Ocean Acidification Affects the Cytoskeleton, Lysozymes, and Nitric Oxide of Hemocytes: A Possible Explanation for the Hampered Phagocytosis in Blood Clams, Tegillarca granosa.
Ocean Acidification Affects the Cytoskeleton, Lysozymes, and Nitric Oxide of Hemocytes: A Possible Explanation for the Hampered Phagocytosis in Blood Clams, Tegillarca granosa.
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海洋酸化影响血细胞的细胞骨架、溶菌酶和一氧化氮：血蛤吞噬作用受阻的可能解释
DOI：
10.3389/fphys.2018.00619
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发表时间：
2018
影响因子：
4
通讯作者：
Liu G
中科院分区：
文献类型：
--
作者：
Su W;Rong J;Zha S;Yan M;Fang J;Liu G
大量人为排放的二氧化碳（CO2）被溶解到海洋中，导致海水pH值降低和化学性质变化，这被称为海洋酸化（OA）。pCO2驱动的酸化对免疫力的影响最近在各种海洋生物中被揭示出来。然而，导致吞噬作用降低的机制仍不清楚。因此，pCO2驱动的OA在目前和不久的将来的水平（pH值为8.1，7.8和7.4）的吞噬率，细胞骨架成分的丰度，一氧化氮（NO）的水平，和溶菌酶（LZM）的浓度和活性的血细胞的影响进行了研究，在商业双壳类，泥蚶（泥蚶）。此外，还分析了OA对调节肌动蛋白骨架和一氧化氮合成2（NOS 2）的基因表达的影响。结果表明，在pH值为7.4的未来OA情景中暴露2周后，血细胞的吞噬率、细胞骨架成分丰度、LZM浓度和活性均显著降低。相反，一个显着增加的浓度与对照组相比，检测到在蛤蜊暴露于OA。此外，调节肌动蛋白细胞骨架和NOS基因的表达显着上调后，OA暴露。虽然根据本研究和以前报道的结果，引起吞噬作用的机制似乎是复杂的，但我们的结果表明，OA可能通过（1）减少细胞骨架成分的丰度，从而阻碍细胞骨架介导的吞噬过程，（2）降低LZM的浓度和活性，并因此抑制被吞噬的病原体通过非氧依赖性途径的降解，和（3）诱导NO的产生，可能会对免疫反应产生负面影响
An enormous amount of anthropogenic carbon dioxide (CO2) has been dissolved into the ocean, leading to a lower pH and changes in the chemical properties of seawater, which has been termed ocean acidification (OA). The impacts of pCO2-driven acidification on immunity have been revealed recently in various marine organisms. However, the mechanism causing the reduction in phagocytosis still remains unclear. Therefore, the impacts of pCO2-driven OA at present and near-future levels (pH values of 8.1, 7.8, and 7.4) on the rate of phagocytosis, the abundance of cytoskeleton components, the levels of nitric oxide (NO), and the concentration and activity of lysozymes (LZM) of hemocytes were investigated in a commercial bivalve species, the blood clam (Tegillarca granosa). In addition, the effects of OA on the expression of genes regulating actin skeleton and nitric oxide synthesis 2 (NOS2) were also analyzed. The results obtained showed that the phagocytic rate, cytoskeleton component abundance, concentration and activity of LZM of hemocytes were all significantly reduced after a 2-week exposure to the future OA scenario of a pH of 7.4. On the contrary, a remarkable increase in the concentration of NO compared to that of the control was detected in clams exposed to OA. Furthermore, the expression of genes regulating the actin cytoskeleton and NOS were significantly up-regulated after OA exposure. Though the mechanism causing phagocytosis seemed to be complicated based on the results obtained in the present study and those reported previously, our results suggested that OA may reduce the phagocytosis of hemocytes by (1) decreasing the abundance of cytoskeleton components and therefore hampering the cytoskeleton-mediated process of engulfment, (2) reducing the concentration and activity of LZM and therefore constraining the degradation of the engulfed pathogen through an oxygen-independent pathway, and (3) inducing the production of NO, which may negatively regulate immune responses.
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