mechanism remains unknown. In the present study, the effects of the realistic future ocean pCO2 levels (pH at 8.1, 7.8, and 7.4) on the total number of haemocyte cells (THC), phagocytosis status, blood cell types composition, and expression levels of twelve genes from the NF-kappa beta signaling and toll-like receptor pathways of a typical bottom burrowing bivalve, blood clam (Tegillarca granosa), were investigated. The results obtained showed that while both THC number and phagocytosis frequency were significantly reduced, the percentage of red and basophil granulocytes were significantly decreased and increased, respectively, upon exposure to elevated pCO2. In addition, exposure to pCO2 acidified seawater generally led to a significant down-regulation in the inducer and key response genes of NF-kappa beta signaling and toll-like receptor pathways. The results of the present study revealed that ocean acidification may hamper immune responses of the bivalve T. granosa which subsequently render individuals more susceptible to pathogens attacks such as those from virus and bacteria.

由二氧化碳分压（pCO2）驱动的海洋酸化对海洋双壳类免疫功能的影响迄今仍不甚明确。截至目前，相关研究仅在少数双壳类物种中开展，其背后的分子机制仍未被揭示。本研究以典型底栖穴居双壳类——泥蚶（Tegillarca granosa）为研究对象，探究了未来现实情境下的海洋pCO2水平（对应海水pH分别为8.1、7.8和7.4）对其血淋巴细胞总数（THC）、吞噬状态、血细胞类型组成，以及核因子κB（NF-kappa beta）信号通路与toll样受体（toll-like receptor）通路中12个基因的表达水平的影响。研究结果显示，在高pCO2环境暴露下，血淋巴细胞总数与吞噬频率均显著降低，而红色粒细胞与嗜碱性粒细胞的占比则分别显著下降与上升。此外，暴露于pCO2酸化海水通常会导致核因子κB信号通路与toll样受体通路中的诱导基因及关键应答基因出现显著下调。本研究结果表明，海洋酸化可能会削弱泥蚶的免疫应答能力，进而使其个体更易遭受病毒、细菌等病原体的侵袭。