Mateus Ana Patrícia, Anjos Liliana, Cardoso João R, Power Deborah M
Comparative Molecular and Integrative Biology, Centro de Ciências do Mar, Universidade do Algarve, Campus de Gambelas, 8005-139 Faro, Portugal; Escola Superior de Saúde, Universidade do Algarve, Av. Dr. Adelino da Palma Carlos, 8000-510 Faro, Portugal.
Comparative Molecular and Integrative Biology, Centro de Ciências do Mar, Universidade do Algarve, Campus de Gambelas, 8005-139 Faro, Portugal.
Mol Immunol. 2017 Jul;87:267-283. doi: 10.1016/j.molimm.2017.04.008. Epub 2017 May 15.
Scale removal in fish triggers a damage-repair program to re-establish the lost epidermis and scale and an associated local immune response. In mammals, chronic stress is known to delay wound healing and to modulate the cutaneous stress axis, but this is unstudied in teleost fish the most successful extant vertebrates. The present study was designed to test the hypothesis that chronic stress impairs cutaneous repair in teleost fish as a consequence of suppression of the immune response. The hypothesis was tested by removing the scales and damaging the skin on one side of the body of fish previously exposed for 4 weeks to a chronic crowding stress and then evaluating cutaneous repair for 1 week. Scale removal caused the loss of the epidermis although at 3days it was re-established. At this stage the basement membrane was significantly thicker (p=0.038) and the hypodermis was significantly thinner (p=0.016) in the regenerating skin of stressed fish relative to the control fish. At 3days, stressed fish also had a significantly lower plasma osmolality (p=0.015) than control fish indicative of reduced barrier function. Chronic stress caused a significant down-regulation of the glucocorticoid receptor (gr) in skin before damage (time 0, p=0.005) and of star at 3 and 7days (p<0.05) after regeneration relative to control fish. In regenerating skin key transcripts of cutaneous repair, pcna, colivα1 and mmp9, and the inflammatory response, tgfβ1, csf-1r, mpo and crtac2, were down-regulated (p<0.05) by chronic stress. Irrespective of chronic stress and in contrast to intact skin many hyper pigmented masses, putative melanomacrophages, infiltrated the epidermis of regenerating skin. This study reveals that chronic stress suppresses the local immune response to scale removal and impairs the expression of key transcripts of wound healing. Elements of the stress axis were identified and modulated by chronic stress during cutaneous repair in gilthead seabream skin.
鱼类的鳞片脱落会触发一个损伤修复程序，以重新建立失去的表皮和鳞片以及相关的局部免疫反应。在哺乳动物中，已知慢性应激会延迟伤口愈合并调节皮肤应激轴，但在硬骨鱼（现存最成功的脊椎动物）中尚未对此进行研究。本研究旨在检验以下假设：慢性应激会因免疫反应受到抑制而损害硬骨鱼的皮肤修复。通过去除先前暴露于慢性拥挤应激4周的鱼体一侧的鳞片并损伤皮肤，然后评估1周的皮肤修复情况来验证该假设。鳞片去除导致表皮缺失，不过在3天时表皮得以重新建立。在此阶段，与对照鱼相比，应激鱼再生皮肤中的基底膜显著更厚（p = 0.038），皮下组织显著更薄（p = 0.016）。在3天时，应激鱼的血浆渗透压也显著低于对照鱼（p = 0.015），表明屏障功能降低。相对于对照鱼，慢性应激导致损伤前皮肤中的糖皮质激素受体（gr）显著下调（时间0，p = 0.005），再生后3天和7天时star也显著下调（p < 0.05）。在再生皮肤中，慢性应激使皮肤修复的关键转录本pcna、colivα1和mmp9以及炎症反应的关键转录本tgfβ1、csf - 1r、mpo和crtac2下调（p < 0.05）。无论是否存在慢性应激，与完整皮肤相反，许多色素沉着过度的团块（假定为黑素巨噬细胞）浸润了再生皮肤的表皮。本研究表明，慢性应激会抑制对鳞片去除的局部免疫反应，并损害伤口愈合关键转录本的表达。在金头鲷皮肤的皮肤修复过程中，慢性应激识别并调节了应激轴的组成部分。
