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Skin damage caused by scale loss modifies the intestine of chronically stressed gilthead sea bream (Sparus aurata, L.)
Developmental & Comparative Immunology ( IF 2.9 ) Pub Date : 2020-12-29 , DOI: 10.1016/j.dci.2020.103989
Ana Patrícia Mateus 1 , Mona Mourad 2 , Deborah M Power 3
Affiliation  

The present study was designed to test if the damage caused by scale loss provokes a change in other innate immune barriers such as the intestine and how chronic stress affects this response. Sea bream (Sparus aurata) were kept in tanks at low density (16 kg m−3, LD) or exposed to a chronic high density (45 kg m−3, HD) stress for 4 weeks. Scales were then removed (approximately 50%) from the left flank in the LD and HD fish. Intestine samples (n = 8/group) were examined before and at 12 h, 3 days and 7 days after scale removal. Changes in the morphology of the intestine revealed that chronic stress and scale loss was associated with intestinal inflammation. Specifically, enterocyte height and the width of the lamina propria, submucosa and muscle layer were significantly increased (p < 0.05) 3 days after skin damage in fish under chronic stress (HD) compared to other treatments (LDWgut3d or HDgut0h). This was associated with a significant up-regulation (p < 0.05) in the intestine of gene transcripts for cell proliferation (pcna) and anti-inflammatory cytokine tgfβ1 and down-regulation of gene transcripts for the pro-inflammatory cytokines tnf-α and il1β (p < 0.05) in HD and LD fish 3 days after scale removal compared to the undamaged control (LDgut0h). Furthermore, a significant up-regulation of kit, a marker of mast cells, in the intestine of HDWgut3d and LDWgut3d fish suggests they may mediate the crosstalk between immune barriers. Skin damage induced an increase in cortisol levels in the anterior intestine in HDWgut12 h fish and significant (p < 0.05) down-regulation of mr expression, irrespective of stress. These results suggest glucocorticoid levels and signalling in the intestine of fish are modified by superficial cutaneous wounds and it likely modulates intestine inflammation.



中文翻译:

水垢损失引起的皮肤损伤会改变长期受压的金头鲷 (Sparus aurata, L.) 的肠道

本研究旨在测试由水垢损失引起的损害是否会引起肠道等其他先天免疫屏障的变化,以及慢性压力如何影响这种反应。海鲷 ( Sparus aurata ) 以低密度 (16 kg m -3 , LD) 保存在水箱中或长期暴露在高密度 (45 kg m -3, HD) 压力 4 周。然后从 LD 和 HD 鱼的左侧去除鳞片(约 50%)。在除垢前和 12 小时、3 天和 7 天检查肠道样本(n = 8/组)。肠道形态的变化表明,慢性压力和规模损失与肠道炎症有关。 具体而言,与其他处理(LDWgut3d 或 HDgut0h)相比,慢性应激(HD)下鱼的皮肤损伤 3 天后肠细胞高度和固有层、黏膜下层和肌肉层的宽度显着增加(p < 0.05)。 这与肠道中细胞增殖 ( pcna ) 和抗炎细胞因子的基因转录物显着上调 ( p < 0.05) 相关 与未受损的对照 (LDgut0h) 相比,去鳞后 3 天 HD 和 LD 鱼中tgfβ1和促炎细胞因子tnf-αil1β基因转录物的下调( p < 0.05)。此外,在 HDWgut3d 和 LDWgut3d 鱼的肠道中,肥大细胞标记物kit的显着上调表明它们可能介导免疫屏障之间的串扰。皮肤损伤导致 HDWgut12 h 鱼前肠皮质醇水平升高,mr显着下调 ( p  < 0.05)表达,与压力无关。这些结果表明,鱼肠道中的糖皮质激素水平和信号传导会受到浅表皮肤伤口的影响,并且它可能会调节肠道炎症。

更新日期:2021-01-06
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