Biomedical Department, Scientific Center of Monaco, Monaco, Monaco.
LIA ROPSE, Laboratoire International Associé, Centre Scientifique de Monaco, Université Côte d'Azur, Nice, France.
Front Immunol. 2023 Nov 22;14:1292410. doi: 10.3389/fimmu.2023.1292410. eCollection 2023.
Climate change is increasing ocean temperatures and consequently impacts marine life (e.g., bacterial communities). In this context, studying host-pathogen interactions in marine organisms is becoming increasingly important, not only for ecological conservation, but also to reduce economic loss due to mass mortalities in cultured species. In this study, we used (), an anemone, as an emerging marine model to better understand the effect of rising temperatures on the infection induced by the pathogenic marine bacterium . The effect of temperature on was examined at 6, 24, or 30 h after bath inoculation with 10 CFU of expressing GFP (Vp-GFP) at 27°C (husbandry temperature) or 31°C (heat stress). Morphological observations of and their Hsps expression demonstrated heat stress induced increasing damage to anemones. The kinetics of the infections revealed that Vp-GFP were localized on the surface of the ectoderm and in the mucus during the first hours of infection and in the mesenterial filaments thereafter. To better identify the cells targeted by Vp-GFP infection, we used spectral flow cytometry. cell types were identified based on their autofluorescent properties. corresponding to different cell types (algae and cnidocytes). We identified an AF10 population whose autofluorescent spectrum was identical to that of human monocytes/macrophage, suggesting that this spectral print could be the hallmark of phagocytic cells called "amebocytes''. AF10 autofluorescent cells had a high capacity to phagocytize Vp-GFP, suggesting their possible role in fighting infection. This was confirmed by microscopy using sorted AF10 and GFP-positive cells (AF10+/GFP+). The number of AF10+/GFP+ cells were reduced at 31°C, demonstrating that increased temperature not only damages tissue but also affects the immune response of . In conclusion, our study provides a springboard for more comprehensive studies of immune defense in marine organisms and paves the way for future studies of the dynamics, activation patterns, and functional responses of immune cells when encountering pathogens.
气候变化正在使海洋温度升高，从而影响海洋生物（例如细菌群落）。在这种情况下，研究海洋生物中的宿主-病原体相互作用变得越来越重要，这不仅对生态保护具有重要意义，而且还有助于减少因养殖物种大量死亡而造成的经济损失。在这项研究中，我们使用（）作为一种新兴的海洋模式生物，以更好地了解温度升高对致病性海洋细菌感染的影响。在 27°C（养殖温度）或 31°C（热应激）下，用 10 CFU 表达 GFP 的 （Vp-GFP）对 进行浴接种后 6、24 或 30 小时，研究了温度对的影响。对 和它们的 Hsps 表达的形态学观察表明，热应激导致海葵受到越来越大的损伤。感染动力学研究表明，Vp-GFP 在感染的最初几个小时内定位于外胚层表面和粘液中，随后定位于中肠丝中。为了更好地识别 Vp-GFP 感染的 细胞，我们使用了光谱流式细胞术。根据细胞的自发荧光特性鉴定了 细胞类型。对应于不同的细胞类型（藻类和刺细胞）。我们鉴定了一个 AF10 群体，其自发荧光光谱与人类单核细胞/巨噬细胞的光谱完全相同，这表明该光谱特征可能是被称为“阿米巴细胞”的吞噬细胞的标志。AF10 自发荧光细胞具有高吞噬 Vp-GFP 的能力，这表明它们在抗感染中可能发挥作用。通过使用分选的 AF10 和 GFP 阳性细胞（AF10+/GFP+）进行显微镜观察证实了这一点。在 31°C 时，AF10+/GFP+细胞的数量减少，这表明高温不仅会损害组织，还会影响的免疫反应。总之，我们的研究为更全面地研究海洋生物的免疫防御提供了一个起点，并为未来研究免疫细胞在遇到病原体时的动态、激活模式和功能反应铺平了道路。
